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AB138015

Anti-RGS1 antibody

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(1 Publication)

Rabbit Polyclonal RGS1 antibody. Suitable for WB and reacts with Human samples. Cited in 1 publication. Immunogen corresponding to Synthetic Peptide within Human RGS1.

View Alternative Names

1R20, BL34, IER1, RGS1, Regulator of G-protein signaling 1, B-cell activation protein BL34, Early response protein 1R20

1 Images
Western blot - Anti-RGS1 antibody (AB138015)
  • WB

Unknown

Western blot - Anti-RGS1 antibody (AB138015)

All lanes:

Western blot - Anti-RGS1 antibody (ab138015) at 1/500 dilution

All lanes:

293 cell lysate at 30 µg

Predicted band size: 24 kDa

false

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

WB

applications

Immunogen

Synthetic Peptide within Human RGS1. The exact immunogen used to generate this antibody is proprietary information.

Q08116

Reactivity data

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Properties and storage information

Form
Liquid
Purification technique
Affinity purification Immunogen
Storage buffer
pH: 7.4 Preservative: 0.02% Sodium azide Constituents: PBS, 50% Glycerol (glycerin, glycerine), 0.88% Sodium chloride
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Regulator of G-protein signaling 1 (RGS1) also known as BL34 or 1R20 acts mechanically as a GTPase-activating protein (GAP) for Gα subunits of heterotrimeric G-proteins. This function speeds up the deactivation of G-proteins by converting GTP to GDP effectively stopping signal transduction. RGS1 has a molecular mass of approximately 25 kDa. This protein is mainly expressed in B and T lymphocytes and you can find it in lymphoid tissues such as the spleen and lymph nodes.
Biological function summary

The RGS1 protein modulates immune cell signaling thereby controlling cell migration and positioning. RGS1 plays a role in reducing signaling from chemokine receptors which affects the movement of lymphocytes within tissues. It does not significantly form part of a larger complex mostly acting independently to exert its function within the immune system.

Pathways

The regulatory activity of RGS1 heavily influences the chemokine signaling pathway and the G-protein coupled receptor (GPCR) signaling pathway. These pathways are important for the directional migration and activation of immune cells. Within these pathways RGS1 interacts with related proteins such as CXCR4 and Gα subunits modulating their signaling outputs to regulate immune cell responses.

RGS1 links to autoimmune diseases and certain cancers. It can modulate the immune response in diseases such as multiple sclerosis where its activity may affect immune cell movement and function. Connections also exist between RGS1 and CXCR4 within cancer pathology where altered signaling could contribute to tumor growth and metastasis. By affecting these pathways RGS1 becomes a potential target for therapeutic intervention in related disorders.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Regulates G protein-coupled receptor signaling cascades, including signaling downstream of the N-formylpeptide chemoattractant receptors and leukotriene receptors (PubMed : 10480894). Inhibits B cell chemotaxis toward CXCL12 (By similarity). Inhibits signal transduction by increasing the GTPase activity of G protein alpha subunits thereby driving them into their inactive GDP-bound form (PubMed : 10480894, PubMed : 18434541).
See full target information RGS1

Publications (1)

Recent publications for all applications. Explore the full list and refine your search

International journal of molecular sciences 26: PubMed40565000

2025

SARS-CoV-2 ORF7a Protein Impedes Type I Interferon-Activated JAK/STAT Signaling by Interacting with HNRNPA2B1.

Applications

Unspecified application

Species

Unspecified reactive species

Yujie Wen,Chaochao Li,Tian Tang,Chao Luo,Shan Lu,Na Lyu,Yongxi Li,Rong Wang
View all publications

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