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Gene Review

KIF2C  -  kinesin family member 2C

Homo sapiens

Synonyms: CT139, KNSL6, Kinesin-like protein 6, Kinesin-like protein KIF2C, MCAK, ...
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Disease relevance of KIF2C

  • In contrast, 9 of 9 colon cancer specimens showed overexpression of KNSL6 mRNA, ranging from 5 to 44 times the level detected in normal colon tissue, indicating that this antigen could also be a valuable therapeutic target [1].
  • These findings suggest the involvement of a PRC1-KIF2C/MCAK complex in breast tumorigenesis, and this complex should be a promising target for the development of novel treatments for breast cancer [2].

High impact information on KIF2C

  • We propose that the chromosomal passenger complex regulates local MCAK activity to permit spindle formation via stabilization of chromatin-associated microtubules [3].
  • The Kin I kinesins are microtubule-destabilizing enzymes important for neuronal transport, spindle assembly, and chromosome segregation. now show that the Kin I MCAK is a microtubule end-stimulated ATPase that can catalytically depolymerize MT's [4].
  • MCAK has one high-affinity binding site per protofilament end, which, when occupied, has both the depolymerase and ATPase activities [5].
  • Tip tracking of MCAK is inhibited by phosphorylation and is dependent on the extreme COOH-terminal tail of MCAK [6].
  • Bipolar spindle assembly was restored in cells lacking Kif2a by treatments that altered microtubule assembly (nocodazole), eliminated kinetochore-microtubule attachment (loss of Nuf2), or stabilized microtubule plus ends at kinetochores (loss of MCAK) [7].

Biological context of KIF2C


Anatomical context of KIF2C

  • MCAK associates with the tips of polymerizing microtubules [6].
  • MCAK, a Kin I kinesin, increases the catastrophe frequency of steady-state HeLa cell microtubules in an ATP-dependent manner in vitro [10].
  • MCAK protein is present in interphase and mitotic CHO cells and is transcribed as a single 3.4-kb message [11].
  • The first involves a role for TOGp in protecting spindle MTs from MCAK activity at the centrosome, which appears essential to prevent the formation of disorganized multipolar spindles [12].
  • With regard to KNSL6 mRNA expression, only trace levels were detected in 15 different normal tissues with the exception of testis, which showed a high level of KNSL6 mRNA expression [1].

Associations of KIF2C with chemical compounds

  • We found that deletions and alanine substitutions of highly conserved positively charged residues in the MCAK neck domain significantly reduced MT depolymerization activity [13].
  • The Interplay of the N- and C-Terminal Domains of MCAK Control Microtubule Depolymerization Activity and Spindle Assembly [14].

Other interactions of KIF2C

  • MCAK is a homodimer that is encoded by a single gene and has no associated subunits [15].

Analytical, diagnostic and therapeutic context of KIF2C


  1. Cancer-related serological recognition of human colon cancer: identification of potential diagnostic and immunotherapeutic targets. Scanlan, M.J., Welt, S., Gordon, C.M., Chen, Y.T., Gure, A.O., Stockert, E., Jungbluth, A.A., Ritter, G., Jäger, D., Jäger, E., Knuth, A., Old, L.J. Cancer Res. (2002) [Pubmed]
  2. Elevated expression of protein regulator of cytokinesis 1, involved in the growth of breast cancer cells. Shimo, A., Nishidate, T., Ohta, T., Fukuda, M., Nakamura, Y., Katagiri, T. Cancer Sci. (2007) [Pubmed]
  3. The chromosomal passenger complex is required for chromatin-induced microtubule stabilization and spindle assembly. Sampath, S.C., Ohi, R., Leismann, O., Salic, A., Pozniakovski, A., Funabiki, H. Cell (2004) [Pubmed]
  4. The Kin I kinesins are microtubule end-stimulated ATPases. Walczak, C.E. Mol. Cell (2003) [Pubmed]
  5. The kinesin-related protein MCAK is a microtubule depolymerase that forms an ATP-hydrolyzing complex at microtubule ends. Hunter, A.W., Caplow, M., Coy, D.L., Hancock, W.O., Diez, S., Wordeman, L., Howard, J. Mol. Cell (2003) [Pubmed]
  6. MCAK associates with the tips of polymerizing microtubules. Moore, A.T., Rankin, K.E., von Dassow, G., Peris, L., Wagenbach, M., Ovechkina, Y., Andrieux, A., Job, D., Wordeman, L. J. Cell Biol. (2005) [Pubmed]
  7. The KinI kinesin Kif2a is required for bipolar spindle assembly through a functional relationship with MCAK. Ganem, N.J., Compton, D.A. J. Cell Biol. (2004) [Pubmed]
  8. Mutations in the ATP-binding domain affect the subcellular distribution of mitotic centromere-associated kinesin (MCAK). Wordeman, L., Wagenbach, M., Maney, T. Cell Biol. Int. (1999) [Pubmed]
  9. Cloning and expression of human mitotic centromere-associated kinesin gene. Kim, I.G., Jun, D.Y., Sohn, U., Kim, Y.H. Biochim. Biophys. Acta (1997) [Pubmed]
  10. MCAK, a Kin I kinesin, increases the catastrophe frequency of steady-state HeLa cell microtubules in an ATP-dependent manner in vitro. Newton, C.N., Wagenbach, M., Ovechkina, Y., Wordeman, L., Wilson, L. FEBS Lett. (2004) [Pubmed]
  11. Identification and partial characterization of mitotic centromere-associated kinesin, a kinesin-related protein that associates with centromeres during mitosis. Wordeman, L., Mitchison, T.J. J. Cell Biol. (1995) [Pubmed]
  12. Differential functional interplay of TOGp/XMAP215 and the KinI kinesin MCAK during interphase and mitosis. Holmfeldt, P., Stenmark, S., Gullberg, M. EMBO J. (2004) [Pubmed]
  13. K-loop insertion restores microtubule depolymerizing activity of a "neckless" MCAK mutant. Ovechkina, Y., Wagenbach, M., Wordeman, L. J. Cell Biol. (2002) [Pubmed]
  14. The Interplay of the N- and C-Terminal Domains of MCAK Control Microtubule Depolymerization Activity and Spindle Assembly. Ems-McClung, S.C., Hertzer, K.M., Zhang, X., Miller, M.W., Walczak, C.E. Mol. Biol. Cell (2007) [Pubmed]
  15. Mitotic centromere-associated kinesin is important for anaphase chromosome segregation. Maney, T., Hunter, A.W., Wagenbach, M., Wordeman, L. J. Cell Biol. (1998) [Pubmed]
  16. Molecular dissection of the microtubule depolymerizing activity of mitotic centromere-associated kinesin. Maney, T., Wagenbach, M., Wordeman, L. J. Biol. Chem. (2001) [Pubmed]
  17. Depletion of centromeric MCAK leads to chromosome congression and segregation defects due to improper kinetochore attachments. Kline-Smith, S.L., Khodjakov, A., Hergert, P., Walczak, C.E. Mol. Biol. Cell (2004) [Pubmed]
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