KRAS Antibody [A18C4] | Primary Antibodies

Application: Reactivity: Human

Lane 1: Hela, Lane 2: 22Rv1, Lane 3: SW480

Usage Information

Dilution
WB1:1000-1:5000

Application
WB, IF, ELISA

Reactivity
Human

Source
Mouse 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
KRAS Antibody [A18C4] detects endogenous levels of total KRAS protein.

Clone
A18C4

Synonym(s)
GTPase Kras; K-Ras 2; Ki-Ras; c-K-ras; c-Ki-ras; KRAS; KRAS2; RASK2

Background
KRAS belongs to the Ras family of small GTPases alongside HRAS and NRAS, cycling between GTP-bound active and GDP-bound inactive states to transduce growth factor signals from receptor tyrosine kinases into intracellular cascades regulating proliferation, survival, and differentiation. KRAS organizes a core G domain for nucleotide binding and hydrolysis with switch I/II regions that undergo conformational shifts upon GTP loading, alongside a hypervariable C-terminus featuring a farnesyl cysteine for membrane anchoring via CAAX motif processing. Oncogenic mutations at G12, G13, or Q61 impair GTPase activity by sterically blocking GAP-mediated arginine finger insertion into the active site, locking KRAS in the GTP conformation that constitutively recruits RAF kinases through switch I effector binding while allosterically engaging PI3K at switch II to activate AKT-mTOR signaling for anabolic metabolism. GTP-KRAS dimers form nanoclusters at the plasma membrane that amplify RAF dimerization and MEK-ERK phosphorylation cascades culminating in MYC and cyclin D1 transcription for G1/S progression, while parallel PI3K pathway activation sustains FOXO exclusion and BCL2 upregulation to evade apoptosis. In physiological contexts, KRAS calibrates lung alveolar development and pancreatic acinar regeneration through precise spatial-temporal activation tuned by SOS GEFs and NF1 GAPs responding to EGFR gradients. Mutant KRAS drives nearly universal pancreatic ductal adenocarcinoma initiation alongside frequent colorectal and lung cancers through autocrine loops sustaining RAF and PI3K outputs despite upstream inhibition.

Background

KRAS belongs to the Ras family of small GTPases alongside HRAS and NRAS, cycling between GTP-bound active and GDP-bound inactive states to transduce growth factor signals from receptor tyrosine kinases into intracellular cascades regulating proliferation, survival, and differentiation. KRAS organizes a core G domain for nucleotide binding and hydrolysis with switch I/II regions that undergo conformational shifts upon GTP loading, alongside a hypervariable C-terminus featuring a farnesyl cysteine for membrane anchoring via CAAX motif processing. Oncogenic mutations at G12, G13, or Q61 impair GTPase activity by sterically blocking GAP-mediated arginine finger insertion into the active site, locking KRAS in the GTP conformation that constitutively recruits RAF kinases through switch I effector binding while allosterically engaging PI3K at switch II to activate AKT-mTOR signaling for anabolic metabolism. GTP-KRAS dimers form nanoclusters at the plasma membrane that amplify RAF dimerization and MEK-ERK phosphorylation cascades culminating in MYC and cyclin D1 transcription for G1/S progression, while parallel PI3K pathway activation sustains FOXO exclusion and BCL2 upregulation to evade apoptosis. In physiological contexts, KRAS calibrates lung alveolar development and pancreatic acinar regeneration through precise spatial-temporal activation tuned by SOS GEFs and NF1 GAPs responding to EGFR gradients. Mutant KRAS drives nearly universal pancreatic ductal adenocarcinoma initiation alongside frequent colorectal and lung cancers through autocrine loops sustaining RAF and PI3K outputs despite upstream inhibition.

References
https://pubmed.ncbi.nlm.nih.gov/33676749/ https://pubmed.ncbi.nlm.nih.gov/20563247/

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%