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05-1072

Sigma-Aldrich

Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2

clone 9A11.2, Upstate®, from mouse

Synonym(s):

Anti-C-K-RAS, Anti-CFC2, Anti-K-RAS2A, Anti-K-RAS2B, Anti-K-RAS4A, Anti-K-RAS4B, Anti-K-Ras, Anti-K-Ras 2, Anti-KI-RAS, Anti-KRAS1, Anti-KRAS2, Anti-NS, Anti-NS3, Anti-OES, Anti-RALD, Anti-RASK2, Anti-c-Ki-ras, Anti-c-Ki-ras2

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About This Item

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

biological source

mouse

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

9A11.2, monoclonal

species reactivity

mouse, rat, human

manufacturer/tradename

Upstate®

technique(s)

immunohistochemistry: suitable (paraffin)
western blot: suitable

isotype

IgG1κ

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

General description

Ras, a proto-oncogene, is a small G-protein that has 3 primary isoforms (H-Ras, N-Ras, and K-Ras) that differ in there approximately 20 C-terminal amino acids. H-Ras was first discovered as a transforming product the retrovirus Harvey murine virus and K-Ras of Kirten sarcoma virus. Ras is a heavily studied target of both academic and pharmaceutical research because of its implications in various pathways and diseases as well as being mutated in a large number of human cancers. Ras is most notably the activator of the Erk/MAPK kinase pathway as activator of Raf, as well as an activator of PI3 Kinase (PI3K). In its oncogenic, mutated state, Ras is unable to hydrolyze GTP to GDP, thus staying in an active state and activating numerous pathways including the MAPK pathway through its activation of Raf, but also others as well that include PI3 Kinase and RalGDS. One path that the pharmaceutical industry has taken to control Ras and its activity is by finding what some consider its Achilles’ heel. For its activation, Ras must localize to the plasma membrane, but interestingly, it lacks a transmembrane domain. To achieve this, Ras must first undergo a post-translational modification (PTM) known as prenylation or geranylation at its C-terminal CAAX motif. For this to take place, a controlled three step process must occur. The first step in the process is the prenylation or geranylation of the C in the CAAX motif that is initiated by the covalent attachment of farnesyl groups to the cysteine that is catalyzed by the heterodimer enzymes farnesyl transferases and . After this modification, the –aaX of the motif is proteolytically removed via Rce1 (Ras Converting Enzyme 1), a membrane associated endoprotease, by a mechanism that is still not fully understood. Finally, the C-terminal prenylcysteine is now methlylated by ICMT (Isoprenylcysteine Carboxymethyl Transferase). These drugs have yet to pass clinical trials though and there is doubt that they will ever be successful in treating tumors associated with Ras activation.

Specificity

Recognizes K-, H-, and N-Ras (all 3 isofroms).

Immunogen

Full length recombinant GST-tagged human H-Ras.

Application

Research Category
Signaling

Apoptosis & Cancer
Research Sub Category
MAP Kinases

G-proteins
This Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2 is validated for use in WB, IH(P) for the detection of Ras.

Quality

routinely evaluated by immunoblot on RIPA lysate from human A431 carcinoma cells, mouse 3T3, mouse brain, orrat brain.

Target description

21 kDa

Physical form

Format: Purified
Protein G Purified
Protein G purified mouse monoclonal in storage buffer containing 0.1M Tris-Glycine (pH 7.4), 15mM NaCl, and 0.05% NaN3.

Storage and Stability

Stable for 1 year at 4°C from date of receipt.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.

Other Notes

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

Legal Information

UPSTATE 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

12 - Non Combustible Liquids

WGK

WGK 1

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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Innate inflammation induced by the 8-oxoguanine DNA glycosylase-1-KRAS-NF-?B pathway.
Aguilera-Aguirre, L; Bacsi, A; Radak, Z; Hazra, TK; Mitra, S; Sur, S; Brasier, AR; Ba, X; Boldogh, I
Journal of immunology (Baltimore, Md. : 1950) (1950)
Xiahui Xiong et al.
Biology open, 8(10) (2019-05-31)
In human, loss of Acid Sphingomeylinase (ASM/SMPD1) causes Niemann-Pick Disease, type A. ASM hydrolyzes sphingomyelins to produce ceramides but protein targets of ASM remain largely unclear. Our mass-spectrometry-based proteomic analyses have identified >100 proteins associated with the ASM-dependent, detergent-resistant membrane
Temporal dissection of K-ras(G12D) mutant in vitro and in vivo using a regulatable K-ras(G12D) mouse allele.
Wang, Z; Feng, Y; Bardeesy, N; Bardessy, N; Wong, KK; Liu, XY; Ji, H
Testing null
Pomme Boissier et al.
Traffic (Copenhagen, Denmark), 14(12), 1255-1271 (2013-10-12)
Eph receptors and their membrane-bound ligands, the ephrins, represent a complex subfamily of receptor tyrosine kinases (RTKs). Eph/ephrin binding can lead to various and opposite cellular behaviors such as adhesion versus repulsion, or cell migration versus cell-adhesion. Recently, Eph endocytosis
Andrew M Waters et al.
Science signaling, 10(498) (2017-09-28)
There is intense interest in developing therapeutic strategies for RAS proteins, the most frequently mutated oncoprotein family in cancer. Development of effective anti-RAS therapies will be aided by the greater appreciation of RAS isoform-specific differences in signaling events that support

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