MAB3291
Anti-H-Ras Antibody, clone 7D7.2
clone 7D7.2, Chemicon®, from mouse
Synonym(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
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
purified antibody
antibody product type
primary antibodies
clone
7D7.2, monoclonal
species reactivity
rat, mouse, human
manufacturer/tradename
Chemicon®
technique(s)
ELISA: suitable
western blot: suitable
isotype
IgG2b
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... HRAS(3265)
Specificity
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
Application
Research Category
Signaling
Signaling
Research Sub Category
MAP Kinases
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.
ELISA
Optimal working dilutions must be determined by end user.
Physical form
0.02M phosphate buffer, 0.25M NaCl, pH 7.6, 0.1% sodium azide
Format: Purified
Storage and Stability
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.
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.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
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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Storage Class Code
10 - Combustible liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘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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