Cell Signaling Technology

Product Pathways - Tyrosine Kinase / Adaptors

MATK/CHK (D2I6U) Rabbit mAb #20729

No. Size Price
20729S 100 µl ( 10 western blots ) ¥3,250.00 现货查询 购买询价 防伪查询
20729 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 52,56 Rabbit IgG
IP 1:100

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,

Specificity / Sensitivity

MATK/CHK (D2I6U) Rabbit mAb recognizes endogenous levels of total MATK/CHK protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Glu97 of human MATK/CHK protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from GDM-1, HL-60 and CMK cell lines using MATK/CHK (D2I6U) Rabbit mAb.



Immunoprecipitation of MATK/CHK protein from GDM-1 cell extracts. Lane 1 is 10% input, lane 2 is Rabbit (DA1E) mAb IgG XP® Isotype Control #3900, and lane 3 is MATK/CHK (D2I6U) Rabbit mAb. Western blot analysis was performed using MATK/CHK (D2I6U) Rabbit mAb


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).

  1. Sakano, S. et al. (1994) Oncogene 9, 1155-61.
  2. Chow, L.M. et al. (1994) Proc Natl Acad Sci U S A 91, 4975-9.
  3. Bennett, B.D. et al. (1994) J Biol Chem 269, 1068-74.
  4. Klages, S. et al. (1994) Proc Natl Acad Sci U S A 91, 2597-601.
  5. Chong, Y.P. et al. (2004) J Biol Chem 279, 20752-66.
  6. Chong, Y.P. et al. (2006) J Biol Chem 281, 32988-99.
  7. Zrihan-Licht, S. et al. (1998) J Biol Chem 273, 4065-72.
  8. Kim, S. et al. (2002) J Biol Chem 277, 36465-70.
  9. Price, D.J. et al. (1997) J Biol Chem 272, 5915-20.
  10. Lee, B.C. et al. (2005) Cancer Res 65, 2840-5.
  11. McShan, G.D. et al. (2002) Int J Oncol 21, 197-205.
  12. Fu, Y. et al. (2006) Int J Oncol 29, 1453-8.
  13. Dokmanovic, M. et al. (2014) Cancer Biol Ther 15, 1029-41.
  14. Zhu, S. et al. (2008) Oncogene 27, 2027-34.
  15. Kim, S.O. et al. (2004) Cancer 101, 1018-27.

Application References

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