Article
Crosstalk between the DNA damage response, histone modifications and neovascularisation.
Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
The international journal of biochemistry & cell biology (impact factor:
4.89).
11/2009;
42(2):193-7.
DOI:10.1016/j.biocel.2009.11.020
pp.193-7
Source: PubMed
- Citations (2)
-
Cited In (0)
-
Article: A view from Kansas on that evolution debate.
Nature 10/1999; 401(6752):423. · 36.28 Impact Factor -
Article: A role for the mitochondrial deacetylase Sirt3 in regulating energy homeostasis.
[show abstract] [hide abstract]
ABSTRACT: Here, we demonstrate a role for the mitochondrial NAD-dependent deacetylase Sirt3 in the maintenance of basal ATP levels and as a regulator of mitochondrial electron transport. We note that Sirt3(-/-) mouse embryonic fibroblasts have a reduction in basal ATP levels. Reconstitution with wild-type but not a deacetylase-deficient form of Sirt3 restored ATP levels in these cells. Furthermore in wild-type mice, the resting level of ATP correlates with organ-specific Sirt3 protein expression. Remarkably, in mice lacking Sirt3, basal levels of ATP in the heart, kidney, and liver were reduced >50%. We further demonstrate that mitochondrial protein acetylation is markedly elevated in Sirt3(-/-) tissues. In addition, in the absence of Sirt3, multiple components of Complex I of the electron transport chain demonstrate increased acetylation. Sirt3 can also physically interact with at least one of the known subunits of Complex I, the 39-kDa protein NDUFA9. Functional studies demonstrate that mitochondria from Sirt3(-/-) animals display a selective inhibition of Complex I activity. Furthermore, incubation of exogenous Sirt3 with mitochondria can augment Complex I activity. These results implicate protein acetylation as an important regulator of Complex I activity and demonstrate that Sirt3 functions in vivo to regulate and maintain basal ATP levels.Proceedings of the National Academy of Sciences 10/2008; 105(38):14447-52. · 9.68 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed.
The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual
current impact factor.
Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence
agreement may be applicable.
Keywords
DNA damage response machinery
eye disorders
factors regulating histone modifications
gene expression
growth factors
histone deacetylases
malignant
neovascularisation
potential interactions
Recent evidence