ik2, DmIKKε, l(2)38Ea, 38D.31, IκB kinase-like 2
IKK-related kinase - a regulator of caspase activation in a nonapoptotic context - promotes degradation of DIAP1 (Thread) through direct phosphorylation - required for proper sensory organ precursor development - acts on the cytoskeleton to regulate egg DV and AP polarity
Gene model reviewed during 5.48
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\IKKε using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\IKKε 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 merge of: ik2 l(2)38Ea
ik2 protein is locally activated (by phosphorylation at residue Ser175) at the tip of growing mechanosensory bristles and controls the rapid shuttling of recycling endosomes. ik2 is also involved in actin bundle organisation. These two processes (recycling endosome dynamics and actin bundle organisation) appear to be independently regulated by ik2.
ik2 is required for dendritic severing during dendrite pruning of ddaC neurons in the pupa.
Both the actin cytoskeleton and the anchoring of microtubule minus-ends are disrupted in ik2 mutants.
When dsRNA constructs are made and transiently transfected into S2 cells in RNAi experiments, a whole range of mitotic abnormalities and spindle abnormalities are seen.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.