IndraLab

Statements


MiR-96 decreases the amount of IRS1. 5 / 9
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"Physiologically, miR-96 is strongly induced by fatty acids and downregulates the expression of the insulin receptor (INSR) and the insulin receptor substrate 1 (IRS-1) to induce a failure in insulin signaling and glycogen synthesis in hepatocytes [XREF_BIBR]."

reach
"To determine if miR-96 represses the expression of IRS-1 directly, we constructed a pGL3-promoter-based 3 ' UTR reporter vector consisting of a luciferase cDNA followed by the 414 nt 3 ' UTR of the IR[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"As INSR and IRS-1 expression is suppressed at the post-transcriptional level by miR-96 in hepatocytes, this study further examined whether the upregulation of miR-96 causes insulin resistance in hepatocytes."

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"Therefore, this data indicates that miR-96 suppresses the expression of IRS-1 at the post-transcriptional level in L6-GLUT4myc myocytes."

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"This suggest that mitochondrial dysfunction increases the level of miR-96, which is predicted to target IRS-1 3 ' UTR, indicating the involvement of miR-96 in the impaired insulin signaling.We have po[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"