RhoB Antibody [G12L1] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 IHC1:600 IF1:800

Application
WB, IHC, IF

Reactivity
Human, Mouse, Rat

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
21 kDa

Positive Control	Mouse brain; Human colon carcinoma; Human non-small cell lung carcinoma; Human non-Hodgkin's lymphoma; Human prostate carcinoma; HCT 116 cells; SK-BR-3 cells; HCC1419 cells
Negative Control	HCC1806 cells; Daudi cells

Datasheet & SDS

Biological Description

Specificity
RhoB (D1J9V) Rabbit mAb detects endogenous levels of total RhoB protein.

Clone
G12L1

Synonym(s)
Rho-related GTP-binding protein RhoB; Rho cDNA clone 6 (h6); RHOB; ARH6; ARHB

Background
RhoB is a small GTPase of the Rho family (RhoA/B/C subfamily) that functions as a molecular switch, cycling between GDP-bound inactive and GTP-bound active states, regulated by guanine nucleotide exchange factors (GEFs) that promote GDP/GTP exchange, GTPase-activating proteins (GAPs) that accelerate GTP hydrolysis, and Rho GDP-dissociation inhibitors (RhoGDIs) that sequester inactive forms. Its unique C-terminal hypervariable region, containing polar serine and glutamine residues rather than the polybasic motif of RhoA and RhoC, enables distinct membrane association, endosomal trafficking, and nuclear localization through specific post-translational modifications such as farnesylation and proteolytic processing. RhoB shares the conserved G-domain with five motifs, the G1 P-loop for nucleotide and magnesium coordination (identical to RhoA and RhoC), Switch I and II for GTP-induced conformational changes exposing effector regions, the Rho-specific Insert helix, and the G3, G4, and G5 motifs, but differs in surface charge distribution, C-terminal polarity, and lack of hyperbasic residues, allowing selective interactions beyond canonical RhoA pathways. In its GTP-bound form, RhoB engages effectors such as ROCKII, mDia1, and Citron kinase to regulate actin dynamics, stress fiber formation, and focal adhesion turnover during cell migration and adhesion, while uniquely controlling endocytic trafficking (such as EGFR internalization), Golgi organization via PKD1 phosphorylation, DNA repair checkpoint activation following genotoxic stress, and apoptosis via Bim upregulation and reactive oxygen species generation. RhoB often opposes RhoA and RhoC, acting as a tumor suppressor by inhibiting invasion and migration (such as in glioblastoma through PKCι and ovarian cancer growth), promoting anoikis, and limiting angiogenesis. Its rapid inducibility by stressors such as UV, hypoxia, and chemotherapeutics marks it as an immediate-early response gene that balances proliferation and survival. RhoB downregulation correlates with poor prognosis in cancers such as breast, lung, and melanoma, as well as with metastasis and chemoresistance, while upregulation enhances therapy sensitivity.

Background

RhoB is a small GTPase of the Rho family (RhoA/B/C subfamily) that functions as a molecular switch, cycling between GDP-bound inactive and GTP-bound active states, regulated by guanine nucleotide exchange factors (GEFs) that promote GDP/GTP exchange, GTPase-activating proteins (GAPs) that accelerate GTP hydrolysis, and Rho GDP-dissociation inhibitors (RhoGDIs) that sequester inactive forms. Its unique C-terminal hypervariable region, containing polar serine and glutamine residues rather than the polybasic motif of RhoA and RhoC, enables distinct membrane association, endosomal trafficking, and nuclear localization through specific post-translational modifications such as farnesylation and proteolytic processing. RhoB shares the conserved G-domain with five motifs, the G1 P-loop for nucleotide and magnesium coordination (identical to RhoA and RhoC), Switch I and II for GTP-induced conformational changes exposing effector regions, the Rho-specific Insert helix, and the G3, G4, and G5 motifs, but differs in surface charge distribution, C-terminal polarity, and lack of hyperbasic residues, allowing selective interactions beyond canonical RhoA pathways. In its GTP-bound form, RhoB engages effectors such as ROCKII, mDia1, and Citron kinase to regulate actin dynamics, stress fiber formation, and focal adhesion turnover during cell migration and adhesion, while uniquely controlling endocytic trafficking (such as EGFR internalization), Golgi organization via PKD1 phosphorylation, DNA repair checkpoint activation following genotoxic stress, and apoptosis via Bim upregulation and reactive oxygen species generation. RhoB often opposes RhoA and RhoC, acting as a tumor suppressor by inhibiting invasion and migration (such as in glioblastoma through PKCι and ovarian cancer growth), promoting anoikis, and limiting angiogenesis. Its rapid inducibility by stressors such as UV, hypoxia, and chemotherapeutics marks it as an immediate-early response gene that balances proliferation and survival. RhoB downregulation correlates with poor prognosis in cancers such as breast, lung, and melanoma, as well as with metastasis and chemoresistance, while upregulation enhances therapy sensitivity.

References
https://pubmed.ncbi.nlm.nih.gov/19956591/ https://pubmed.ncbi.nlm.nih.gov/27875099/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%