EGF Receptor (E746-A750del Specific) Antibody [L24P14]

Catalog No.: F0430

Application: Reactivity: Human

Lane 1: H3255, Lane 2: H1975, Lane 3: NCI-H1650

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:1000 IP1:100 IHC1:100 - 1:400 IF1:100 - 1:200 FCM1:250 - 1:1000

Application
WB, IP, IHC, IF, FCM

Source
Rabbit Monoclonal Antibody

Reactivity
Human

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
175 kDa

Datasheet & SDS

生物学的記述

Specificity
EGF Receptor (E746-A750del Specific) Antibody [L24P14] detects endogenous levels of total EGF E746-A750del mutant Receptor protein.

Clone
L24P14

Synonym(s)
Epidermal growth factor receptor; Proto-oncogene c-ErbB-1;Receptor tyrosine-protein kinase erbB-1; EGFR; ERBB; ERBB1; HER1

Background
EGF Receptor (E746-A750del Specific) is a common exon 19 in-frame deletion mutation in the epidermal growth factor receptor (EGFR), a receptor tyrosine kinase of the ErbB/HER family, resulting in the loss of five amino acids (Glu746-Ala750) from the kinase domain’s C-helix proximal region and accounting for about 90% of exon 19 deletions in non-small cell lung cancer (NSCLC). This deletion (c.2236_2250del15) repositions the C-helix N-terminally toward the N-lobe, stabilizing an active αC-β4 kinase conformation, which increases ATP-site accessibility and promotes allosteric asymmetric dimerization for trans-autophosphorylation. As a result, E746-A750del leads to ligand-independent constitutive kinase activation, hyperstimulating oncogenic signaling cascades such as RAS-RAF-MEK-ERK, PI3K-AKT-mTOR, and PLCγ to drive tumor growth, invasion, and metastasis, especially in EGFR-mutant NSCLC among non-smokers. Clinically, this mutation predicts high sensitivity to first- and third-generation tyrosine kinase inhibitors (TKIs) like osimertinib, although secondary T790M mutation can confer drug resistance.

Background

EGF Receptor (E746-A750del Specific) is a common exon 19 in-frame deletion mutation in the epidermal growth factor receptor (EGFR), a receptor tyrosine kinase of the ErbB/HER family, resulting in the loss of five amino acids (Glu746-Ala750) from the kinase domain’s C-helix proximal region and accounting for about 90% of exon 19 deletions in non-small cell lung cancer (NSCLC). This deletion (c.2236_2250del15) repositions the C-helix N-terminally toward the N-lobe, stabilizing an active αC-β4 kinase conformation, which increases ATP-site accessibility and promotes allosteric asymmetric dimerization for trans-autophosphorylation. As a result, E746-A750del leads to ligand-independent constitutive kinase activation, hyperstimulating oncogenic signaling cascades such as RAS-RAF-MEK-ERK, PI3K-AKT-mTOR, and PLCγ to drive tumor growth, invasion, and metastasis, especially in EGFR-mutant NSCLC among non-smokers. Clinically, this mutation predicts high sensitivity to first- and third-generation tyrosine kinase inhibitors (TKIs) like osimertinib, although secondary T790M mutation can confer drug resistance.

References
[1] Galdadas I, et al. Elife. 2021 Jul 28;10:e65824. [2] Red Brewer M, et al. Proc Natl Acad Sci U S A. 2013 Sep 17;110(38):E3595-604.

PVDFメンブレン孔径参考表

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%