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18070
Mutant Ras Antibody Sampler Kit
Primary Antibodies

Mutant Ras Antibody Sampler Kit #18070

Western Blotting Image 1

Western blot analysis of extracts from various cell lines using Ras (G12V Mutant Specific) (D2H12) Rabbit mAb (upper), Ras (D2C1) Rabbit mAb #8955 (middle), and β-Actin (D6A8) #8457 (lower).

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Western Blotting Image 2

Western blot analysis of extracts from various cell lines using Ras (G12D Mutant Specific) (D8H7) Rabbit mAb (upper), Ras (D2C1) Rabbit mAb #8955 (middle), and β-Actin (D6A8) #8457 (lower).

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Western Blotting Image 3

Western blot analysis of extracts from various cell lines using Ras (D2C1) Rabbit mAb.

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Western Blotting Image 4

After the primary antibody is bound to the target protein, a complex with HRP-linked secondary antibody is formed. The LumiGLO® is added and emits light during enzyme catalyzed decomposition.

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Product Includes Quantity Applications Reactivity MW(kDa) Isotype
Ras (G12V Mutant Specific) (D2H12) Rabbit mAb 14412 20 µl
  • WB
H 21 Rabbit IgG
Ras (G12D Mutant Specific) (D8H7) Rabbit mAb 14429 20 µl
  • WB
H 21 Rabbit IgG
Ras (D2C1) Rabbit mAb 8955 20 µl
  • WB
H M R Mk 21 Rabbit IgG
Anti-rabbit IgG, HRP-linked Antibody 7074 100 µl
  • WB
Goat 

The Mutant Ras Antibody Sampler Kit provides an economical means of detecting common mutation in the Ras protein. The kit contains enough primary and secondary antibodies to perform at least two western blot experiments.

Each antibody in the Mutant Ras Antibody Sampler kit detects endogenous levels of its target protein. Ras (D2C1) Rabbit mAb recognizes endogenous levels of total Ras protein, specifically K-Ras and N-Ras. This antibody does not cross-react with H-Ras or R-Ras.

Monoclonal antibodies are produced by immunizing rabbits with synthetic peptides corresponding to G12V and G12D mutant sequences of human Ras protein. Ras (D2C1) Rabbit mAb was produced by immunizing rabbits with a recombinant protein specific to human K-Ras protein.

The 21 kDa guanine-nucleotide binding proteins (K-Ras, H-Ras, and N-Ras) cycle between active (GTP-bound) and inactive (GDP-bound) forms (1). Receptor tyrosine kinases and G protein-coupled receptors activate Ras, which then stimulates the Raf-MEK-MAPK pathway (2-4). GTPase-activating proteins (GAP) normally facilitate the inactivation of Ras. However, research studies have shown that in 30% of human tumors, point mutations in Ras prevent the GAP-mediated inhibition of this pathway (5). The most common oncogenic Ras mutation found in tumors is Gly12 to Asp12 (G12D), which prevents Ras inactivation, possibly by increasing the overall rigidity of the protein (5,6). Additional oncogenic mutations of Ras have been observed at varying frequencies at codons 12, 13, and 61. The Gly12 to Val12 (G12V) mutation has been detected in a number of different cancers, including colorectal and thyroid cancer (7,8).

  1. Boguski, M.S. and McCormick, F. (1993) Nature 366, 643-54.
  2. Avruch, J. et al. (1994) Trends Biochem Sci 19, 279-83.
  3. Buday, L. and Downward, J. (1993) Cell 73, 611-20.
  4. Huang, D.C. et al. (1993) Mol Cell Biol 13, 2420-31.
  5. Bos, J.L. (1989) Cancer Res 49, 4682-9.
  6. Ma, J. and Karplus, M. (1997) J Mol Biol 274, 114-31.
  7. Prior, I.A. et al. (2012) Cancer Res 72, 2457-67.
  8. Winder, T. et al. (2009) Oncol Rep 21, 1283-7.
Entrez-Gene Id
3845 , 4893
Swiss-Prot Acc.
P01116 , P01111
For Research Use Only. Not For Use In Diagnostic Procedures.

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