ID:DOK4_HUMAN DESCRIPTION: RecName: Full=Docking protein 4; AltName: Full=Downstream of tyrosine kinase 4; AltName: Full=Insulin receptor substrate 5; Short=IRS-5; Short=IRS5; FUNCTION: DOK proteins are enzymatically inert adaptor or scaffolding proteins. They provide a docking platform for the assembly of multimolecular signaling complexes. DOK4 functions in RET-mediated neurite outgrowth and plays a positive role in activation of the MAP kinase pathway (By similarity). Putative link with downstream effectors of RET in neuronal differentiation. May be involved in the regulation of the immune response induced by T-cells. SUBUNIT: Interacts with RET and TEK/TIE2. Interaction with RET is mediated through the PTB domain and requires phosphorylation of RET 'Tyr-1062' (By similarity). TISSUE SPECIFICITY: Widely expressed. High expression in skeletal muscle, heart, kidney and liver. Weaker expression in spleen, lung and small intestine, brain, heart and. Expressed in both resting and activated peripheral blood T-cells. DOMAIN: PTB domain mediates receptor interaction (By similarity). PTM: Phosphorylated on tyrosine residues in response to insulin, IGF1 or RET stimulation. SIMILARITY: Belongs to the DOK family. Type B subfamily. SIMILARITY: Contains 1 IRS-type PTB domain. SIMILARITY: Contains 1 PH domain. SEQUENCE CAUTION: Sequence=AAC24310.1; Type=Erroneous gene model prediction;
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q8TEW6
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.