Ecto-NOX Disulfide-Thiol Exchanger 2 Protéines (ENOX2)

Human Ecto-NOX Disulfide-Thiol Exchanger 2 (ENOX2) interaction partners

1. The tumor-associated NADH oxidase (tNOX)-mediated modulation of the NAD+ concentration and SIRT1 are involved in oxaliplatin-induced apoptosis.

2. These findings not only shed light on the molecular mechanism of the anticancer properties of capsaicin, but also the transcription regulation of tNOX expression that may potentially explain how POU3F2 is associated with tumorigenesis.

3. The findings support a role for arNOX as a major source of oxidative damage leading to cross-linking of skin proteins.

4. The results suggest that phosphorylation of serine-504 by PKCdelta modulates the biological function of tNOX.

5. this result suggests that hnRNP F directs formation of the exon 4 minus variant of ENOX2.

6. increased NADH levels resulting from ENOX2 inhibition result in decreased prosurvival sphingosine-1-phosphate and increased proapoptotic ceramide, both of which may be important to initiation of the ENOX2 inhibitor-induced apoptotic cascade.

7. ENOX2 is a dimeric protein containing 4 coppers/dimer capable of carrying out concerted four electron transfers from NADH or ubiquinol to molecular oxygen as required to form water.

8. arNOX activity correlates with age and reaches a maximum at about age 65 in males and 55 in females.

9. Enhanced arNOX activity correlates with age and with oxidative changes contributing to skin aging.

10. tNOX is both necessary and sufficient for the cellular anticancer activities attributed to both EGCg and capsaicin. *tNOX enzyme

11. results indicate that shRNA targeting of tNOX inhibits the growth of cervical cancer cells, and reduces cell migration via a decrease in the membrane association of Rac.

12. A relationship of tNOX to unregulated growth of cancer cells was provided by data where growth of HeLa cells was inhibited by transfection with the exon 5 antisense oligonucleotides

13. These results indicate that tNOX is suppressed during apoptosis and demonstrate that tNOX down-regulation sensitizes cells to stress-induced growth reduction, suggesting that tNOX is required for transformed cell growth.