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05-1072 Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2

100 µg  
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      Key Specifications Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      H, M, RWB, IH(P)MPurifiedMonoclonal Antibody
      Catalogue Number05-1072
      Brand Family Upstate
      Trade Name
      • Upstate
      DescriptionAnti-Ras Antibody, (K-, H-, N-), clone 9A11.2
      Background InformationRas, 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.
      Product Information
      PresentationProtein G purified mouse monoclonal in storage buffer containing 0.1M Tris-Glycine (pH 7.4), 15mM NaCl, and 0.05% NaN3.
      Quality LevelMQ100
      ApplicationThis Anti-Ras Antibody, (K-, H-, N-), clone 9A11.2 is validated for use in WB, IH(P) for the detection of Ras.
      Key Applications
      • Western Blotting
      • Immunohistochemistry (Paraffin)
      Biological Information
      ImmunogenFull length recombinant GST-tagged human H-Ras.
      ConcentrationPlease refer to the Certificate of Analysis for the lot-specific concentration.
      SpecificityRecognizes K-, H-, and N-Ras (all 3 isofroms).
      Species Reactivity
      • Human
      • Mouse
      • Rat
      Antibody TypeMonoclonal Antibody
      Entrez Gene Number
      Entrez Gene SummaryMembers of the RAS superfamily of GTP-binding proteins, which includes MRAS, are membrane-anchored, intracellular signal transducers responsible for a variety of normal cellular functions. They are oncogenically activated in a significant fraction of tumors.[supplied by OMIM]
      Gene Symbol
      • K-Ras
      • Ki-Ras
      • K-Ras2
      • Kras-2
      • p21B
      • KRAS
      • RASK2
      • HRAS
      • HA_RAS
      • N-RAS
      • H-RAS
      • NRAS
      • NRAS1
      • ALPS4
      Purification MethodProtein G Purified
      UniProt Number
      UniProt SummaryFUNCTION: Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
      Enzyme regulation:Alternate between an inactive form bound to GDP and an active form bound to GTP. Activated by a guanine nucleotide-exchange factor (GEF) and inactivated by a GTPase-activating protein (GAP).
      SIZE: 189 amino acids; 21,656 Da
      SUBUNIT: Interacts with PHLPP (By similarity).
      SUBCELLULAR LOCATION: Cell membrane; Lipid-anchor; Cytoplasmic side.
      Involvement in disease:
      Defects in KRAS are a cause of acute myelogenous leukemia (AML) [MIM:601626]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development.

      Defects in KRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. It is characterized by leukocytosis with tissue infiltration and in vitro hypersensitivity of myeloid progenitors to granulocyte-macrophage colony stimulating factor.

      Defects in KRAS are the cause of Noonan syndrome 3 (NS3) [MIM:609942]. Noonan syndrome (NS) [MIM:163950] is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Rarely, NS is associated with juvenile myelomonocytic leukemia (JMML). NS3 inheritance is autosomal dominant.

      Defects in KRAS are a cause of cardiofaciocutaneous syndrome (CFC syndrome) [MIM:115150]; also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. The inheritance of CFC syndrome is autosomal dominant.

      KRAS mutations are involved in cancer development.
      Molecular Weight21 kDa
      Physicochemical Information
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Quality Assuranceroutinely evaluated by immunoblot on RIPA lysate from human A431 carcinoma cells, mouse 3T3, mouse brain, orrat brain.
      Usage Statement
      • 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.
      Storage and Shipping Information
      Storage ConditionsStable 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.
      Packaging Information
      Material Size100 µg
      Transport Information
      Supplemental Information


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


      Safety Data Sheet (SDS) 

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

      TitleLot Number
      Anti-Ras (K-,H-,N-), clone 9A11.2 - 2444150 2444150
      Anti-Ras (K-,H-,N-), clone 9A11.2 - NG1752500 NG1752500
      Anti-Ras (K-,H-,N-), clone 9A11.2 - 2198978 2198978
      Anti-Ras (K-,H-,N-), clone 9A11.2 - 2325713 2325713
      Anti-Ras (K-,H-,N-), clone 9A11.2 - 2363937 2363937
      Anti-Ras (K-,H-,N-), clone 9A11.2 - 2517760 2517760
      Anti-Ras (K-,H-,N-), clone 9A11.2 - 3249934 3249934
      Anti-Ras (K-,H-,N-), clone 9A11.2 - 3385816 3385816
      Anti-Ras (K-,H-,N-), clone 9A11.2 - 3499850 3499850
      Anti-Ras (K-,H-,N-), clone 9A11.2 - 3695879 3695879


      Reference overviewApplicationPub Med ID
      Innate inflammation induced by the 8-oxoguanine DNA glycosylase-1-KRAS-NF-κB 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)  193  4643-53  2014

      Show Abstract
      25267977 25267977
      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
      PloS one  7  e37308  2012

      Show Abstract
      Western Blotting22606359 22606359

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      Life Science Research > Antibodies and Assays > Primary Antibodies