Upstream / Downstream

Explore pathways related to this product.

Antibody Guarantee

CST Antibody Performance Guarantee



Find answers on our FAQs page.


Visit PhosphoSitePlus®

PTM information and tools available.


Product Includes Quantity Applications Reactivity MW(kDa) Isotype
c-Fos Antibody 4384 40 µl
H M R 62 Rabbit 
c-Abl Antibody 2862 40 µl
H M R 135 (c-Abl); 210 (Bcr-Abl) Rabbit 
c-Jun (60A8) Rabbit mAb 9165 40 µl
H M R Mk 43, 48 Rabbit IgG
c-Kit (D13A2) XP® Rabbit mAb 3074 40 µl
H M 120 and 145 Rabbit 
c-Myc (D84C12) XP® Rabbit mAb 5605 40 µl
H M R 57-65 Rabbit IgG
c-Raf Antibody 9422 40 µl
H M R Mk 65 to 75 Rabbit 
Ras (27H5) Rabbit mAb 3339 40 µl
H M R Mk Dm Sc 21 Rabbit IgG
c-Rel Antibody 4727 40 µl
H Mk 78 Rabbit 
Src (36D10) Rabbit mAb 2109 40 µl
H M R Hm Mk B Pg 60 Rabbit IgG
Anti-rabbit IgG, HRP-linked Antibody 7074 100 µl
All Goat 

Product Description

The c-Oncogene Antibody Sampler Kit provides an economical means of evaluating total levels of various oncogenic proteins. The kit contains enough primary and secondary antibodies to perform four Western blot experiments.

Specificity / Sensitivity

Unless otherwise indicated, each antibody in the c-Oncogene Antibody Sampler Kit detects endogenous levels of total target protein and does not cross-react with related proteins. c-Jun (60A8) Rabbit mAb detects endogenous levels of total c-Jun protein, regardless of phosphorylation state. Ras (27H5) Rabbit mAb detects endogenous levels of total K-Ras, H-Ras and N-Ras proteins. Src (36D10) Rabbit mAb detects endogenous levels of Src proteins and may cross-react with other Src family members. The c-Myc (D84C12) Rabbit mAb detects endogenous levels of total c-Myc protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with synthetic peptides corresponding to residues near the carboxy terminus of human c-Rel, residues near the carboxy-terminus of human c-Fos, and corresponding to the sequence close to the carboxy-terminus of human c-Abl. Antibodies are purified by protein A and peptide affinity chromatography. Monoclonal antibody is produced by immunizing animals with synthetic peptides corresponding to residues near the carboxy terminus of human Src, residues near the amino terminus of human K-Ras, from the amino-terminal sequence of human c-Jun, residues near the amino terminus of c-Myc and corresponding to the residues surrounding Tyr703 of human c-Kit.

The regulation of cell growth, differentiation and programmed death is coordinated by several sets of proteins that comprise essential signal transduction pathways. Many of these key regulatory proteins are encoded by proto-oncogenes, which can be activated (altered) to change the typical cell program to one of abnormal cell growth and unregulated development. Proteins encoded by proto-oncogenes include growth factors and other ligands, receptor proteins, tyrosine kinases, various regulatory proteins (i.e. GTPases) and transcription factors. Together these proteins comprise the basic elements of cell signaling pathways; altered expression or mutation of one or more of these components can lead to oncogenic growth (reviewed in 1).

Non-receptor (i.e. cytoplasmic, nuclear) tyrosine kinases such as c-Abl and Src play key roles in the regulation of cell proliferation, differentiation, apoptosis, cell adhesion and stress responses (2,3). Alteration of the corresponding c-Abl and Src proto-oncogenes is associated with oncogenesis; Abl1-BCR gene translocations result in chronic myelogenous leukemia (CML) while constitutively active Src is seen in some patients with colon cancer and altered Src expression is seen in a wide array of cancers (2,4). Regulation of Raf tyrosine kinase by Ras GTPase controls downstream kinases in the MEK/MAPK signaling pathway (5). Activation of the Ras and Raf proto-oncogenes are common in human cancers and both proteins are seen as potential therapeutic targets (6). The receptor tyrosine kinase c-Kit plays a critical role in activation and growth of hematopoietic stem cells (7); mutations that inhibit c-Kit kinase activity are associated with a variety of developmental disorders while mutations producing constitutively active c-Kit can result in mastocytosis and gastrointestinal stromal tumors (8). The alteration of key transcription factors such as c-Fos, c-Jun, c-Myc and c-Rel that are normally responsible for regulating cell and tissue growth, differentiation and the inflammation/immune response, can also result in unregulated, oncogenic cell growth (9-12).

1.  Croce, C.M. (2008) N Engl J Med 358, 502-11.

2.  Thomas, S.M. and Brugge, J.S. (1997) Annu Rev Cell Dev Biol 13, 513-609.

3.  Avruch, J. et al. (1994) Trends Biochem Sci 19, 279-83.

4.  Wang, J.Y. (2000) Oncogene 19, 5643-50.

5.  Gommerman, J.L. et al. (1997) J Biol Chem 272, 30519-25.

6.  Dehm, S.M. and Bonham, K. (2004) Biochem Cell Biol 82, 263-74.

7.  Nocka, K. et al. (1990) EMBO J 9, 1805-13.

8.  Stites, E.C. et al. (2007) Science 318, 463-7.

9.  Shaulian, E. and Karin, M. (2002) Nat Cell Biol 4, E131-6.

10.  Milde-Langosch, K. (2005) Eur J Cancer 41, 2449-61.

11.  Yokota, J. et al. (1986) Science 231, 261-5.

12.  Rayet, B. and Gélinas, C. (1999) Oncogene 18, 6938-47.

Entrez-Gene Id 3265, 3845, 4893
Swiss-Prot Acc. P01112, P01116, P01111

Protein Specific References

Jeong WJ et al. (2012) Sci Signal 5, ra30

For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.
U.S. Patent No. 5,675,063.