Abstract
Objectives: The expression level of hepatic LDL receptor (LDLR) plays a key role in LDL-cholesterol metabolism. LDLR gene transcription is negatively regulated by elevated intracellular cholesterol levels. Additionally, alterations in LDLR mRNA decay rate provide a rapid means for cells to modulate LDLR expression in response to demand for LDL-derived cholesterol. The regulation of LDLR mRNA stability is mediated through its 3' untranslated region (3'UTR). Our previous studies identified hnRNP D as a key mRNA binding protein that interacts with the regulatory sequences in 3'UTR to induce LDLR mRNA degradation.
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