slimb, shiva, ica, shv, wel
beta-transducin family Trp-Asp repeats family - subunit of a multi-protein complex that targets proteins for degradation by the ubiquitin-proteasome pathway - an important regulator of Wingless, Hedgehog and Dorsal pathways
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\slmb using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\slmb in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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 GBrowse for alignment of the cDNAs and ESTs to the gene model.
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.
Source for identity of: slmb CG3412
Source for merge of: slmb CG3412
Source for merge of: slmb wel
Source for merge of: slmb BcDNA:GM02031
Source for merge of: slmb shv
Source for merge of: slmb ica
Source for merge of: slmb MENE(3R)-B
Identified as a component of the hh signalling pathway in a genome-wide RNAi screen. dsRNA made from templates generated with primers directed affects the extent of expression of a hh signaling reporter construct in Clone 8 cells.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Isolated in an EMS screen for recessive mutations that alter normal adult patterning in somatic clones.
Strong alleles cause embryonic lethality while weak alleles cause larval and pupal lethality.
Identified in an adult mosaic screen for negative regulators of cell proliferation.
Given the name "pingiel", after one of Pavlov's dogs.
To reflect the fact that many of the mutants isolated in this screen disrupt Avic\GFP-stau localisation to the anterior and/or posterior pole of the oocyte, many of the complementation groups identified in the screen have been named after polar explorers who failed to reach the North or South pole.