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MAB3291

Sigma-Aldrich

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

clone 7D7.2, Chemicon®, from mouse

Synonym(e):

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

UNSPSC-Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

Biologische Quelle

mouse

Qualitätsniveau

100

Antikörperform

purified antibody

Antikörper-Produkttyp

primary antibodies

Klon

7D7.2, monoclonal

Speziesreaktivität

rat, mouse, human

Hersteller/Markenname

Chemicon®

Methode(n)

ELISA: suitable
western blot: suitable

Isotyp

IgG2b

NCBI-Hinterlegungsnummer

NM_005343.2
NM_176795.2

UniProt-Hinterlegungsnummer

P01112

Versandbedingung

wet ice

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... HRAS(3265)

Spezifität

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

Immunogen

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

Anwendung

Research Category
Zelluläre Signaltransduktion
Research Sub Category
MAP-Kinasen
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.

Physikalische Form

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

Lagerung und Haltbarkeit

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.

Sonstige Hinweise

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

Rechtliche Hinweise

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

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 2

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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Die Dokumentenbibliothek aufrufen

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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