{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fahrenbach JP"],"funding":["American Heart Association","NCATS NIH HHS","National Heart, Lung, and Blood Institute","NHLBI NIH HHS","NIAMS NIH HHS"],"pagination":["2804-15"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4062826"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["28(7)"],"pubmed_abstract":["The newborn heart adapts to postnatal life by shifting from a fetal glycolytic metabolism to a mitochondrial oxidative metabolism. Abcc9, an ATP-binding cassette family member, increases expression concomitant with this metabolic shift. Abcc9 encodes a membrane-associated receptor that partners with a potassium channel to become the major potassium-sensitive ATP channel in the heart. Abcc9 also encodes a smaller protein enriched in the mitochondria. We now deleted exon 5 of Abcc9 to ablate expression of both plasma membrane and mitochondria-associated Abcc9-encoded proteins, and found that the myocardium failed to acquire normal mature metabolism, resulting in neonatal cardiomyopathy. Unlike wild-type neonatal cardiomyocytes, mitochondria from Ex5 cardiomyocytes were unresponsive to the KA"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["Abcc9 is required for the transition to oxidative metabolism in the newborn heart."],"pmcid":["PMC4062826"],"funding_grant_id":["F32‐HL097587","R01 HL078926","R21 HL093626","F32-HL097587","11GRNT7600070","UL1 TR000430","K08 HL098565","U54 AR052646","R01‐HL57414","R21‐HL93626","0630268N","R21-HL93626","R01 HL057414","F32 HL097587","K08-HL098565","R01‐HL078926","R01-HL078926","R01-HL57414","K08‐HL098565"],"pubmed_authors":["Yerokun B","Makielski JC","McNally EM","Shi NQ","Kim G","Stoller D","Aggarwal N","Hadhazy M","Fahrenbach JP","Earley JU"],"additional_accession":[]},"is_claimable":false,"name":"Abcc9 is required for the transition to oxidative metabolism in the newborn heart.","description":"The newborn heart adapts to postnatal life by shifting from a fetal glycolytic metabolism to a mitochondrial oxidative metabolism. Abcc9, an ATP-binding cassette family member, increases expression concomitant with this metabolic shift. Abcc9 encodes a membrane-associated receptor that partners with a potassium channel to become the major potassium-sensitive ATP channel in the heart. Abcc9 also encodes a smaller protein enriched in the mitochondria. We now deleted exon 5 of Abcc9 to ablate expression of both plasma membrane and mitochondria-associated Abcc9-encoded proteins, and found that the myocardium failed to acquire normal mature metabolism, resulting in neonatal cardiomyopathy. Unlike wild-type neonatal cardiomyocytes, mitochondria from Ex5 cardiomyocytes were unresponsive to the KA","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jul","modification":"2025-04-22T17:39:49.671Z","creation":"2019-03-27T01:30:26Z"},"accession":"S-EPMC4062826","cross_references":{"pubmed":["24648545"],"doi":["10.1096/fj.13-244459"]}}