CDC42 Antibody [B14M24] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat, Bovine

Usage Information

Dilution
WB1:1000

Application
WB

Reactivity
Human, Mouse, Rat, Bovine

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

Datasheet & SDS

Biological Description

Specificity
CDC42 Antibody [B14M24] detects endogenous levels of total CDC42 protein.

Clone
B14M24

Synonym(s)
CDC42, CDC42Hs, Cell division control protein 42 homolog, cell division cycle 42, G25K, G25K GTP-binding protein, growth-regulating protein, GTP binding protein, 25kDa, GTP-binding protein, 25kD, small GTP binding protein CDC42, TKS

Background
CDC42 is a small Rho‑family GTPase that acts as a conserved molecular switch controlling actin cytoskeleton organization, cell polarity, membrane trafficking, and signaling pathways that regulate growth and differentiation across diverse mammalian tissues. The protein contains a canonical small GTPase fold with a P‑loop NTP‑binding domain, switch I and II regions that change conformation upon GTP binding and hydrolysis, and a C‑terminal CAAX motif that is prenylated to anchor CDC42 at specific membrane compartments where receptors and scaffolding proteins recruit its dedicated guanine nucleotide exchange factors and GTPase‑activating proteins. CDC42 cycles between GDP‑bound inactive and GTP‑bound active states under the coordinated action of GEFs that catalyze GDP–GTP exchange, GAPs that accelerate intrinsic GTP hydrolysis, and RhoGDIs that bind GDP‑loaded CDC42 and retain it in the cytosol until appropriate signals release it for membrane targeting and activation. Active CDC42 engages multiple effector proteins, including p21‑activated kinases, N‑WASP/WASP, and PAR polarity complexes, and these effectors connect CDC42 activation to Arp2/3‑dependent actin nucleation, formation of actin‑rich filopodia, establishment of apical–basal polarity, and organization of adherens and tight junctions, which coordinates epithelial morphogenesis, directed migration, and lumen and barrier formation. CDC42 also interacts with IQGAP proteins, MRCK kinases, and regulators at the Golgi and plasma membrane to integrate actomyosin contractility with vesicle trafficking and microtubule dynamics, shaping junctional stability, polarized secretion, and organelle positioning. In endocrine tissues, glucose‑stimulated CDC42 activation functions as an early signal in stimulus–secretion coupling for insulin, where CDC42 regulates cortical actin remodeling and recruitment of exocytotic machinery required for the sustained second phase of insulin release. In signaling networks controlling proliferation and survival, CDC42 modulates pathways such as EGFR–mTORC1 and contributes to activation of downstream cascades including MAPK and PI3K, which influence transcriptional programs and cell‑cycle progression. Germline mutations and dysregulated CDC42 activity associate with developmental and autoinflammatory syndromes, while overexpression or hyperactivation in tumors correlates with enhanced motility, invasive behavior, and metastatic dissemination.

Background

CDC42 is a small Rho‑family GTPase that acts as a conserved molecular switch controlling actin cytoskeleton organization, cell polarity, membrane trafficking, and signaling pathways that regulate growth and differentiation across diverse mammalian tissues. The protein contains a canonical small GTPase fold with a P‑loop NTP‑binding domain, switch I and II regions that change conformation upon GTP binding and hydrolysis, and a C‑terminal CAAX motif that is prenylated to anchor CDC42 at specific membrane compartments where receptors and scaffolding proteins recruit its dedicated guanine nucleotide exchange factors and GTPase‑activating proteins. CDC42 cycles between GDP‑bound inactive and GTP‑bound active states under the coordinated action of GEFs that catalyze GDP–GTP exchange, GAPs that accelerate intrinsic GTP hydrolysis, and RhoGDIs that bind GDP‑loaded CDC42 and retain it in the cytosol until appropriate signals release it for membrane targeting and activation. Active CDC42 engages multiple effector proteins, including p21‑activated kinases, N‑WASP/WASP, and PAR polarity complexes, and these effectors connect CDC42 activation to Arp2/3‑dependent actin nucleation, formation of actin‑rich filopodia, establishment of apical–basal polarity, and organization of adherens and tight junctions, which coordinates epithelial morphogenesis, directed migration, and lumen and barrier formation. CDC42 also interacts with IQGAP proteins, MRCK kinases, and regulators at the Golgi and plasma membrane to integrate actomyosin contractility with vesicle trafficking and microtubule dynamics, shaping junctional stability, polarized secretion, and organelle positioning. In endocrine tissues, glucose‑stimulated CDC42 activation functions as an early signal in stimulus–secretion coupling for insulin, where CDC42 regulates cortical actin remodeling and recruitment of exocytotic machinery required for the sustained second phase of insulin release. In signaling networks controlling proliferation and survival, CDC42 modulates pathways such as EGFR–mTORC1 and contributes to activation of downstream cascades including MAPK and PI3K, which influence transcriptional programs and cell‑cycle progression. Germline mutations and dysregulated CDC42 activity associate with developmental and autoinflammatory syndromes, while overexpression or hyperactivation in tumors correlates with enhanced motility, invasive behavior, and metastatic dissemination.

References
https://pubmed.ncbi.nlm.nih.gov/35154449/ https://pubmed.ncbi.nlm.nih.gov/21115489/

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%