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Literature summary for 4.2.1.22 extracted from

  • Chakraborty, P.K.; Murphy, B.; Mustafi, S.B.; Dey, A.; Xiong, X.; Rao, G.; Naz, S.; Zhang, M.; Yang, D.; Dhanasekaran, D.N.; Bhattacharya, R.; Mukherjee, P.
    Cystathionine beta-synthase regulates mitochondrial morphogenesis in ovarian cancer (2018), FASEB J., 32, 4145-4157 .
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Homo sapiens
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General Information

General Information Comment Organism
physiological function cystathionine beta-synthase reprograms mitochondrial morphogenesis in ovarian cancer cells by selectively regulating the stability of mitofusin MFN2. Clinically, high expression of both CBS and MFN2 implicates poor overall survival of ovarian cancer patients, and a significant association between CBS andMFN2 expression exists in individual patients in the same data set. The silencing of CBS by siRNA or its inhibition of creates oxidative stress that activates JNK. Activated JNK phosphorylates MFN2 to recruit homologous to the E6-AP carboxyl terminus' domain-containing ubiquitin E3 ligase for its degradation via the ubiquitin-proteasome system. In CBS-silenced orthotopic xenograft tumor tissues,MFN2 but notMFN1 is selectively downregulated Homo sapiens