anti-NADPH Oxidase 3 (NOX3) Anticorps

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

1. Hsp70 (Montrer HSP70 Anticorps) activates Stat3 (Montrer STAT3 Anticorps) and suppresses Nox3 via TLR4 (Montrer TLR4 Anticorps)

2. Together, these findings reveal that Nox2 (Montrer CYBB Anticorps) 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 (Montrer ROS1 Anticorps) generation and that NOX3-derived ROS (Montrer ROS1 Anticorps) may drive palmitate-induced hepatic insulin (Montrer INS Anticorps) resistance through JNK (Montrer MAPK8 Anticorps) and p38(MAPK (Montrer MAPK14 Anticorps)) 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 (Montrer ROS1 Anticorps) generation in the cochlear and vestibular systems and that NOX3-dependent ROS (Montrer ROS1 Anticorps) generation might contribute to hearing loss and balance problems in response to ototoxic drugs.

Human NADPH Oxidase 3 (NOX3) interaction partners

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

2. In lung transplants, our study highlights a donor-recipient interaction of NOX3 and NFE2L2 (Montrer NFE2L2 Anticorps) that increases the risk of PGD (Montrer PGD Anticorps).

3. Reduced matrigel invasion was mediated by reduced ROS (Montrer ROS1 Anticorps) levels coinciding with decreased expression of NADPH oxidase 2 (Montrer CYBB Anticorps), 3, 4 and 5 involved in ROS (Montrer ROS1 Anticorps) production.

4. palmitate-induced ROS (Montrer ROS1 Anticorps) generation and that NOX3-derived ROS (Montrer ROS1 Anticorps) may drive palmitate-induced hepatic insulin (Montrer INS Anticorps) resistance through JNK (Montrer MAPK8 Anticorps) and p38(MAPK (Montrer MAPK14 Anticorps)) pathways.

5. Down-regulation of NOX3 using siRNA prevented TNF-alpha (Montrer TNF Anticorps)-induced decrease of cellular glycogen (Montrer GYS1 Anticorps).

6. Nox3 is regulated by NOXO1 (Montrer NOXO1 Anticorps), p47phox, and p67phox (Montrer NCF2 Anticorps)

7. Nox3 functions together with p22(phox (Montrer CYBA Anticorps)) as an enzyme constitutively producing superoxide

8. Rac1 (Montrer RAC1 Anticorps) regulates both oxidases Nox1 (Montrer NOX1 Anticorps) and Nox3 through the Nox activators

9. In conclusion, the results demonstrate that NOX3, a reactive oxygen species generating NADPH oxidase (Montrer NOX1 Anticorps), plays an integral role in insulin (Montrer INS Anticorps)-induced p42 (Montrer EPB42 Anticorps)/44 Mitogen-activated protein kinase (Montrer MAPK1 Anticorps) signal transmission and VEGF-A (Montrer VEGFA Anticorps) production.

10. Roles for p22phox (Montrer CYBA Anticorps) at several distinct points in the maturation and assembly of a functionally competent Nox3 in the plasma membrane.