SREBP
links: reference: 9-6-2021
Sterol regulatory element-binding protein #
- (Sometimes Sterol response element BP, which is maybe a bit more intuitive)
- Travis: *“As far as I know, the only thing that causes Acne is SREBP: activated exclusively by either androgens or IGF-1”… Studies have shown that sebum from people with acne have a higher viscosity, melting point, and characterized by an unbalance of lipids—namely: squalene, wax esters, and triglycerides. *
- And then amongst other things, SREPB increases squalene synthesis through it, and they upregulate wax ester synthase. Larger lipids are produced, raising sebum viscosity, leading to a clog.
- SREPB → Wax ester synthase/diacylglycerol acyltransferase (WS/DGAT)
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https://raypeatforum.com/community/threads/the-travis-corner.21611/post-371120
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IGF-1 induces SREBP-1 expression and lipogenesis in SEB-1 sebocytes via activation of the phosphoinositide 3-kinase/Akt pathway
- Increase in expression of SREBP-1 induced by IGF-1 was blocked in the presence of the PI3-K inhibitor but not in the presence of the MAPK/ERK inhibitor. Furthermore, inhibition of the PI3-K pathway also blocked the IGF-1-induced transcription of SREBP target genes and sebocyte lipogenesis.
- Involvement of the SREBP pathway in the mode of action of androgens in sebaceous glands in vivo
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IGF-1 induces SREBP-1 expression and lipogenesis in SEB-1 sebocytes via activation of the phosphoinositide 3-kinase/Akt pathway
- Increases Sebum quantity and viscosity, regulating lipid/sterol biosynthesis, but also the pentose phosphate pathway.
- The sole mediator of wax synthase
- Located on the endoplasmic reticulum, but androgens/IGF release the active form which activates transcription of its targets.
- Transcription is repressed by FGF21
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Diabetes and insulin in regulation of brain cholesterol metabolism
- in insulin-deficient diabetic mice, there is a reduction in expression of the major transcriptional regulator of cholesterol metabolism, SREBP-2, and its downstream genes in the hypothalamus and other areas of the brain, leading to a reduction in brain cholesterol synthesis and synaptosomal cholesterol content