R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
MATK/CHK (D2I6U) Rabbit mAb #20729
Filter:
- WB
- IP
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 52,56 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
MATK/CHK (D2I6U) Rabbit mAb recognizes endogenous levels of total MATK/CHK protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Glu97 of human MATK/CHK protein.
Background
MATK/CHK (CTK, NTK and HYL) is a non-receptor tyrosine kinase structually and functionally homologous to Csk kinase. The kinase was identified through molecular cloning from multiple tissues by different research groups. Like Csk, MATK/CHK has a N-terminal SH3 domain, followed by an SH2 domain and a C-terminal catalytic kinase domain (1-4). MATK/CHK inhibits Src family members in several different ways. First, it directly phosphorylates the inhibitory C-terminal tyrosine of Src (as well as other Src family members). This induces a Src protein conformational change from the active to inactive state (2,4). Second, it binds directly to activated Src and induces a conformational change to the inactive state (5,6). The SH2 domain of MATK/CHK directly interacts with the phosphorylated tyrosine of activated receptor tyrosine kinases, such as ErbB-2 and c-Kit, to inhibit receptor function (7-9). MATK/CHK negatively regulates tumor cell growth, migration and invasion (10-13). Decreased expression of the protein has been correlated with brain tumors as well as colon cancers in research studies (14-15).
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- Klages, S. et al. (1994) Proc Natl Acad Sci U S A 91, 2597-601.
- Chong, Y.P. et al. (2004) J Biol Chem 279, 20752-66.
- Chong, Y.P. et al. (2006) J Biol Chem 281, 32988-99.
- Zrihan-Licht, S. et al. (1998) J Biol Chem 273, 4065-72.
- Kim, S. et al. (2002) J Biol Chem 277, 36465-70.
- Price, D.J. et al. (1997) J Biol Chem 272, 5915-20.
- Lee, B.C. et al. (2005) Cancer Res 65, 2840-5.
- McShan, G.D. et al. (2002) Int J Oncol 21, 197-205.
- Fu, Y. et al. (2006) Int J Oncol 29, 1453-8.
- Dokmanovic, M. et al. (2014) Cancer Biol Ther 15, 1029-41.
- Zhu, S. et al. (2008) Oncogene 27, 2027-34.
- Kim, S.O. et al. (2004) Cancer 101, 1018-27.
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