anti-NADPH Oxidase 3 (NOX3) Anticorps

Mouse (Murine) NADPH Oxidase 3 (NOX3) interaction partners

1. Hsp70 activates Stat3 and suppresses Nox3 via TLR4

2. Together, these findings reveal that Nox2 is a Zn(2+)-regulated enzyme that mediates ZnD-induced oxidative stress and kidney hypertrophy. Understanding the specific mechanisms by which ZnD contributes to kidney damage may have an important impact on the treatment of chronic kidney disease.

3. Nox3 mutants and heterozygotes demonstrated a greater susceptibility to noise-induced hearing loss.

4. Although Nox3 overexpression revealed no apparent effect, depletion of Nox3 decreased the number of spermatogonial stem cells in both cultured spermatogonia and freshly isolated testis cells.

5. Mutations of Nox3 include retrovirus insertion, missense mutations, splice donor mutation, a splice acceptor mutation and premature translational termination.

6. palmitate-induced ROS generation and that NOX3-derived ROS may drive palmitate-induced hepatic insulin resistance through JNK and p38(MAPK) pathways.

7. an allelic series of mutations at the otoconia-deficient head tilt (het) locus, affecting the gene for NADPH oxidase 3 (Nox3), identifies Nox3 as a protein with a clear enzymatic function indispensable for otoconia morphogenesis

8. NOX3 is a relevant source of ROS generation in the cochlear and vestibular systems and that NOX3-dependent ROS generation might contribute to hearing loss and balance problems in response to ototoxic drugs.

Human NADPH Oxidase 3 (NOX3) interaction partners

1. The results suggested that rs6557421 variant in Nox3 and rs3744439 variant in Tbx4 might have potential effect on individual susceptibility to pulmonary hypertension.

2. genetic variants in NOX3 may confer susceptibility to antithyroid drug-induced apoptosis of granulocytes.

3. In lung transplants, our study highlights a donor-recipient interaction of NOX3 and NFE2L2 that increases the risk of PGD.

4. Reduced matrigel invasion was mediated by reduced ROS levels coinciding with decreased expression of NADPH oxidase 2, 3, 4 and 5 involved in ROS production.

5. palmitate-induced ROS generation and that NOX3-derived ROS may drive palmitate-induced hepatic insulin resistance through JNK and p38(MAPK) pathways.

6. Down-regulation of NOX3 using siRNA prevented TNF-alpha-induced decrease of cellular glycogen.

7. Nox3 is regulated by NOXO1, p47phox, and p67phox

8. Nox3 functions together with p22(phox) as an enzyme constitutively producing superoxide

9. Rac1 regulates both oxidases Nox1 and Nox3 through the Nox activators

10. In conclusion, the results demonstrate that NOX3, a reactive oxygen species generating NADPH oxidase, plays an integral role in insulin-induced p42/44 Mitogen-activated protein kinase signal transmission and VEGF-A production.

11. Roles for p22phox at several distinct points in the maturation and assembly of a functionally competent Nox3 in the plasma membrane.

12. Potential candidate genes in these regions that have been implicated in diabetic nephropathy and/or renal damage in models of hypertension include CYBA (or P22PHOX) (16q24), NOX1 (10q22), and NOX3 (6q25.1-q26).