FB2025_01 , released February 20, 2025
Gene: Dmel\Ras85D
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General Information
Symbol
Dmel\Ras85D
Species
D. melanogaster
Name
Ras oncogene at 85D
Annotation Symbol
CG9375
Feature Type
FlyBase ID
FBgn0003205
Gene Model Status
Stock Availability
Gene Summary
Ras oncogene at 85D (Ras85D) encodes a protein that acts downstream of several cell signals, most notably from Receptor Tyrosine Kinases, to regulate tissue growth and development. When abnormally activated it can direct developmental defects and tissue hyperplasia, mimicking aspects of human disease including Rasopathies and cancer, respectively. [Date last reviewed: 2019-03-14] (FlyBase Gene Snapshot)
Also Known As

Ras, Ras1, Dras1, RasV12, dRas

Key Links
Genomic Location
Cytogenetic map
Sequence location
Recombination map
3-48
RefSeq locus
NT_033777 REGION:9510561..9513067
Sequence
Genomic Maps
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
Gene Ontology (GO) Annotations (77 terms)
Molecular Function (7 terms)
Terms Based on Experimental Evidence (5 terms)
CV Term
Evidence
References
inferred from direct assay
inferred from direct assay
inferred from physical interaction with FLYBASE:spri; FB:FBgn0085443
inferred from physical interaction with FLYBASE:Rgl; FB:FBgn0026376
inferred from direct assay
Terms Based on Predictions or Assertions (3 terms)
CV Term
Evidence
References
enables GDP binding
inferred from biological aspect of ancestor with PANTHER:PTN000631348
enables GTP binding
inferred from biological aspect of ancestor with PANTHER:PTN000631348
inferred from biological aspect of ancestor with PANTHER:PTN000631348
inferred from electronic annotation with InterPro:IPR001806
Biological Process (68 terms)
Terms Based on Experimental Evidence (67 terms)
CV Term
Evidence
References
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
involved_in dorsal closure
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:btl; FB:FBgn0285896
inferred from mutant phenotype
involved_in gastrulation
inferred from mutant phenotype
involved_in hemocyte migration
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from expression pattern
inferred from mutant phenotype
involved_in MAPK cascade
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:htl; FB:FBgn0010389
involved_in metamorphosis
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:htl; FB:FBgn0010389
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:egr; FB:FBgn0033483
inferred from genetic interaction with FLYBASE:hid; FB:FBgn0003997
inferred from genetic interaction with FLYBASE:rpr; FB:FBgn0011706
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with UniProtKB:P51023
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:rho; FB:FBgn0004635
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:l(2)gl; FB:FBgn0002121
inferred from genetic interaction with FLYBASE:scrib; FB:FBgn0263289
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:csw; FB:FBgn0000382,FLYBASE:sev; FB:FBgn0003366
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from high throughput genetic interaction with FLYBASE:Ras85D; FB:FBgn0003205
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:scrib; FB:FBgn0263289
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:tor; FB:FBgn0003733
inferred from genetic interaction with FLYBASE:14-3-3ζ; FB:FBgn0004907
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
Terms Based on Predictions or Assertions (3 terms)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN008604616
inferred from electronic annotation with InterPro:IPR020849
Cellular Component (2 terms)
Terms Based on Experimental Evidence (2 terms)
CV Term
Evidence
References
located_in membrane
inferred from direct assay
located_in plasma membrane
inferred from direct assay
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
located_in membrane
inferred from electronic annotation with InterPro:IPR020849
is_active_in plasma membrane
inferred from biological aspect of ancestor with PANTHER:PTN000631348
Gene Group (FlyBase)
Protein Family (UniProt)
Belongs to the small GTPase superfamily. Ras family. (P08646)
Catalytic Activity (EC/Rhea)
GTPase activity
RHEA 19669:
Summaries
Gene Snapshot
Ras oncogene at 85D (Ras85D) encodes a protein that acts downstream of several cell signals, most notably from Receptor Tyrosine Kinases, to regulate tissue growth and development. When abnormally activated it can direct developmental defects and tissue hyperplasia, mimicking aspects of human disease including Rasopathies and cancer, respectively. [Date last reviewed: 2019-03-14]
Gene Group (FlyBase)
RAS GTPASES -
The Ras family are members of the Ras superfamily of small GTPases. Ras proteins act in signal transduction cascades, generally the activated GTPase recruits and activates downstream effectors. Members this family are typically membrane-associated via isoprenylation of a CaaX motif in the C-terminus. (Adapted from PMID:15731001).
Pathway (FlyBase)
Torso Signaling Pathway Core Components -
The formation of Drosophila embryonic termini is controlled by the localized activation of Torso (tor) receptor tyrosine kinase. The Torso signaling pathway acts via the canonical Ras/Raf/MAP kinase cascade. (Adapted from FBrf0157176.)
Sevenless Signaling Pathway Core Components -
The specification of the R7 photoreceptor cell in each ommatidium of the developing Drosophila eye is dependent on activation of Sevenless receptor tyrosine kinase, which acts via the canonical Ras/Raf/MAP kinase cascade to promote the expression of lz and pros. sev, expressed in presumptive R7 cells, is activated by binding to Bride of Sevenless (boss), a seven-transmembrane protein expressed in R8 cells. (Adapted from FBrf0127283 and FBrf0221727).
EGFR Signaling Pathway Core Components -
The Epidermal Growth Factor Receptor (EGFR) signaling pathway is used multiple times during development (FBrf0190321). It is activated by the binding of a secreted ligand to the receptor tyrosine kinase Egfr and acts via the canonical Ras/Raf/MAP kinase (ERK) cascade. (Adapted from FBrf0190321 and FBrf0221727).
FGFR Signaling Pathway Core Components -
Fibroblast Growth Factor Receptor (FGFR) signaling pathway is initiated by the binding of secreted FGFs - bnl or ths/pyr to receptor tyrosine kinases btl or htl, respectively, to initiate signaling primarily via the canonical Ras/Raf/MAP kinase (ERK) cascade. (Adapted from FBrf0221038).
Pvr Signaling Pathway Core Components -
PDGF/VEGF (Platelet-Derived Growth Factor/Vascular Endothelial Growth Factor)-receptor related (Pvr) encodes a receptor tyrosine kinase activated by the binding of PDGF- and VEGF-related factors (Pvf1,Pvf2 or Pvf3). Pvr has been shown to activate the canonical Ras/Raf/MAP kinase (ERK) cascade, the PI3K kinase pathway, TORC1 (FBrf0222697), Rho family small GTPases (FBrf0221764, FBrf0180198) and the JNK cascade (FBrf0180198), in a context-dependent manner. (Adapted from FBrf0222697 and FBrf0221727).
Protein Function (UniProtKB)
Ras proteins bind GDP/GTP and possess intrinsic GTPase activity (By similarity). Plays a role in eye development by regulating cell growth, survival of postmitotic ommatidial cells and differentiation of photoreceptor cells (PubMed:11290305). During larval development, mediates Ptth/tor signaling leading to the production of ecdysone, a hormone required for the initiation of metamorphosis (PubMed:19965758).
(UniProt, P08646)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
Ras1: Ras proto-oncogene sequence
Codes for a polypeptide of 21.6 kilodaltons; residues 1-121 and 137-64 exhibit 75% homology with vertebrate H-ras protein.
Summary (Interactive Fly)

ras homolog - establishes follicular cell fate during oogenesis, functions in Torso signal transduction, functions downstream EGF-R in the establishment of ventral ectoderm fate, functions downstream of Breathless in tracheal and midline glia migration, functions downstream of FGF receptor in muscle precursors and in the central nervous system, functions downstream of the EGF-R and Sevenless in differentiation in photoreceptors

Gene Model and Products
Number of Transcripts
1
Number of Unique Polypeptides
1

Please see the JBrowse view of Dmel\Ras85D for information on other features

To submit a correction to a gene model please use the Contact FlyBase form

Protein Domains (via Pfam)
Isoform displayed:
Pfam protein domains
InterPro name
classification
start
end
Protein Domains (via SMART)
Isoform displayed:
SMART protein domains
InterPro name
classification
start
end
Structure
Protein 3D structure   (Predicted by AlphaFold)   (AlphaFold entry P08646)

If you don't see a structure in the viewer, refresh your browser.
Model Confidence:
  • Very high (pLDDT > 90)
  • Confident (90 > pLDDT > 70)
  • Low (70 > pLDDT > 50)
  • Very low (pLDDT < 50)

AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.

Experimentally Determined Structures
Crossreferences
Comments on Gene Model

Gene model reviewed during 5.41

Annotated transcripts do not represent all supported alternative splices within 5' UTR.

Low-frequency RNA-Seq exon junction(s) not annotated.

Gene model reviewed during 5.47

Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0082122
1958
189
Additional Transcript Data and Comments
Reported size (kB)

2.0, 1.3 (northern blot)

1.3 (northern blot)

Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
UniProt
RefSeq ID
GenBank
FBpp0081600
21.6
189
8.01
Polypeptides with Identical Sequences

There is only one protein coding transcript and one polypeptide associated with this gene

Additional Polypeptide Data and Comments
Reported size (kDa)
Comments
External Data
Crossreferences
Linkouts
Sequences Consistent with the Gene Model
Nucleotide / Polypeptide Records
 
Mapped Features

Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Ras85D using the Feature Mapper tool.

External Data
Crossreferences
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
Linkouts
Expression Data
Testis-specificity index

The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).

-1.05

Transcript Expression
Polypeptide Expression
mass spectroscopy
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
Marker for
 
Subcellular Localization
CV Term
Evidence
References
located_in membrane
inferred from direct assay
located_in plasma membrane
inferred from direct assay
Expression Deduced from Reporters
High-Throughput Expression Data
Associated Tools

JBrowse - Visual display of RNA-Seq signals

View Dmel\Ras85D in JBrowse
RNA-Seq by Region - Search RNA-Seq expression levels by exon or genomic region
Reference
See Gelbart and Emmert, 2013 for analysis details and data files for all genes.
Developmental Proteome: Life Cycle
Developmental Proteome: Embryogenesis
External Data and Images
Linkouts
BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
Images
Alleles, Insertions, Transgenic Constructs, and Aberrations
Classical and Insertion Alleles ( 64 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 93 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of Ras85D
Transgenic constructs containing regulatory region of Ras85D
Aberrations (Deficiencies and Duplications) ( 5 )
Variants
Variant Molecular Consequences
Alleles Representing Disease-Implicated Variants
Phenotypes
For more details about a specific phenotype click on the relevant allele symbol.
Lethality
Allele
Sterility
Allele
Other Phenotypes
Allele
Phenotype manifest in
Allele
dorsal mesothoracic disc & peripodial epithelium | somatic clone, with Scer\GAL4αTub84B.PL
eye disc & photoreceptor cell, with Scer\GAL4Act5C.PP
glial cell & antennal disc, with Scer\GAL4hs.PB
larval optic lobe & glial cell | somatic clone | cell non-autonomous, with Scer\GAL4αTub84B.PP
medulla cortex & glial cell | somatic clone | cell non-autonomous, with Scer\GAL4αTub84B.PP
mesothoracic tarsal segment 1 & bract
mesothoracic tarsal segment 1 & bract | ectopic
mesothoracic tergum & macrochaeta | ectopic, with Scer\GAL4sca-C253
mesothoracic tergum & macrochaeta | supernumerary, with Scer\GAL4sca-C253
muscle founder cell & visceral muscle primordium | ectopic, with Scer\GAL4twi.2PE
photoreceptor cell & axon & eye disc, with Scer\GAL4bi-omb-Gal4
sensory neuron & axon & embryo, with Scer\GAL4repo
subretinal glial cell & eye disc, with Scer\GAL4bi-omb-Gal4
subretinal glial cell & larval optic stalk, with Scer\GAL4bi-omb-Gal4
Orthologs
Human Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Homo sapiens (Human) (63)
12 of 14
Yes
Yes
3  
12 of 14
Yes
Yes
2  
11 of 14
No
Yes
5 of 14
No
No
2  
4 of 14
No
No
3  
4 of 14
No
No
3  
4 of 14
No
No
3 of 14
No
Yes
3 of 14
No
Yes
3 of 14
No
No
1  
3 of 14
No
No
1  
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
2 of 14
No
No
1  
2 of 14
No
No
1  
2 of 14
No
No
2 of 14
No
No
1  
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1  
2 of 14
No
No
1  
2 of 14
No
No
1  
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1  
2 of 14
No
No
2 of 14
No
No
1  
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
5  
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
Model Organism Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Rattus norvegicus (Norway rat) (33)
12 of 14
Yes
Yes
11 of 14
No
Yes
11 of 14
No
Yes
5 of 14
No
No
4 of 14
No
Yes
4 of 14
No
No
4 of 14
No
No
4 of 14
No
No
3 of 14
No
Yes
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
Mus musculus (laboratory mouse) (36)
12 of 14
Yes
Yes
12 of 14
Yes
Yes
11 of 14
No
Yes
5 of 14
No
No
4 of 14
No
Yes
4 of 14
No
No
4 of 14
No
No
4 of 14
No
No
3 of 14
No
Yes
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
Xenopus tropicalis (Western clawed frog) (44)
10 of 13
Yes
Yes
9 of 13
No
Yes
7 of 13
No
Yes
4 of 13
No
Yes
3 of 13
No
No
2 of 13
No
No
2 of 13
No
No
2 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
Danio rerio (Zebrafish) (43)
12 of 14
Yes
Yes
12 of 14
Yes
Yes
12 of 14
Yes
Yes
11 of 14
No
Yes
11 of 14
No
Yes
5 of 14
No
No
4 of 14
No
No
4 of 14
No
No
4 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
Caenorhabditis elegans (Nematode, roundworm) (31)
13 of 14
Yes
Yes
4 of 14
No
No
4 of 14
No
No
3 of 14
No
No
3 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
Anopheles gambiae (African malaria mosquito) (27)
11 of 12
Yes
Yes
Arabidopsis thaliana (thale-cress) (18)
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
Saccharomyces cerevisiae (Brewer's yeast) (9)
6 of 13
Yes
No
6 of 13
Yes
No
4 of 13
No
No
2 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
Schizosaccharomyces pombe (Fission yeast) (2)
6 of 12
Yes
No
1 of 12
No
No
Escherichia coli (enterobacterium) (0)
Other Organism Orthologs (via OrthoDB)
Data provided directly from OrthoDB:Ras85D. Refer to their site for version information.
Paralogs
Paralogs (via DIOPT v9.1)
Drosophila melanogaster (Fruit fly) (27)
8 of 13
7 of 13
6 of 13
5 of 13
5 of 13
4 of 13
4 of 13
4 of 13
3 of 13
3 of 13
3 of 13
3 of 13
3 of 13
3 of 13
2 of 13
2 of 13
2 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
Human Disease Associations
FlyBase Human Disease Model Reports
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 16 )
Allele
Disease
Evidence
References
model of  cancer
Potential Models Based on Orthology ( 26 )
Human Ortholog
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 18 )
Allele
Disease
Interaction
References
model of  cancer
is exacerbated by ITPUAS.F
model of  cancer
is ameliorated by InRGL00139
is ameliorated by InRJF01183
is ameliorated by InRJF01482
is ameliorated by NetBΔ
is ameliorated by NetBKK103672
is ameliorated by unc-5MI04273
is ameliorated by bskDN.UAS
is ameliorated by bskHMS00777
is exacerbated by hepAct.UAS
is exacerbated by imdUAS.cGa
is ameliorated by JraNIG.2275R
is ameliorated by TimpUAS.cPa
ameliorates  cancer
model of  kidney cancer
is ameliorated by Pka-C1B3
is ameliorated by mTorΔP
model of  cancer
is exacerbated by exe1
is exacerbated by Ptp61FΔ
is exacerbated by M6W186stop
is ameliorated by Ptip3804
is exacerbated by p53UAS.cUa
is ameliorated by Ilp8MI00727
Disease Associations of Human Orthologs (via DIOPT v9.1 and OMIM)
Note that ortholog calls supported by only 1 or 2 algorithms (DIOPT score < 3) are not shown.
Homo sapiens (Human)
Gene name
Score
OMIM
OMIM Phenotype
DO term
Complementation?
Transgene?
Functional Complementation Data
Functional complementation data is computed by FlyBase using a combination of the orthology data obtained from DIOPT and OrthoDB and the allele-level genetic interaction data curated from the literature.
Interactions
Summary of Physical Interactions
esyN Network Diagram
Show neighbor-neighbor interactions:
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(data from AllianceMine provided by esyN)
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Protein
RNA
Selected Interactor(s)
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Please see the Physical Interaction reports below for full details
protein-protein
Physical Interaction
Assay
References
Summary of Genetic Interactions
esyN Network Diagram
Show/hide secondary interactors 
(data from AllianceMine provided by esyN)
esyN Network Key:
Suppression
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Please look at the allele data for full details of the genetic interactions
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
External Data
Linkouts
BioGRID - A database of protein and genetic interactions.
DroID - A comprehensive database of gene and protein interactions.
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
Pathways
Signaling Pathways (FlyBase)
Metabolic Pathways
FlyBase
External Links
External Data
Linkouts
SignaLink - A signaling pathway resource with multi-layered regulatory networks.
Class of Gene
Genomic Location and Detailed Mapping Data
Chromosome (arm)
3R
Recombination map
3-48
Cytogenetic map
Sequence location
FlyBase Computed Cytological Location
Cytogenetic map
Evidence for location
85D19-85D19
Limits computationally determined from genome sequence between P{PZ}ps10615&P{PZ}Ras85D06677 and P{EP}CG9393EP3122
Experimentally Determined Cytological Location
Cytogenetic map
Notes
References
85D18-85D20
(determined by in situ hybridisation)
85D10-85D10
(determined by in situ hybridisation)
85D-85D
(determined by in situ hybridisation)
Experimentally Determined Recombination Data
Left of (cM)
Right of (cM)
Notes
Stocks and Reagents
Stocks (278)
Genomic Clones (15)
 

Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete

cDNA Clones (156)
 

Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.

cDNA clones, fully sequenced
BDGP DGC clones
Other clones
Drosophila Genomics Resource Center cDNA clones

For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.

cDNA Clones, End Sequenced (ESTs)
Other clones
RNAi and Array Information
Linkouts
DRSC - Results frm RNAi screens
Antibody Information
Laboratory Generated Antibodies
Commercially Available Antibodies
 
Cell Line Information
Other Comments

dsRNA made from templates generated with primers directed against this gene.

Ras85D plays a role in the regulation of compartment size in embryos.

dsRNA has been made from templates generated with primers directed against this gene.

Ras85D activity in the prothoracic gland regulates body size and the duration of each larval stage by regulating ecdysone release.

dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.

Area matching Drosophila EST AA141103.

Ras85D controls growth, survival and differentiation in the eye. These three functions are mediated by distinct thresholds of MAPK activity.

Ras85D functions in the developing wing to regulate cellular growth.

Ras85D-mediated signalling pathways are not influenced by R levels. Ras85D and R seem to function via distinct pathways.

The N-terminal portion of the cnk protein strongly cooperates with Ras85D, whereas the C-terminal portion efficiently blocks Ras85D (Ras) and phl (Raf) signalling when overexpressed in the eye. Two domains in the N-terminal portion of cnk are critical for cooperation with Ras85D. cnk functions in more than one pathway downstream of Ras85D.

Activation of the Egfr/Ras85D/rl pathway specifically inhibits the proapoptotic activity of W.

The MAPK cascade is required for Ras85D mitogenic response, loss of function mutations in phl, Dsor1, rl and ksr dominantly suppress hyperplastic growth, as do mutations in the Ras85D effector loop that disrupt the Ras85D-phl interaction.

Ectopic expression of activated Ras85D during imaginal disc development is sufficient to drive cell proliferation and causes hyperplastic growth of imaginal discs. Activated Ras85D induces hyperplasia of both the eye imaginal disc and the adult eye when expressed under the control of an ey enhancer fragment. In addition activated Ras85D causes non-autonomous cell death in imaginal discs and at high expression levels can lead to the complete ablation of the adult eye.

Ras85D functions as a potent negative regulator of apoptosis, acting by downregulating the proapoptotic activity of W. Egfr activation of Ras85D is required for cell survival in the embryo.

The role of Ras85D in phl activation is not limited to the translocation of phl to the membrane through a Ras85D-phl association. Ras85D is essential for the activation of an additional factor which in turn activates phl.

The signal promoting survival of cells in the interommatidial lattice is part of a balance between N and Ras85D pathways, which appear to act in opposition to regulate the number of interommatidial cells permitted to remain. Ras signalling promotes the 2o/3o pigment cell fate at the expense of programmed cell death in the interommatidial lattice.

Ras85D has a novel signaling function that prevents programmed cell death in the eye.

Ras85D is a positive modifier of pb activity, while the Ras85D-antagonist Gap1 has an opposite effect. Ras85D+ activity also modulates Scr and Ubx function.

Genetic studies indicate that 14-3-3ζ acts downstream of Ras85D and upstream of phl in the developing eye disc.

Expression of Ras85D at different times during oogenesis suggests transient Ras85D activity early in oogenesis is sufficient to cause anterior follicle cells to express posterior follicle cell markers, but is not sufficient to inhibit anterior follicle cell differentiation. Ras85D activity later in oogenesis did inhibit anterior follicle cell differentiation, antagonising the expression and activity of the slbo gene. Therefore, it appears that a sustained Ras85D signal is required first to initiate posterior follicle cell differentiation and subsequently to inhibit anterior follicle cell differentiation.

Analysis of genetic interactions among faf and R and Ras85D reveals that in addition to its critical role anterior to the morphogenetic furrow, faf has a function in undifferentiated cells alter in eye development that involves, probably indirectly, Ras85D and R. These results suggest that cells outside the facet influence cell fates within the facet.

The mechanism by which cno product controls cone cell formation in the developing compound eye is studied.

Shows no genetic interaction with sdk.

Ras85D function is required for the determination and differentiation of the midline glia.

The csw SH2-containing tyrosine phosphatase is required during signalling by sev, Ras85D and phl.

Targetted mesodermal expression of an activated form of Ras85D partially rescues the htl mutant phenotype.

Inactivated mutations of Ras85D enhance the P{sevhs-cswCS} phenotype.

A dominant mutation in Ras85D has been used as a starting point to identify mutations in genes functioning downstream of the Ras85D function.

pros gene becomes transcriptionally activated at a low level in all sev-competent cells prior to sev signaling and this requires the activities of Ras85D and two ETS transcription factors, aop and pnt. Restriction of high level pros expression to the R7 cell appears as a subsequent event, which requires sev activation of the Ras85D kinase pathway.

dos functions upstream or independent of Ras85D and defines a signalling pathway that is independent of direct binding of the drk SH2/SH3 adaptor protein to the sev receptor tyrosine kinase.

Studies of interaction between argos and members of the Ras/MAPK pathway demonstrate the argos gene product is a negative regulator of signal transduction that acts upstream of the Ras/MAPK cascade.

Ras85D is required early and late in oogenesis and to determine the dorsoventral fate of the embryo in addition to that of the eggshell. Double mutant analysis demonstrates a role for Ras85D gene product downstream of Egfr.

The mts product positively and negatively regulates Ras85D-mediated photoreceptor development.

Loss of function alleles of Ras85D are enhancers of the cswEsev1A-3EC.sev and cswEsev1A-eOP.sev phenotype.

Genetic data suggest phyl acts downstream of Ras85D, phl and aop to promote neuronal differentiation in R1, R6 and R7. Ectopic expression of phyl in the cone cell precursors mimics the effect of ectopic activation of Ras85D suggesting that phyl expression is regulated by Ras85D.

Ras85D is proposed to be an activator in longitudinal vein formation. There is a distinct signalling pathway activated by Egfr that interacts with Ras85D signal transduction cascade to induce crossvein formation in the wing that might be used for signalling processes elsewhere in the developing fly.

phl can be activated by tor in the complete absence of Ras85D, phl can be activated by RPTK in a Ras-independent pathway.

phl can be activated by tor in the complete absence of Ras85D function.

Ras CAAX peptidomimetic treatment rescues the activated Ras85D eye phenotype by suppressing the formation of supernumerary R7 cells in the compound eye. Suppression requires the CAAX element.

The N-terminal drk SH3 domain is primarily responsible for binding to the tail of the Sos product in vitro, and for signalling to the Ras85D product in vivo.

A screen to identify mutations affecting the Ras85D signalling pathway identified alleles of phl, Dsor1, rl, aop, βggt-I, mts, ksr and phyl.

Synaptic current and modulation of K+ current triggered by Pacap38 are mediated by coactivation of the Ras/Raf (Ras85D/phl) and rut cyclase pathways.

Genetic analysis suggests that pnt is a downstream effector of Ras85D.

Dosage-dependent genetic interaction between S and sev, Ras85D and Sos (involved in receptor tyrosine kinase signalling) supports a role for S in cell-cell signalling.

Heat shock induced expression, embryonic injection and female mosaic analysis demonstrates that Ras85D and its positive regulator Sos are involved in the tor signalling pathway.

rho gene product acts synergistically with Egfr signalling components.

The phl serine/threonine kinase plays a crucial role in the R7 pathway: genetic evidence suggests that phl acts downstream of Ras85D and upstream of sina in the sev R7 signal transduction pathway.

Ras85D activation may account for all the signalling action of the sev gene product. An activated Ras85DV12 protein can rescue the normal R7 precursor from transformation into a cone cell in sev and boss mutants and induces the formation of supernumerary R7 cells.

Ras85D is required for photoreceptor development, acts in the developing R7 cell to attenuate the signalling by the sev gene product and is a suppressor of the Egfr phenotype to restore the eye to a nearly normal appearance.

The transcription pattern of Ras85D was analyzed in neuroblasts derived from tumerous larval brain of l(2)gl larvae and S2 tissue culture cells. Ras85D expresses constitutive as well as maternal/embryonic-specific transcripts.

Ras85D has been cloned and sequenced.

Codes for a polypeptide of 21.6 kilodaltons; residues 1-121 and 137-64 exhibit 75% homology with vertebrate H-ras protein.

Relationship to Other Genes
Source for database merge of

Source for merge of: Ras85D l(3)06677

Additional comments

Loss-of-function mutations are homozygous lethal; enhance sev and EgfrE1 in heterozygotes (M. Simon).

Nomenclature History
Source for database identify of
Nomenclature comments
Etymology
Synonyms and Secondary IDs (61)
Reported As
Symbol Synonym
C-ras1
DRas85D/Ras
Dm Ras1
Dmras85D
Ras
(Fangninou et al., 2024, Fischer et al., 2024, Fukuda et al., 2024, Karunaraj et al., 2024, Leung et al., 2024, Li et al., 2024, Aida et al., 2023, Cabrera et al., 2023, Colombani and Andersen, 2023, Deng et al., 2023, Fangninou et al., 2023, Kim et al., 2023, Parisi et al., 2023, Shimell and O'Connor, 2023, Zheng et al., 2023, Almeida Machado Costa et al., 2022, Cuevas-Navarro et al., 2022, Ding et al., 2022, Enomoto and Igaki, 2022, Jiang et al., 2022, Kim et al., 2022, Marchetti et al., 2022, Ohhara et al., 2022, Thangadurai et al., 2022, Tsai et al., 2022, Wang et al., 2022, Weina et al., 2022, Yang et al., 2022, Zhao et al., 2022, Adams et al., 2021, Alvarez-Ochoa et al., 2021, Charlton-Perkins et al., 2021, Cheng et al., 2021, Cong et al., 2021, Dong et al., 2021, Gong et al., 2021, Harnish et al., 2021, Herrera and Bach, 2021, Hodgson et al., 2021, Kannangara et al., 2021, Khezri et al., 2021, Kong et al., 2021, Lam Wong and Verheyen, 2021, Lu et al., 2021, Mark et al., 2021, Morata, 2021, Nászai et al., 2021, Nishida et al., 2021, Noyes et al., 2021, Paraskevopoulos and McGuigan, 2021, Rambur et al., 2021, Shahzad et al., 2021, Snigdha et al., 2021, Soler Beatty et al., 2021, Sood et al., 2021, Spratford et al., 2021, Wei et al., 2021, Wei et al., 2021, Cruz et al., 2020, Gangwani et al., 2020, Guo et al., 2020, Gutiérrez-Martínez et al., 2020, Hayashi and Ogura, 2020, Howe et al., 2020, Jacqueline et al., 2020, Jasper, 2020, Jin et al., 2020, Kamdem et al., 2020, Kanda and Igaki, 2020, Koyama et al., 2020, Krautz et al., 2020, Kurihara et al., 2020, Kushnir et al., 2020, Liang et al., 2020, Mariano et al., 2020, Morata and Calleja, 2020, Morris et al., 2020, Noyes et al., 2020, Rambur et al., 2020, Sawyer et al., 2020, Sênos Demarco et al., 2020, Sun et al., 2020, Washington et al., 2020, Zurita and Murillo-Maldonado, 2020, Banerjee et al., 2019, Campbell et al., 2019, Chatterjee and Deng, 2019, Fenckova et al., 2019, Khezri and Rusten, 2019, Kurelac et al., 2019, Mishra-Gorur et al., 2019, Murcia et al., 2019, Zhang et al., 2019, Zhang et al., 2019, Amcheslavsky et al., 2018, Benhra et al., 2018, Dunn et al., 2018, Poon et al., 2018, Sriskanthadevan-Pirahas et al., 2018, Tsuboi et al., 2018, Vicente et al., 2018, Arnal et al., 2017, Baril et al., 2017, Bhattacharya et al., 2017, Fei et al., 2017, Ismail et al., 2017, Katheder et al., 2017, Li et al., 2017, Ma et al., 2017, Ma et al., 2017, Manent et al., 2017, Moeller et al., 2017, Pascual et al., 2017, Pérez et al., 2017, Rahman et al., 2017, Rives-Quinto et al., 2017, San Martin et al., 2017, Shu et al., 2017, Tauc et al., 2017, Taylor et al., 2017, Xiang et al., 2017, Bielmeier et al., 2016, Bosveld et al., 2016, Casas-Tintó et al., 2016, Fagegaltier et al., 2016, Hudry et al., 2016, Mbodj et al., 2016, Ou et al., 2016, Pan et al., 2016, Snee et al., 2016, Toggweiler et al., 2016, Doggett et al., 2015, Feng and Martin, 2015, Figueroa-Clarevega and Bilder, 2015, Grifoni and Bellosta, 2015, Grifoni et al., 2015, Grillo-Hill et al., 2015, Legent et al., 2015, Meng and Biteau, 2015, Nie et al., 2015, Pasco et al., 2015, Srivastava, 2015, Turkel et al., 2015, Baril et al., 2014, Chabu and Xu, 2014, Claudius et al., 2014, Cordero et al., 2014, Guo et al., 2014, Handke et al., 2014, Huang et al., 2014, Ma et al., 2014, Ohsawa et al., 2014, Parisi et al., 2014, Stickel and Su, 2014, Das et al., 2013, Gaur et al., 2013, Khan et al., 2013, Khoo et al., 2013, Li et al., 2013, Lin et al., 2013, Mbodj et al., 2013, Molnar and de Celis, 2013, Pagarigan et al., 2013, Pastor-Pareja and Xu, 2013, Petzoldt et al., 2013, Yamanaka et al., 2013, Zhang et al., 2013, Andreu et al., 2012, Bond and Foley, 2012, Dahlgaard et al., 2012, Herranz et al., 2012, Jones et al., 2012, Justiniano et al., 2012, Kim et al., 2012, Maeng et al., 2012, Mavromatakis and Tomlinson, 2012, Mou et al., 2012, Sannang et al., 2012, Turski et al., 2012, Ajuria et al., 2011, Charlton-Perkins et al., 2011, Grigorian et al., 2011, Helman et al., 2011, Jiang et al., 2011, Jiang et al., 2011, Kawamori et al., 2011, Ou et al., 2011, Ashton-Beaucage et al., 2010, Chi et al., 2010, Li et al., 2010, Rendina et al., 2010, Roignant and Treisman, 2010, Salzer et al., 2010, Wu et al., 2010, Yan et al., 2010, Yogev et al., 2010, Zeng et al., 2010, Zhang et al., 2010, Almudi et al., 2009, Baker et al., 2009, Firth and Baker, 2009, Huh et al., 2009, Jiang and Edgar, 2009, Lembong et al., 2009, Moressis et al., 2009, Terriente-Félix and de Celis, 2009, Yan et al., 2009, Atreya and Fernandes, 2008, Hou et al., 2008, Lyulcheva et al., 2008, Miura et al., 2008, Pastor-Pareja et al., 2008, Patel and Jacobs, 2008, Read and Thomas, 2008, Roukens et al., 2008, Simcox et al., 2008, Zhang and Therrien, 2008, Almudí et al., 2007, Berry and Baehrecke, 2007, Firth and Baker, 2007, Jovceva et al., 2007, Juhász et al., 2007, Khoo et al., 2007, Lavery and Stern, 2007, Lavery et al., 2007, Letizia et al., 2007, O'Keefe et al., 2007, Srivastava et al., 2007, Tong et al., 2007, Tseng et al., 2007, Vidal et al., 2007, Yoneda et al., 2007, Beckett and Baylies, 2006, Brown et al., 2006, Caldwell et al., 2006, Carmena et al., 2006, Cela and Llimargas, 2006, Daftary et al., 2006, Friedman and Perrimon, 2006, Hannan et al., 2006, Kim et al., 2006, Lavery and Stern, 2006, Luo et al., 2006, Montell, 2006, Nolo et al., 2006, Pallavi et al., 2006, Philippakis et al., 2006, Poulton and Deng, 2006, Qiao et al., 2006, Sternberg, 2006, Caldwell et al., 2005, Caldwell et al., 2005, Galindo et al., 2005, Haralalka and Abmayr, 2005, Igaki et al., 2005, Jekely et al., 2005, Jekely et al., 2005, Moon et al., 2005, Richardson et al., 2005, Roignant et al., 2005, Rutkowski and Warren, 2005, Sen et al., 2005, Song et al., 2005, Sotillos and De Celis, 2005, Sustar and Schubiger, 2005, Barolo and Posakony, 2004, Bilder, 2004, Bruckner et al., 2004, Bruckner et al., 2004, Cordero et al., 2004, Cork and Purugganan, 2004, Kim and Bar-Sagi, 2004, Kim et al., 2004, Meister, 2004, Pan et al., 2004, Patel et al., 2004, Pollock et al., 2004, Raymond et al., 2004, Sinenko and Mathey-Prevot, 2004, Ward and Berg, 2004, Asha et al., 2003, Baena-Lopez and Garcia-Bellido, 2003, Botella et al., 2003, Carmena and Baylies, 2003, Ghabrial et al., 2003, Guan et al., 2003, Jekely, 2003, Kshetrapal and Shashidhara, 2003, Lee et al., 2003, Neufeld, 2003, Pagliarini and Xu, 2003, Rintelen et al., 2003, Shilo, 2003, Tayler and Garrity, 2003, Tootle et al., 2003, Uv et al., 2003, Wernet et al., 2003, Amiri and Stein, 2002, Beckett et al., 2002, Brumby and Richardson, 2002, Claeys et al., 2002, Fazio et al., 2002, Furlong et al., 2002, Gorski and Marra, 2002, James et al., 2002, Lee et al., 2002, Lin, 2002, Meyerowitz, 2002, Morey et al., 2002, Muller et al., 2002, Prober and Edgar, 2002, Rebay, 2002, Roch et al., 2002, Roy and Therrien, 2002, Roy et al., 2002, Skeath and Alvarez, 2002, Voas and Rebay, 2002, Xin et al., 2002, Zecca and Struhl, 2002, Bai et al., 2001, Baker, 2001, Baker and Yu, 2001, Campuzano, 2001, del Alamo and Diaz-Benjumea, 2001, Duchek and Rorth, 2001, Fiorini et al., 2001, Freeman, 2001, Halfar et al., 2001, Jacinto et al., 2001, Marty et al., 2001, Morrison, 2001, Peltonen and Mckusick, 2001, Silver et al., 2001, Tapon et al., 2001, Bangs et al., 2000, Baonza et al., 2000, Brennan and Moses, 2000, Brill et al., 2000, Carmena et al., 2000, Chen and Courey, 2000, Chen et al., 2000, Foley and Sprenger, 2000, Gibson et al., 2000, Halfon et al., 2000, Kumar and Moses, 2000, Kumar and Moses, 2000, Oldham et al., 2000, Potter et al., 2000, Rebay et al., 2000, Smith et al., 2000, Sotillos and Campuzano, 2000, Strasser and Vaux, 2000, Tittel and Steller, 2000, Weinkove and Leevers, 2000, Wilson and Leptin, 2000, Carmena et al., 1999, Casci and Freeman, 1999, Chen et al., 1999, Huang and Rubin, 1999, Leevers, 1999, Martin-Bermudo et al., 1999, Montell, 1999, Prokop, 1999, Ridley, 1999, Ruden et al., 1999, Stronach and Perrimon, 1999, Therrien et al., 1999, Wilson, 1999, Bergmann et al., 1998, Brill et al., 1998, Deng and Bownes, 1998, Dickson, 1998, Hayashi et al., 1998, Kurada et al., 1998, Nunez and del Peso, 1998, Roark and Bier, 1998, Spencer and Cagan, 1998, Vincent et al., 1998, Cagan et al., 1997, Freeman, 1997, Greenwood and Struhl, 1997, Guo et al., 1997, Lee and Montell, 1997, Szuts et al., 1997, VanBerkum, 1997, Yarnitzky et al., 1997, Badenhorst et al., 1996, Lee and Montell, 1996, Downward, 1995, Perrimon et al., 1995, Brown and Hartley, 1994, Pawson, 1993, Pawson et al., 1993, Baringa, 1992)
Ras1
(Ostalé et al., 2024, Bindhani et al., 2022, Das and Arur, 2022, Neophytou and Pitsouli, 2022, Costa-Rodrigues et al., 2021, Vega-Cuesta et al., 2020, Xu et al., 2020, Fenckova et al., 2019, Mirzoyan et al., 2019, Ray and Lakhotia, 2019, Zhou et al., 2019, Enomoto et al., 2018, He et al., 2018, Ashton-Beaucage et al., 2016, Kim et al., 2016, Yang et al., 2016, Leshchiner et al., 2015, Peláez et al., 2015, Levayer and Moreno, 2013, Mora et al., 2013, Pickering et al., 2013, Sieglitz et al., 2013, Sopko and Perrimon, 2013, Bangi et al., 2012, Morris et al., 2012, Smith et al., 2012, Yang and Terman, 2012, Apidianakis and Rahme, 2011, Bangi et al., 2011, Friedman et al., 2011, Geiger et al., 2011, Lin and Hackam, 2011, Read, 2011, Ding et al., 2010, Sung et al., 2010, Swaminathan and Pile, 2010, Apidianakis et al., 2009, Hurlbut et al., 2009, Jiang and Edgar, 2009, Leatherbarrow and Halfon, 2009, Nie et al., 2009, Sims et al., 2009, Wu et al., 2009, Xia et al., 2008, Yakoby et al., 2008, Boettner and Van Aelst, 2007, de Navascués and Modolell, 2007, Estrada et al., 2007, Halfon and Leatherbarrow, 2007, Carmena et al., 2006, Estrada et al., 2006, Orme et al., 2006, Polesello et al., 2006, Polesello et al., 2006, Walker et al., 2006, Dupuy et al., 2005, Formstecher et al., 2005, Go, 2005, Kon et al., 2005, Mittelman and Lev, 2005, Sundaram, 2005, Vidal et al., 2005, Zhu et al., 2005, Bajpai et al., 2004, Dearborn and Kunes, 2004, Ishimaru et al., 2004, Boettner et al., 2003, Botella et al., 2003, Firth and Baker, 2003, Li and Li, 2003, Li et al., 2003, Mirey et al., 2003, Park et al., 2003, Rawlins et al., 2003, Behan et al., 2002, Cripps and Olson, 2002, Doronkin et al., 2002, Fazio et al., 2002, Fetchko et al., 2002, Harden et al., 2002, Held, 2002, Koh et al., 2002, Li et al., 2002, Mattila et al., 2002, Rohrbaugh et al., 2002, Shamloula et al., 2002, Aoyagi and Wassarman, 2001, Baker, 2001, Borland et al., 2001, Culi et al., 2001, Hernandez-Hernandez and Ferrus, 2001, James and Berg, 2001, James and Berg, 2001, Janssens and Goris, 2001, Prober and Edgar, 2001, Schnorr et al., 2001, Schnorr et al., 2001, Tepass et al., 2001, van Steensel et al., 2001, Williams et al., 2001, Carthew et al., 2000, Fanto, 2000, Fanto et al., 2000, Firth et al., 2000, Halfon et al., 2000, Harikrishnan et al., 2000, Hayashi and Saigo, 2000, Huang and Rubin, 2000, Huang and Rubin, 2000, James et al., 2000, Li et al., 2000, Luschnig et al., 2000, Prober and Edgar, 2000, Prober and Edgar, 2000, Robertson et al., 2000, Selva and Perrimon, 2000, Taguchi et al., 2000, Takatsu et al., 2000, Teeter et al., 2000, Therrien et al., 2000, White and Jarman, 2000, Xu et al., 2000, Zimmerman et al., 2000, Asha et al., 1999, Bonini and Fortini, 1999, Casci et al., 1999, Chou et al., 1999, Feldmann et al., 1999, Feng, 1999, Halfar et al., 1999, Halfar et al., 1999, Harden et al., 1999, Harden et al., 1999, Hipfner and Cohen, 1999, Ishimaru et al., 1999, Iyadurai et al., 1999, James et al., 1999, Karim and Rubin, 1999, Kramer et al., 1999, Li and Perrimon, 1999, Lu and Li, 1999, Martin-Blanco et al., 1999, Prober and Edgar, 1999, Rangarajan et al., 1999, Sawamoto et al., 1999, Sawamoto et al., 1999, Schulz and Gajewski, 1999, Spana and Perrimon, 1999, Staehling-Hampton et al., 1999, Therrien et al., 1999, Thomas and Wassarman, 1999, Vinos et al., 1999, Wilson, 1999, Zhang et al., 1999, Boube et al., 1998, Bourbon et al., 1998, Carmena et al., 1998, Chou et al., 1998, Dominguez et al., 1998, Gajewski et al., 1998, Hayashi et al., 1998, Hsu et al., 1998, Iyadurai et al., 1998, James and Berg, 1998, Karim and Rubin, 1998, Karim and Rubin, 1998, Li et al., 1998, Li et al., 1998, Lu and Li, 1998, Maixner et al., 1998, Mantrova and Hsu, 1998, Michelson et al., 1998, Michelson et al., 1998, Neufeld et al., 1998, Rommel and Hafen, 1998, Savranski et al., 1998, Sawamoto et al., 1998, Boube et al., 1997, Chang and Rubin, 1997, Chen et al., 1997, Chou and Britt, 1997, Dominguez et al., 1997, Fischer et al., 1997, Karim and Rubin, 1997, Karim et al., 1997, Kockel et al., 1997, Kramer et al., 1997, Li et al., 1997, Li et al., 1997, Li et al., 1997, Lim et al., 1997, Matsuo et al., 1997, Matsuo et al., 1997, Michelson et al., 1997, O'Keefe et al., 1997, Okabe and Okano, 1997, Okabe and Okano, 1997, Rubin et al., 1997, Rubin et al., 1997, Schnorr and Berg, 1997, Tang et al., 1997, The et al., 1997, Yamamoto et al., 1997, Allard et al., 1996, Allard et al., 1996, Boube et al., 1996, Carroll et al., 1996, Dickson et al., 1996, Duffy and Perrimon, 1996, Gisselbrecht et al., 1996, Herbst et al., 1996, Karim et al., 1996, Kauffmann et al., 1996, Lai et al., 1996, MacDougall and Waterfield, 1996, Raabe et al., 1996, Rorth, 1996, Sauer et al., 1996, Sawamoto et al., 1996, Schnorr and Berg, 1996, Schnorr and Berg, 1996, Takahashi et al., 1996, The et al., 1996, Wassarman et al., 1996, Wes et al., 1996, Carroll et al., 1995, Chang et al., 1995, Dickson, 1995, Dickson et al., 1995, Doberstein et al., 1995, Hariharan et al., 1995, Hou et al., 1995, Kauffmann et al., 1995, Kramer et al., 1995, Lee and Montell, 1995, Rebay and Rubin, 1995, Schweitzer et al., 1995, Therrien et al., 1995, Therrien et al., 1995, Wassarman et al., 1995, Winge, 1995.6.4, Zhong, 1995, Zhong, 1995, Biggs et al., 1994, Bohmann et al., 1994, Brunner et al., 1994, Carthew et al., 1994, Chang et al., 1994, Chang et al., 1994, Diaz-Benjumea and Hafen, 1994, Duffy and Perrimon, 1994, Ezer et al., 1994, Freeman, 1994, Kramer and Cagan, 1994, Moodie and Wolfman, 1994, Perrimon, 1994, Simon, 1994, Thomas et al., 1994, Wilson, 1994, Cutforth et al., 1993, Dickson and Hafen, 1993, Hafen et al., 1993, Hafen et al., 1993, Heberlein et al., 1993, Kramer, 1993, Kussick et al., 1993, Lev, 1993.6.4, Livingston and Wilt, 1993, Lu et al., 1993, Lu et al., 1993, Raabe et al., 1993, Simon et al., 1993, Yamamoto, 1993, Berg and Schnorr, 1992, Fortini et al., 1992, Lai and Rubin, 1992, Simon et al., 1992, Woods and Bryant, 1992, Simon et al., 1991)
Ras85D
(Luo et al., 2024, Barbaste et al., 2023, Zhang et al., 2023, Zhang et al., 2023, Jarabo et al., 2022, Azuma et al., 2021, Bilder et al., 2021, Bonfini et al., 2021, DeAngelis et al., 2021, Dillard et al., 2021, Ito and Igaki, 2021, Liu et al., 2021, Salim et al., 2021, Brown Rackley et al., 2020, Denton et al., 2020, Iwashita et al., 2020, Kim et al., 2020, La Marca and Richardson, 2020, Mehrotra et al., 2020, Noyes et al., 2020, Port et al., 2020, Ramond et al., 2020, Williams et al., 2020, Bangi et al., 2019, Bhattacharjee et al., 2019, Chai et al., 2019, Chen and Read, 2019, Coelho and Moreno, 2019, Fahey-Lozano et al., 2019, Ji et al., 2019, Kim and Choi, 2019, Meltzer et al., 2019, Moreno et al., 2019, Portela et al., 2019, Saavedra and Perrimon, 2019, Singh et al., 2019, Snigdha et al., 2019, Su, 2019, Tenedini et al., 2019, Cho et al., 2018, Duncan et al., 2018, Jia et al., 2018, Muñoz-Soriano et al., 2018, Stephano et al., 2018, Zoranovic et al., 2018, Ashton-Beaucage and Therrien, 2017, Houtz et al., 2017, Jordán-Álvarez et al., 2017, Kim et al., 2017, Li et al., 2017, Ozasa et al., 2017, Revaitis et al., 2017, Suisse et al., 2017, Transgenic RNAi Project members, 2017-, Wolfstetter et al., 2017, Ashton-Beaucage et al., 2016, Gallant, 2016.4.27, Kahn et al., 2016, Malartre, 2016, Padash Barmchi et al., 2016, Sarov et al., 2016, Shimaji et al., 2016, Fischer et al., 2015, Li et al., 2015, Matsuda et al., 2015, Morán et al., 2015, Panneton et al., 2015, Turkel et al., 2015, Van Bortle et al., 2015, Xia et al., 2015, Ashton-Beaucage et al., 2014, Baril et al., 2014, Handke et al., 2014, Hauling et al., 2014, Lu et al., 2014, Tchankouo-Nguetcheu et al., 2014, Bergwitz et al., 2013, Carter, 2013, Hahn et al., 2013, Külshammer and Uhlirova, 2013, Lin et al., 2013, Ma et al., 2013, Muha and Müller, 2013, Parsons and Foley, 2013, Sen et al., 2013, Shen et al., 2013, Tran et al., 2013, Upadhyai and Campbell, 2013, Wang et al., 2013, Willoughby et al., 2013, Yu et al., 2013, Zhang et al., 2013, Avet-Rochex et al., 2012, Butchar et al., 2012, Chen et al., 2012, Maeng et al., 2012, Morris et al., 2012, Zhai et al., 2012, Brumby et al., 2011, Diez et al., 2011, Fauvarque and Williams, 2011, Friedman et al., 2011, Friedman et al., 2011, Lindquist et al., 2011, Murillo-Maldonado et al., 2011, Ragab et al., 2011, Takemura and Adachi-Yamada, 2011, Beam and Moberg, 2010, Buchon et al., 2010, Chi et al., 2010, Sung et al., 2010, Wu et al., 2010, Bond and Foley, 2009, Chittaranjan et al., 2009, Franzdóttir et al., 2009, Lembong et al., 2009, Mohseni et al., 2009, Mortimer and Moberg, 2009, Oishi et al., 2009, Shalaby et al., 2009, Shen et al., 2009, Sims et al., 2009, Yan et al., 2009, Aritakula and Ramasamy, 2008, Burgio et al., 2008, Day et al., 2008, Franciscovich et al., 2008, Simcox et al., 2008, Yakoby et al., 2008, Yan et al., 2008, Zartman et al., 2008, Beltran et al., 2007, de Navascués and Modolell, 2007, Kankel et al., 2007, Baril and Therrien, 2006, Gilboa and Lehmann, 2006, Igaki et al., 2006, Mahoney et al., 2006, Molnar et al., 2006, Oishi et al., 2006, Harrison et al., 2005, Lievens et al., 2005, Rawlings et al., 2004, Gim et al., 2001, Pickeral et al., 2000)
S35097
fs(3)05703
l(3)s1747
ras
(Datta et al., 2023, Floc'hlay et al., 2023, Bourouliti and Skoulakis, 2022, Jiang et al., 2022, Valencia-Expósito et al., 2022, Zipper et al., 2022, Santabárbara-Ruiz and Léopold, 2021, Sheng and Du, 2020, Ma et al., 2019, Campbell et al., 2018, Courgeon et al., 2018, Molnar et al., 2018, Selcho et al., 2017, Atkins et al., 2016, Bangi et al., 2016, Sheng et al., 2016, Andersen et al., 2015, Hall and Verheyen, 2015, Külshammer et al., 2015, Matsuda et al., 2015, Slack et al., 2015, Ballesteros-Arias et al., 2014, Deng and Kerppola, 2013, Turski et al., 2012, Biteau and Jasper, 2011, Carrasco-Rando et al., 2011, Grillo et al., 2011, Jiang et al., 2011, Knox et al., 2011, Herz et al., 2010, Menéndez et al., 2010, Cruz et al., 2009, Genevet et al., 2009, Martinez et al., 2009, Ninov et al., 2009, Wu et al., 2009, Jones et al., 2008, Wang et al., 2008, Yakoby et al., 2008, Fernandes and Krishan, 2007, Luo et al., 2007, Polesello and Tapon, 2007, Galindo et al., 2006, Liu et al., 2006, MacMullin and Jacobs, 2006, Miura et al., 2006, Parker, 2006, Roignant et al., 2006, Uhlirova and Bohmann, 2006, Yang and Baker, 2006, Baonza and Freeman, 2005, Cabernard and Affolter, 2005, Duchek and Baum, 2005, Hariharan, 2005, Pollock et al., 2005, Vidal et al., 2005, Dotto and Silke, 2004, Alvarez et al., 2003, Artero et al., 2003, Bach et al., 2003, Bergmann and Lane, 2003, Matsuda et al., 2003, Pallavi and Shashidhara, 2003, Settle et al., 2003, Voas and Rebay, 2003, Merabet et al., 2002, Reich and Shilo, 2002, Zecca and Struhl, 2002, Hidalgo et al., 2001, Tang et al., 2001, Affolter, 2000, Bui et al., 2000, Dobens and Raftery, 2000, Johnson Hamlet and Perkins, 2000, Pazman and Haynes, 2000, Prober and Edgar, 2000, Smith et al., 2000, Yun et al., 2000, Bergmann et al., 1999, Murakami et al., 1999, Bergmann et al., 1998, Bergmann et al., 1998, Hazelett et al., 1998, Mathias et al., 1998, Nguyen et al., 1997, Peverali et al., 1996, Marshall, 1994, Schupbach and Roth, 1994, Wolpert, 1994)
Secondary FlyBase IDs
  • FBgn0011008
  • FBgn0011548
Datasets (1)
Study focus (1)
Experimental Role
Project
Project Type
Title
  • bait_protein
Interaction map generated by purification of receptor tyrosine kinase pathway factors, with identification of copurifying proteins by mass spectrometry.
Study result (0)
Result
Result Type
Title
External Crossreferences and Linkouts ( 110 )
Sequence Crossreferences
NCBI Gene - Gene integrates information from a wide range of species. A record may include nomenclature, Reference Sequences (RefSeqs), maps, pathways, variations, phenotypes, and links to genome-, phenotype-, and locus-specific resources worldwide.
GenBank Protein - A collection of sequences from several sources, including translations from annotated coding regions in GenBank, RefSeq and TPA, as well as records from SwissProt, PIR, PRF, and PDB.
RefSeq - A comprehensive, integrated, non-redundant, well-annotated set of reference sequences including genomic, transcript, and protein.
UniProt/GCRP - The gene-centric reference proteome (GCRP) provides a 1:1 mapping between genes and UniProt accessions in which a single 'canonical' isoform represents the product(s) of each protein-coding gene.
UniProt/Swiss-Prot - Manually annotated and reviewed records of protein sequence and functional information
Other crossreferences
AlphaFold DB - AlphaFold provides open access to protein structure predictions for the human proteome and other key proteins of interest, to accelerate scientific research.
BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
FlyMine - An integrated database for Drosophila genomics
KEGG Genes - Molecular building blocks of life in the genomic space.
MARRVEL_MODEL - MARRVEL (model organism gene)
Linkouts
BioGRID - A database of protein and genetic interactions.
Cell Signaling Technology - Commercial vendor for primary antibodies and antibody conjugates.
Drosophila Genomics Resource Center - Drosophila Genomics Resource Center (DGRC) cDNA clones
DroID - A comprehensive database of gene and protein interactions.
DRSC - Results frm RNAi screens
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
FlyCyc Genes - Genes from a BioCyc PGDB for Dmel
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
iBeetle-Base - RNAi phenotypes in the red flour beetle (Tribolium castaneum)
Interactive Fly - A cyberspace guide to Drosophila development and metazoan evolution
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
SignaLink - A signaling pathway resource with multi-layered regulatory networks.
References (1,409)