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J Biol Chem. 2011 Jun 10;286(23):20292-6. doi: 10.1074/jbc.M110.198523. Epub 2011 Feb 23.

Knockdown of DAPIT (diabetes-associated protein in insulin-sensitive tissue) results in loss of ATP synthase in mitochondria.

Author information

  • 1International Cooperative Research Project ATP-Synthesis Regulation Project, Japan Science and Technology Agency, 2-3-6 Aomi, Koto-Ku, Tokyo 135-0064, Japan.

Abstract

It was found recently that a diabetes-associated protein in insulin-sensitive tissue (DAPIT) is associated with mitochondrial ATP synthase. Here, we report that the suppressed expression of DAPIT in DAPIT-knockdown HeLa cells causes loss of the population of ATP synthase in mitochondria. Consequently, DAPIT-knockdown cells show smaller mitochondrial ATP synthesis activity, slower growth in normal medium, and poorer viability in glucose-free medium than the control cells. The mRNA levels of α- and β-subunits of ATP synthase remain unchanged by DAPIT knockdown. These results indicate a critical role of DAPIT in maintaining the ATP synthase population in mitochondria and raise an intriguing possibility of active role of DAPIT in cellular energy metabolism.

PMID:
21345788
[PubMed - indexed for MEDLINE]
PMCID:
PMC3121504
Free PMC Article

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