Symbol: Name: ID: |
SH2B2 SH2B adaptor protein 2 GFS:6459 |
Gene name: | SH2B2 |
Chromosome: | 7q22.1 |
Previous Symbols: | |
Previous Names: | |
Aliases: | APS |
Name Aliases: | adaptor protein with pleckstrin homology and src |
Locus Type: | gene with protein product |
Mouse Genome Database ID: | MGI:1345171 | Rat Genome Database ID: | RGD:69284 |
HGNC ID: | HGNC:17381 | RefSeq IDs: | NM_020979 |
Entrez Gene ID: | 10603 | Ensembl Gene ID: | ENSG00000160999 |
VEGA IDs: | OTTHUMG00000150652 | UniProt ID: | O14492 |
UCSC ID: | uc011kko.1 | OMIM ID: | 605300 |
Pubmed: | PMID9233773 | ||
CCDS IDs: |
SH2B adapter protein 2 is a protein that in humans is encoded by the SH2B2 gene.
The protein encoded by this gene is expressed in B lymphocytes and contains pleckstrin homology and src homology 2 (SH2) domains. In Burkitt's lymphoma cell lines, it is tyrosine-phosphorylated in response to B cell receptor stimulation. Because it binds Shc independent of stimulation and Grb2 after stimulation, it appears to play a role in signal transduction from the receptor to the Shc/Grb2 pathway. [provided by RefSeq, Jun 2009]. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Gene record to access additional publications.
Function: Adapter protein for several members of the tyrosine kinase receptor family. Involved in multiple signaling pathways. May be involved in coupling from immunoreceptor 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. May induce cytoskeletal reorganization via interaction with VAV3.
Products for SH2B2 gene
Catalog | Product Name | Application | Company |
GFS:E06459 | SH2B adaptor protein 2; ELISA kit | ELISA | n/a |
GFS:A06459 | SH2B adaptor protein 2; Anti | ANTIBODIES | n/a |
GFS:P06459 | SH2B adaptor protein 2; Protien | Protien | n/a |