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MAB3291

Sigma-Aldrich

Anti-H-Ras Antibody, clone 7D7.2

clone 7D7.2, Chemicon®, from mouse

Sinônimo(s):

Anti-C-BAS/HAS, Anti-C-H-RAS, Anti-C-HA-RAS1, Anti-CTLO, Anti-H-RASIDX, Anti-HAMSV, Anti-HRAS1, Anti-RASH1, Anti-p21ras

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About This Item

Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

fonte biológica

mouse

Nível de qualidade

100

forma do anticorpo

purified antibody

tipo de produto de anticorpo

primary antibodies

clone

7D7.2, monoclonal

reatividade de espécies

rat, mouse, human

fabricante/nome comercial

Chemicon®

técnica(s)

ELISA: suitable
western blot: suitable

Isotipo

IgG2b

nº de adesão NCBI

NM_005343.2
NM_176795.2

nº de adesão UniProt

P01112

Condições de expedição

wet ice

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... HRAS(3265)

Especificidade

Recognizes H-Ras (the oncogene of Harvey murine sarcoma virus). Approximate molecular weight of 21 kDa.

Imunogênio

Full-length recombinant human H-Ras - GST fusion protein

Aplicação

Research Category
Signaling
Research Sub Category
MAP Kinases
This Anti-H-Ras Antibody, clone 7D7.2 is validated for use in ELISA, WB for the detection of H-Ras.
Western blot

ELISA

Optimal working dilutions must be determined by end user.

forma física

0.02M phosphate buffer, 0.25M NaCl, pH 7.6, 0.1% sodium azide
Format: Purified

Armazenamento e estabilidade

Maintain refrigerated at 2-8°C in undiluted aliquots for up to 6 months.

WARNING: The monoclonal reagent solution contains 0.1% sodium azide as a preservative. Due to potential hazards arising from the build up of this material in pipes, spent reagent should be disposed of with liberal volumes of water.

Outras notas

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Informações legais

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Exoneração de responsabilidade

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

WGK 2

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.

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Ho-June Lee et al.
Molecular cancer therapeutics, 16(4), 694-704 (2017-02-01)
Cancer cell line profiling to identify previously unrecognized kinase dependencies revealed a novel nonmutational dependency on the DNA damage response checkpoint kinase Chk1. Although Chk1 is a promising therapeutic target in p53-deficient cancers, we found that Ras-MEK signaling engages Chk1
Wouter W Kallemeijn et al.
Nature protocols, 16(11), 5083-5122 (2021-10-29)
Protein lipidation is one of the most widespread post-translational modifications (PTMs) found in nature, regulating protein function, structure and subcellular localization. Lipid transferases and their substrate proteins are also attracting increasing interest as drug targets because of their dysregulation in
Candida Zuchegna et al.
Redox report : communications in free radical research, 27(1), 150-157 (2022-07-14)
Although the protooncogenes small GTPases Ras are redox-sensitive proteins, how they are regulated by redox signaling in the central nervous system (CNS) is still poorly understood. Alteration in redox-sensitive targets by redox signaling may have myriad effects on Ras stability
Atsushi Hoshino et al.
Nature communications, 4, 2308-2308 (2013-08-07)
Cumulative evidence indicates that mitochondrial dysfunction has a role in heart failure progression, but whether mitochondrial quality control mechanisms are involved in the development of cardiac dysfunction remains unclear. Here we show that cytosolic p53 impairs autophagic degradation of damaged

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