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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

CMTM8  -  CKLF-like MARVEL transmembrane domain...

Homo sapiens

Synonyms: CKLF-like MARVEL transmembrane domain-containing protein 8, CKLFSF8, CKLFSF8-V2, Chemokine-like factor superfamily member 8
 
 
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High impact information on CMTM8

  • Previous research in our laboratory also demonstrated CMTM8 attenuated EGFR-mediated signaling pathways by decreasing ERK1/2phosphorylation levels [1].
  • Caspase-dependent and independent mediated apoptosis, induced by CMTM8 overexpression, was facilitated by the mitochondria and inhibited by knockdown of Bad or overexpression of Bcl-xL [1].
  • In cells overexpressing CKLFSF8, the initial activation of EGFR was not affected, but subsequent desensitization of EGF-induced signaling occurred rapidly [2].
  • In contrast, knockdown of CKLFSF8 by siCKLFSF8 delayed EGFR endocytosis [2].
  • The characteristics of CKLFSF2-7 are intermediate between CKLFSF1 and CKLFSF8 [3].
 

Biological context of CMTM8

  • CMTM8 induces caspase-dependent and -independent apoptosis through a mitochondria-mediated pathway [1].
 

Other interactions of CMTM8

  • These data implicate CMTM8 as a negative regulator of EGF-induced signaling, with potential use as a novel therapeutic gene for EGFR-targeted anticancer gene therapy [1].
  • CKLFSF8 shares 39.3% amino acid identity with TM4SF11 [3].
 

Analytical, diagnostic and therapeutic context of CMTM8

References

  1. CMTM8 induces caspase-dependent and -independent apoptosis through a mitochondria-mediated pathway. Jin, C., Wang, Y., Han, W., Zhang, Y., He, Q., Li, D., Yin, C., Tian, L., Liu, D., Song, Q., Ma, D. J. Cell. Physiol. (2007) [Pubmed]
  2. Regulation of EGF receptor signaling by the MARVEL domain-containing protein CKLFSF8. Jin, C., Ding, P., Wang, Y., Ma, D. FEBS Lett. (2005) [Pubmed]
  3. Identification of eight genes encoding chemokine-like factor superfamily members 1-8 (CKLFSF1-8) by in silico cloning and experimental validation. Han, W., Ding, P., Xu, M., Wang, L., Rui, M., Shi, S., Liu, Y., Zheng, Y., Chen, Y., Yang, T., Ma, D. Genomics (2003) [Pubmed]
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