APS
an adapter protein involved in coupling immunoreceptors to Ras signaling. Acts as a negative regulator of cytokine signaling in collaboration with CBL. Binds to EPOR and suppresses EPO-induced STAT5 activation, possibly through a masking effect on STAT5 docking sites in EPOR. Suppresses PDGF-induced mitogenesis. Interacts with several proteins including KIT/c-KIT, SHC, GRB2, EPOR, CBL/c-CBL, PDGFR, VAV1 and VAV3. Interacts with SHC through its N-terminal region, with GRB2 via the phosphorylated C-terminus and with EPOR and KIT via its SH2 domain. Interacts with GRB2 after B-cell antigen receptor stimulation. Interacts with VAV3 via its PH domain, inducing cytoskeletal reorganization. Expressed in spleen, prostrate, testis, uterus, small intestine and skeletal muscle. Among haematopoietic cell lines, expressed exclusively in B-cells. Not expressed in most tumor cell lines. Tyrosine phosphorylated by JAK2, KIT and other kinases activated by B-cell receptor in response to stimulation with cytokines, IL3, IL5, PDGF, IGF1, IGF2, CSF2/GM-CSF and cross-linking of the B-cell receptor complex. Note: This description may include information from UniProtKB.
Alt. Names/Synonyms: Adapter protein with pleckstrin homology and Src homology 2 domains; adaptor protein with pleckstrin homology and src homology 2 domains; APS; SH2 and PH domain-containing adapter protein APS; SH2B adapter protein 2; SH2B adaptor protein 2; SH2B2
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.
