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The expression of SREBP1 is an independent risk factor affecting the overall survival of patients with pancreatic cancer. In addition, SREBP1 knockdown inhibited the de novo lipogenesis and growth of pancreatic cancer cells.
SREBF2 and SREBF1 are key players in cholesterol metabolism. These genes code for transcriptional regulators of cholesterol synthesis known as sterol regulatory element-binding proteins (SREBPs) (e.g., SREBP-1a/c and SREBP2).
Sterol regulatory element binding proteins (SREBPs) are a family of transcription factors that regulate lipid homeostasis by controlling the expression of a range of enzymes required for endogenous cholesterol, fatty acid (FA), triacylglycerol and phospholipid synthesis.
The SREBPs play related but distinct roles: SREBP-1c, the predominant SREBP-1 isoform in adult liver, preferentially activates genes required for fatty acid synthesis, while SREBP-2 preferentially activates the LDL receptor gene and various genes required for cholesterol synthesis.
Sterol-regulatory-element-binding proteins (SREBPs) are cleaved and released from membranes when cells are deprived of cholesterol or fatty acids. They migrate to the nucleus and up-regulate genes required for lipid synthesis and uptake.
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Sterol regulatory element binding proteins (SREBPs) are a family of transcription factors that regulate lipid homeostasis by controlling the expression of a range of enzymes required for endogenous cholesterol, fatty acid (FA), triacylglycerol and phospholipid synthesis.

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