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Excess protein synthesis is the major pathological manifestation of cardiac hypertrophy; however, the underlying mechanism remains elusive. Here we found that a SAM transporter Slc25a26 translocated to mitochondria during cardiac hypertrophy. Silencing Slc25a26 aggravated phenylephrine-induced cardi...
ORGANISM(S): Rattus norvegicus 
2022-01-05 | GSE173737 | GEO
Targeting Cytoplasmic SAM by Expressing Slc25a26 Inhibits Protein Synthesis in Cardiac Hypertrophy via SAMTOR/mTOR signaling
The SLC25A26 gene encodes a mitochondrial inner membrane carrier that transports S-adenosylmethionine (SAM) into the mitochondrial matrix in exchange for S-adenosylhomocysteine (SAH). SAM is the predominant methyl-group donor for most cellular methylation processes, of which SAH is produced as a by-...
ORGANISM(S): Drosophila melanogaster (Fruit fly) 
2022-01-19 | PXD026900 | Pride
This study evaluated the expression of depression-associated genes (GAR1, PER3, MTPAP, SLC25A26, CD19) in whole-blood samples from 100 patients with depression and 100 healthy controls using SYBR Green-based quantitative RT-PCR on the Rotor-Gene Q system.
ORGANISM(S): Homo sapiens 
FBXO24 targets SLC25A26 for K6-linked polyubiquitination to maintain mitochondrial function during spermiogenesis
ORGANISM(S): Mus Musculus 
Mus musculus Transcriptome or Gene expression
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