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GRB2 Rabbit mAb
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IP, ICC |
|---|---|
| Primary Accession | P62993 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Monoclonal Antibody |
| Calculated MW | 25206 Da |
| Gene ID | 2885 |
|---|---|
| Other Names | GRB2 |
| Dilution | WB~~1/500-1/1000 |
| Format | Liquid |
| Name | GRB2 |
|---|---|
| Synonyms | ASH |
| Function | Non-enzymatic adapter protein that plays a pivotal role in precisely regulated signaling cascades from cell surface receptors to cellular responses, including signaling transduction and gene expression (PubMed:11726515, PubMed:37626338). Thus, participates in many biological processes including regulation of innate and adaptive immunity, autophagy, DNA repair or necroptosis (PubMed:35831301, PubMed:37626338, PubMed:38182563). Controls signaling complexes at the T-cell antigen receptor to facilitate the activation, differentiation, and function of T-cells (PubMed:9489702, PubMed:36864087). Mechanistically, engagement of the TCR leads to phosphorylation of the adapter protein LAT, which serves as docking site for GRB2 (PubMed:9489702). In turn, GRB2 establishes a a connection with SOS1 that acts as a guanine nucleotide exchange factor and serves as a critical regulator of KRAS/RAF1 leading to MAPKs translocation to the nucleus and activation (PubMed:12171928, PubMed:25870599). Functions also a role in B-cell activation by amplifying Ca(2+) mobilization and activation of the ERK MAP kinase pathway upon recruitment to the phosphorylated B-cell antigen receptor (BCR) (PubMed:25413232, PubMed:29523808). Plays a role in switching between autophagy and programmed necrosis upstream of EGFR by interacting with components of necrosomes including RIPK1 and with autophagy regulators SQSTM1 and BECN1 (PubMed:35831301, PubMed:38182563). Regulates miRNA biogenesis by forming a functional ternary complex with AGO2 and DICER1 (PubMed:37328606). Functions in the replication stress response by protecting DNA at stalled replication forks from MRE11-mediated degradation. Mechanistically, inhibits RAD51 ATPase activity to stabilize RAD51 on stalled replication forks (PubMed:38459011). Additionally, directly recruits and later releases MRE11 at DNA damage sites during the homology-directed repair (HDR) process (PubMed:34348893). |
| Cellular Location | Nucleus. Cytoplasm. Endosome. Golgi apparatus {ECO:0000250|UniProtKB:Q60631} |
Research Areas
Citations (0)
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info@abcepta.com, and receive a free "I Love Antibodies" mug.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
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$ 350.00
Cat# AP78702
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