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Canonical pathway analysis, using Ingenuity Pathway Analysis software, revealed that the only genes in the "superpathway of cholesterol biosynthesis" were Idi1 (upregulated) and Hmgcs2 (downregulated). The Idi1 and Hmgcs2 genes have regulatory roles in atrial lipotoxic myopathy associated with atrial enlargement
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Our data also suggested that apart from heart, the expression of HMGCS2 was also different in kidney and spleen between control and STZ treated mice. In conclusion, The HMGCS2 molecule may potentially be involved in T1D induced cardiac dysfunction.
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several nutrients as well as specific nutritional related hormonal conditions are able to affect significantly HMGCS2 gene expression.
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miR-107-mediated decrease of HMGCS2 indicates poor outcomes and promotes cell migration in hepatocellular carcinoma
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this studies demonstrate that HMGCS2 functions as a transcriptional factor that binds to peroxisome proliferator-activated receptor alpha (PPARalpha), resulting in Src expression and activation in a metabolically independent manner
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HMGCS2 shares with ketone bodies common features in autophagic clearance of APP, suggesting that ketone bodies play an important role in HMGCS2 regulation of the autophagy.
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High expression of either HSD17B2 or HMGCS2 predicted poor susceptibility of rectal cancer to preoperative chemoradiotherapy.
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FABP7 and HMGCS2 may have roles in apocrine differentiation categorizing apocrine carcinoma of the breast
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In Fe-S cluster-deficient muscles, results show a dramatic up-regulation of the ketogenic enzyme HMGCS2 and the secreted protein FGF21 (fibroblast growth factor 21).
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An alternative transcript of HMGCS2 carrying a deletion of exon 4, and two alternative transcripts of HMGCL with deletions of exons 5 and 6, and exons 5, 6 and 7, respectively, were detected.
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Human HMGCS2 regulates mitochondrial fatty acid oxidation and FGF21 expression
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The authors report high-resolution crystal structures of the human cytosolic (hHMGCS1) and mitochondrial (hHMGCS2) isoforms in binary product complexes.
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Ketogenesis is an undesirable metabolic characteristic of the proliferating cell, which is down-regulated through c-Myc-mediated repression of the key metabolic gene HMGCS2.
