Anti-RhoG [1F3-B3-E5] Antibody

This mouse IgG2bk  monoclonal antibody [1F3-B3-E5] was generated against a KLH synthetic peptide encompassing Ras homology Growth-related (RhoG) amino acids 161-180 and is reactive against human, mouse and rat RhoG.


  • Reacts with human, mouse and rat RhoG
  • Suitable for Western Blot and ELISA applications

RhoG (ARGH) is a member of the Ras super-family of small G-proteins and a member of the Rac subfamily of Rho Family of GTPases. RhoG is a small G-protein (GTPase) who is activated by a GEF (guanine nucleotide exchange factor). The GEF displaces GDP from the binding site of RhoG and allows GTP to bind in its place rendering the protein active. This active RhoG binds downstream effector molecules that include ELMO and DOCK180. RhoG then cleaves GTP to GDP making it inactive. RhoG is believed to be crucial for integrin-mediated Rac activation and cell spreading. RhoG is believed to be active upstream of Rac and work independently of Rac.

From the laboratory of Martin A. Schwartz, PhD, University of Virginia.

The Investigator's Annexe Part of The Investigator's Annexe program.

Catalog Number Product DataSheet Size AVAILABILITY Price Qty
Anti-RhoG [1F3-B3-E5] Antibody
100ug 4-6 weeks
Regular Price:$335.00
On Sale:

Product Type: Antibody
Antigen: RhoG
Accession ID: P84095 , NM_001665
Molecular Weight: 21 kDa
Isotype: IgG2bk
Clonality: Monoclonal
Clone Name: 1F3-B3-E5
Reactivity: Human, mouse and rat
Immunogen: KLH synthetic peptide encompassing amino acids RhoG 161-180
Species Immunized: Mouse
Epitope: AA 161-180
Purification Method: Protein G Affinity Chromatography
Buffer: PBS, 0.05% (w/v) Sodium Azide
Tested Applications: WB, ELISA
Storage: -20C
Shipped: Cold packs



Does not cross-react with Rac, Rho (A, B, C), or Cdc42

From the laboratory of Martin A. Schwartz, PhD, University of Virginia.
  1. Meller J, Vidali L, Schwartz MA. Endogenous RhoG is dispensable for integrin-mediated cell spreading but contributes to Rac-independent migration. J Cell Sci. 2008 Jun 15;121(Pt 12):1981-9.

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