SH2B Adaptor Protein 2 (SH2B2) Antibody
221€ (50 µg)
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935106861
info@markelab.com
name
SH2B Adaptor Protein 2 (SH2B2) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx327510
tested applications
ELISA, WB
Description
SH2B2 Antibody is a Rabbit Polyclonal against SH2B2.
Documents del producto
Instrucciones
Data sheet
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | SH2B Adaptor Protein 2 (SH2B2) |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Recommended Dilution | ELISA: 1/20000, WB: 1/500 - 1/2000. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Purification | Purified by affinity chromatography. |
| Size 1 | 50 µg |
| Size 2 | 100 µg |
| Form | Liquid |
| Tested Applications | ELISA, WB |
| Buffer | PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide. |
| Availability | Shipped within 5-10 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | O14492 |
| Gene ID | 10603 |
| Alias | SH2B2, APS, SH2B adaptor protein 2 |
| Background | Antibody anti-SH2B2 |
| Status | RUO |
Descripción
SH2B2, also known as APS (adaptor protein containing PH and SH2 domains), is an adaptor protein that regulates signal transduction downstream of receptor tyrosine kinases, including insulin receptor and c-KIT. It binds phosphorylated receptors and recruits downstream effectors such as PI3K and SOCS proteins, modulating pathways involved in insulin signaling, glucose uptake, and cell proliferation. SH2B2 is highly expressed in insulin-sensitive tissues and hematopoietic cells, where it regulates glucose homeostasis, hematopoiesis, and mast cell activation. It is also involved in negative feedback regulation by recruiting SOCS proteins, which inhibit receptor signaling and prevent excessive activation. Dysregulation of SH2B2 is linked to metabolic disorders, insulin resistance, and hematopoietic abnormalities. Knockout studies reveal defects in glucose metabolism, impaired hematopoiesis, and altered mast cell responses, underscoring its role in fine-tuning receptor-mediated signaling pathways.
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