The NADPH oxidase subunit p22phox inhibits the function of the tumor suppressor protein tuberin.

@article{Block2010TheNO,
  title={The NADPH oxidase subunit p22phox inhibits the function of the tumor suppressor protein tuberin.},
  author={K. Block and Y. Gorin and David D. New and A. Eid and Tomasz Chelmicki and A. Reed and G. G. Choudhury and D. Parekh and H. Abboud},
  journal={The American journal of pathology},
  year={2010},
  volume={176 5},
  pages={
          2447-55
        }
}
Mutations in the von Hippel-Lindau (VHL) gene give rise to renal cell carcinoma. Reactive oxygen species, generated by Nox oxidases, are involved in tumorigenesis. We have previously demonstrated that in VHL-deficient cells, p22(phox)-dependent Nox1 and Nox4 oxidases maintain hypoxia inducible factor-2alpha (HIF-2alpha) protein expression through an Akt-dependent translational pathway. Phosphorylation of tuberin, by Akt, results in its inactivation. Here we show that diphenyleneiodonium… Expand
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TLDR
The data demonstrate that VHL protein exerts its tumor suppressor action, at least partially, via inhibition of p22phox-based Nox4/Nox1 NADPH oxidase-dependent reactive oxygen species generation. Expand
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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Direct Interaction of the Novel Nox Proteins with p22phox Is Required for the Formation of a Functionally Active NADPH Oxidase*
TLDR
Evidence is provided that p22phox directly interacts with Nox1 and Nox4, to form an superoxide-generating NADPH oxidase and it is demonstrated that mutation of the potential heme binding site in the Nox proteins disrupts the complex formation of Nox 1 and NOx4 with p 22phox. Expand
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TLDR
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