protein tyrosine phosphatase H (transmembrane-type protein-tyrosine phosphatase type H, stomach cancer-associated protein tyrosine phosphatase 1, SAP-1, PTPRH, SAP1)

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Function

may contribute to contact inhibition of cell growth & motility by mediating the dephosphorylation of focal adhesion- associated substrates & thus negatively regulating integrin- promoted signaling processes
induces apoptotosis by at least 2 distinct mechanisms:
inhibition of cell survival
signaling mediated by PI 3-kinase, Akt, & ILK & activation of a caspase-dependent proapoptotic pathway
inhibits basal activity of LCK & its activation in response to TCR stimulation & TCR-induced activation of MAP kinase & surface expression of CD69
inhibits TCR-induced tyrosine phosphorylation of LAT & ZAP-70
inhibits both basal activity of DOK1 & its CD2-induced tyrosine phosphorylation
induces dephosphorylation of p130cas, focal adhesion kinase & c-Src
reduces migratory activity of Jurkat cells
regulated by reversible dimerization
dimerization reduces its catalytic activity
interacts with LCK

protein tyrosine phosphate + H2O <--> protein tyrosine + phosphate

homodimer; disulfide-linked (probable)
extracellular domain mediates homodimerization
one or more Cys in the extracellular domain is essential for the formation of dimers probably by forming a disulfide bond
cytoplasmic domain mediates the interaction with LCK
belongs to the protein-tyrosine phosphatase family receptor class 3 subfamily
contains 8 fibronectin F3 modules
contains 1 tyrosine-protein phosphatase domain

expressed in pancreatic cancer & colorectal cancer cells, but not in normal pancreas or colon
expression in hepatocellular carcinoma is related to the differentiation status of the tumor & expression is inversely related to tumor aggressiveness
induced at the early stage of hepatocellular carcinoma & is suppressed at later stages