Show simple item record

dc.contributor.author Melanie Paillard
dc.contributor.author Csordás György
dc.contributor.author Szanda Gergő
dc.contributor.author Golenár Tünde
dc.contributor.author Valentina Debattisti
dc.contributor.author Bartók Ádám
dc.contributor.author Nadan Wang
dc.contributor.author Cynthia Moffat
dc.contributor.author Erin L. Seifert
dc.contributor.author Spät András
dc.contributor.author Hajnóczky György
dc.date.accessioned 2018-10-05T07:03:11Z
dc.date.available 2018-10-05T07:03:11Z
dc.date.issued 2017
dc.identifier 85014549297
dc.identifier.citation pagination=2291-2300; journalVolume=18; journalIssueNumber=10; journalTitle=CELL REPORTS;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/4837
dc.identifier.uri doi:10.1016/j.celrep.2017.02.032
dc.description.abstract Mitochondrial Ca2+ uptake through the Ca2+ uniporter supports cell functions, including oxidative metabolism, while meeting tissue-specific calcium signaling patterns and energy needs. The molecular mechanisms underlying tissue-specific control of the uniporter are unknown. Here, we investigated a possible role for tissue-specific stoichiometry between the Ca2+-sensing regulators (MICUs) and pore unit (MCU) of the uniporter. Low MICU1:MCU protein ratio lowered the [Ca2+] threshold for Ca2+ uptake and activation of oxidative metabolism but decreased the cooperativity of uniporter activation in heart and skeletal muscle compared to liver. In MICU1-overexpressing cells, MICU1 was pulled down by MCU proportionally to MICU1 overexpression, suggesting that MICU1:MCU protein ratio directly reflected their association. Overexpressing MICU1 in the heart increased MICU1:MCU ratio, leading to liver-like mitochondrial Ca2+ uptake phenotype and cardiac contractile dysfunction. Thus, the proportion of MICU1-free and MICU1-associated MCU controls these tissue-specific uniporter phenotypes and downstream Ca2+ tuning of oxidative metabolism. © 2017
dc.relation.ispartof urn:issn:2211-1247
dc.title Tissue-Specific Mitochondrial Decoding of Cytoplasmic Ca2+ Signals Is Controlled by the Stoichiometry of MICU1/2 and MCU
dc.type Journal Article
dc.date.updated 2018-02-19T11:50:52Z
dc.language.rfc3066 en
dc.identifier.mtmt 3201118


Files in this item

xmlui.dri2xhtml.METS-1.0.onlyFromAllowedIP

View/Open

This item appears in the following Collection(s)

Show simple item record

Search DSpace


Advanced Search

Browse

My Account