FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2000221281> ?p ?o ?g. }

• W2000221281 endingPage "1217" @default.
• W2000221281 startingPage "1209" @default.
• W2000221281 abstract "The mitochondrial phosphate carrier (PiC) is critical for ATP synthesis by serving as the primary means for mitochondrial phosphate import across the inner membrane. In addition to its role in energy production, PiC is hypothesized to have a role in cell death as either a component or a regulator of the mitochondrial permeability transition pore (MPTP) complex. Here, we have generated a mouse model with inducible and cardiac-specific deletion of the Slc25a3 gene (PiC protein). Loss of PiC protein did not prevent MPTP opening, suggesting it is not a direct pore-forming component of this complex. However, Slc25a3 deletion in the heart blunted MPTP opening in response to Ca2+ challenge and led to a greater Ca2+ uptake capacity. This desensitization of MPTP opening due to loss or reduction in PiC protein attenuated cardiac ischemic-reperfusion injury, as well as partially protected cells in culture from Ca2+ overload induced death. Intriguingly, deletion of the Slc25a3 gene from the heart long-term resulted in profound hypertrophy with ventricular dilation and depressed cardiac function, all features that reflect the cardiomyopathy observed in humans with mutations in SLC25A3. Together, these results demonstrate that although the PiC is not a direct component of the MPTP, it can regulate its activity, suggesting a novel therapeutic target for reducing necrotic cell death. In addition, mice lacking Slc25a3 in the heart serve as a novel model of metabolic, mitochondrial-driven cardiomyopathy." @default.
• W2000221281 created "2016-06-24" @default.
• W2000221281 creator A5016899347 @default.
• W2000221281 creator A5032442021 @default.
• W2000221281 creator A5036179300 @default.
• W2000221281 creator A5040025655 @default.
• W2000221281 creator A5064270709 @default.
• W2000221281 creator A5071684244 @default.
• W2000221281 creator A5075550603 @default.
• W2000221281 creator A5085011121 @default.
• W2000221281 date "2014-03-21" @default.
• W2000221281 modified "2023-10-16" @default.
• W2000221281 title "Genetic deletion of the mitochondrial phosphate carrier desensitizes the mitochondrial permeability transition pore and causes cardiomyopathy" @default.
• W2000221281 cites W1506478670 @default.
• W2000221281 cites W1518141245 @default.
• W2000221281 cites W1543177856 @default.
• W2000221281 cites W1558847742 @default.
• W2000221281 cites W1583113219 @default.
• W2000221281 cites W1968091682 @default.
• W2000221281 cites W1972249421 @default.
• W2000221281 cites W1973144114 @default.
• W2000221281 cites W1973925468 @default.
• W2000221281 cites W1980959570 @default.
• W2000221281 cites W1981575376 @default.
• W2000221281 cites W1983845733 @default.
• W2000221281 cites W1989545610 @default.
• W2000221281 cites W1993418135 @default.
• W2000221281 cites W1994442108 @default.
• W2000221281 cites W1995873637 @default.
• W2000221281 cites W1996738096 @default.
• W2000221281 cites W2004224253 @default.
• W2000221281 cites W2007088638 @default.
• W2000221281 cites W2013299408 @default.
• W2000221281 cites W2017213538 @default.
• W2000221281 cites W2030548279 @default.
• W2000221281 cites W2038837845 @default.
• W2000221281 cites W2047322721 @default.
• W2000221281 cites W2055571680 @default.
• W2000221281 cites W2056596287 @default.
• W2000221281 cites W2063099262 @default.
• W2000221281 cites W2074800090 @default.
• W2000221281 cites W2081358044 @default.
• W2000221281 cites W2083770619 @default.
• W2000221281 cites W2084947365 @default.
• W2000221281 cites W2092288031 @default.
• W2000221281 cites W2094580473 @default.
• W2000221281 cites W2097270551 @default.
• W2000221281 cites W2116444561 @default.
• W2000221281 cites W2117714847 @default.
• W2000221281 cites W2118321705 @default.
• W2000221281 cites W2134208169 @default.
• W2000221281 cites W2139284714 @default.
• W2000221281 cites W2143046500 @default.
• W2000221281 cites W2164931274 @default.
• W2000221281 cites W4254119740 @default.
• W2000221281 cites W4362172418 @default.
• W2000221281 doi "https://doi.org/10.1038/cdd.2014.36" @default.
• W2000221281 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4085527" @default.
• W2000221281 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24658400" @default.
• W2000221281 hasPublicationYear "2014" @default.
• W2000221281 type Work @default.
• W2000221281 sameAs 2000221281 @default.
• W2000221281 citedByCount "138" @default.
• W2000221281 countsByYear W20002212812014 @default.
• W2000221281 countsByYear W20002212812015 @default.
• W2000221281 countsByYear W20002212812016 @default.
• W2000221281 countsByYear W20002212812017 @default.
• W2000221281 countsByYear W20002212812018 @default.
• W2000221281 countsByYear W20002212812019 @default.
• W2000221281 countsByYear W20002212812020 @default.
• W2000221281 countsByYear W20002212812021 @default.
• W2000221281 countsByYear W20002212812022 @default.
• W2000221281 countsByYear W20002212812023 @default.
• W2000221281 crossrefType "journal-article" @default.
• W2000221281 hasAuthorship W2000221281A5016899347 @default.
• W2000221281 hasAuthorship W2000221281A5032442021 @default.
• W2000221281 hasAuthorship W2000221281A5036179300 @default.
• W2000221281 hasAuthorship W2000221281A5040025655 @default.
• W2000221281 hasAuthorship W2000221281A5064270709 @default.
• W2000221281 hasAuthorship W2000221281A5071684244 @default.
• W2000221281 hasAuthorship W2000221281A5075550603 @default.
• W2000221281 hasAuthorship W2000221281A5085011121 @default.
• W2000221281 hasBestOaLocation W20002212811 @default.
• W2000221281 hasConcept C126322002 @default.
• W2000221281 hasConcept C134018914 @default.
• W2000221281 hasConcept C13591479 @default.
• W2000221281 hasConcept C137183658 @default.
• W2000221281 hasConcept C185592680 @default.
• W2000221281 hasConcept C190283241 @default.
• W2000221281 hasConcept C2778198053 @default.
• W2000221281 hasConcept C2778674702 @default.
• W2000221281 hasConcept C2778797674 @default.
• W2000221281 hasConcept C28859421 @default.
• W2000221281 hasConcept C31573885 @default.
• W2000221281 hasConcept C513476851 @default.
• W2000221281 hasConcept C55493867 @default.
• W2000221281 hasConcept C71924100 @default.
• W2000221281 hasConcept C74897846 @default.

• next