Protein phosphatase that may contribute to contact inhibition of cell growth and motility by mediating the dephosphorylation of focal adhesion-associated substrates and thus negatively regulating integrin-promoted signaling processes. Induces apoptotic cell death by at least two distinct mechanisms: inhibition of cell survival signaling mediated by PI 3-kinase, Akt, and ILK and activation of a caspase-dependent proapoptotic pathway. Inhibits the basal activity of LCK and its activation in response to TCR stimulation and TCR-induced activation of MAP kinase and surface expression of CD69. Inhibits TCR-induced tyrosine phosphorylation of LAT and ZAP70. Inhibits both basal activity of DOK1 and its CD2-induced tyrosine phosphorylation. Induces dephosphorylation of BCAR1, focal adhesion kinase and SRC. Reduces migratory activity of Jurkat cells (By similarity). Reduces tyrosine phosphorylation of CEACAM20 and thereby contributes to suppress the intestinal immune response (PubMed:26195794). H2O + O-phospho-L-tyrosyl-[protein] = L-tyrosyl-[protein] + phosphate Homodimer; disulfide-linked (By similarity). Interacts with LCK (By similarity). Interacts (phosphorylated form) with GRB2 (via SH2 domain) (PubMed:20398064). Interacts (phosphorylated form) with FYN (via SH2 domain) (PubMed:20398064). Interacts (via extracellular domain) with CEACAM20 (via extracellular domain); the interaction dephosphorylates CEACAM20 (PubMed:26195794). Colocalizes with CEACAM20 at the apical brush border of intestinal cells. Expressed strongly in the intestinal tract, with particularly high levels in the duodenum and jejunum (at protein level). Also expressed at low level in the testis (at protein level). Not detected in other tissues tested (at protein level). Detected from embryonic stage 16.5 dpc onwards, with marked increase in expression level after birth. Viable and fertile (PubMed:19170756). No significant effect on body weight or nutrient absorption (PubMed:19170756). Morphology of intestinal epithelium cells appears to be normal (PubMed:19170756). Double knockouts with APC heterozygotes, a model for intestinal tumorigenesis, show reduced adenoma growth (PubMed:19170756). Double knockouts with IL10, a model of inflammatory bowel disease, show significantly increased colonic inflammation in the presence of commensal bacteria and reduced survival rates (PubMed:26195794).