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 (Montrer SIRT1 Protéines) 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 (Montrer POU3F2 Protéines) is associated with tumorigenesis.

3. The results suggest that phosphorylation of serine-504 by PKCdelta (Montrer PKCd Protéines) modulates the biological function of tNOX.

4. this result suggests that hnRNP F (Montrer HNRNPF Protéines) directs formation of the exon 4 minus variant of ENOX2.

5. 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.

6. 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.

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

8. 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 (Montrer AKT1 Protéines).

9. 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

10. 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.

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

1. this result suggests that hnRNP F (Montrer HNRNPF Protéines) directs formation of the exon 4 minus variant of ENOX2

2. Data show that growth of transgenic mouse embryonic fibroblasts overexpressing tNOX is inhibited by low concentrations of the anticarcinogenic tNOX inhibitors epigallocatechin-3-gallate and phenoxodiol.

3. The tissue expression of tNOX mRNA was greatest in heart, lung and liver. When these tissues were analyzed for cell size.