ID:KIRR1_HUMAN DESCRIPTION: RecName: Full=Kin of IRRE-like protein 1; AltName: Full=Kin of irregular chiasm-like protein 1; AltName: Full=Nephrin-like protein 1; Flags: Precursor; FUNCTION: Plays a significant role in the normal development and function of the glomerular permeability. Signaling protein that needs the presence of TEC kinases to fully trans-activate the transcription factor AP-1 (By similarity). SUBUNIT: Interacts with TJP1/ZO-1 and with NPHS2/podocin (via the C-terminus). Interacts with NPHS1/nephrin (via the Ig-like domains); this interaction is dependent on KIRREL glycosylation. Homodimer (via the Ig-like domains). Interacts when tyrosine- phosphorylated with GRB2 (By similarity). SUBCELLULAR LOCATION: Cell membrane; Single-pass type I membrane protein (Potential). Note=Predominantly located at podocyte slit diaphragm. TISSUE SPECIFICITY: Abundantly expressed in kidney. Specifically expressed in podocytes of kidney glomeruli. PTM: Phosphorylation probably regulates the interaction with NSH2. Phosphorylated at Tyr-605 and Tyr-606 by FYN, leading to GRB2 binding (By similarity). PTM: N-glycosylated (By similarity). SIMILARITY: Belongs to the immunoglobulin superfamily. SIMILARITY: Contains 5 Ig-like C2-type (immunoglobulin-like) domains. SEQUENCE CAUTION: Sequence=AAP59845.1; Type=Frameshift; Positions=19; Sequence=BAA91850.1; Type=Erroneous initiation; Sequence=BAB14192.1; Type=Erroneous initiation;
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 Q96J84
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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.