UCP3 is associated with Hax-1 in mitochondria in the presence of calcium ion.
UCP3 is associated with Hax-1 in mitochondria in the presence of calcium ion.
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DOI:
10.1016/j.bbrc.2016.02.075
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发表时间:
2016-03-25
影响因子:
3.1
通讯作者:
Nikawa, Takeshi
中科院分区:
文献类型:
--
作者:
Hirasaka, Katsuya;Mills, Edward M.;Haruna, Marie;Bando, Aki;Ikeda, Chika;Abe, Tomoki;Kohno, Shohei;Nowinski, Sara M.;Lago, Cory U.;Akagi, Ken-ichi;Tochio, Hidehito;Ohno, Ayako;Teshima-Kondo, Shigetada;Okumura, Yuushi;Nikawa, Takeshi
Uncoupling protein 3 (UCP3) is known to regulate energy dissipation, proton leakage, fatty acid oxidation, and oxidative stress. To identify the putative protein regulators of UCP3, we performed yeast two-hybrid screens. Here we report that UCP3 interacted with HS-1 associated protein X-1 (Hax-1), an anti-apoptotic protein that was localized in the mitochondria, and is involved in cellular responses to Ca2+. The hydrophilic sequences within loop 2, and the matrix-localized hydrophilic domain of mouse UCP3, were necessary for binding to Hax-1 at the C-terminal domain, adjacent to the mitochondrial inner membrane. Interestingly, interaction of these proteins occurred in a calcium-dependent manner. Moreover, the NMR spectrum of the C-terminal domain of Hax-1 was dramatically changed by removal of Ca2+, suggesting that the C-terminal domain of Hax-1 underwent a Ca2+-induced conformational change. In the Ca2+-free state, the C-terminal Hax-1 tended to unfold, suggesting that Ca2+ binding may induce protein folding of the Hax-1 C-terminus. These results suggested that the UCP3-Hax-1 complex may regulate mitochondrial functional changes caused by mitochondrial Ca2+.
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影响因子:
4.3
作者:
Csordas, Gyoergy;Hajnoczky, Gyoergy
通讯作者:
Hajnoczky, Gyoergy
影响因子:
13.8
作者:
Azzu, Vian;Brand, Martin D.
通讯作者:
Brand, Martin D.
影响因子:
7.7
作者:
Iwig JS;Vercoulen Y;Das R;Barros T;Limnander A;Che Y;Pelton JG;Wemmer DE;Roose JP;Kuriyan J
通讯作者:
Kuriyan J
影响因子:
2.9
作者:
Hopper, RK;Carroll, S;Balaban, RS
通讯作者:
Balaban, RS
DOI:
10.1073/pnas.0906998106
发表时间:
2009-12-08
影响因子:
11.1
作者:
Zhao, Wen;Waggoner, Jason R.;Kranias, Evangelia G.
通讯作者:
Kranias, Evangelia G.