PPAR
2022-02-01 links: reference: Travis - PPARs And Keratin
Peroxisome proliferator-activated receptor #
Transcription factors and nuclear receptor proteins. They all dimerize with RXR.
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There are: 
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α, β/δ (same thing I guess), γ1, γ2, γ3 types. 
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PPAR-β/δ competes with PPAR-α and PPAR-γ. Downregulation of β/δ can increase Keratin 20 expression several fold. 
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Overexpression of PPAR-γ on the skin protects rats against Hair Loss. 
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PPAR-γ agonists administered to the brain increase insulin transport/sensitivity to the brain. 
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- [Inhibition of Peroxisome Proliferator Signaling Pathways by Thyroid Hormone Receptor: Competitive Binding to the Response Element]
- I.e. thyroid hormone (-RXR heteromers) binds to PPRE, inhibiting it.
- Both PPAR and TR bind to PPRE although only PPAR mediates transcriptional activation via PPRE. TRzRXR heterodimers are potential competitors with PPAR•RXR for binding to PPREs.
- Thyroid hormone response element and PP response element have an almost perfectly inverse relationship: 
 
 
 
- [Inhibition of Peroxisome Proliferator Signaling Pathways by Thyroid Hormone Receptor: Competitive Binding to the Response Element]
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Androgens increase the expression of PPAR-α1 PPAR γ coactivator 
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Causes and consequences of low grade endotoxemia and inflammatory diseases - the expression of PPARs promotes an M2 polarization and is responsible for maintaining the basal anti-inflammatory tone of adipose tissue via promoting the co-repression of pro-inflammatory genes through co-repressors nuclear receptor corepressor 1 or 2 (NCoR). However, in our studies and in others, PPAR expression is inhibited after TLR4 stimulation by LPS, and complete knock out of this nuclear receptor promotes inflammation and IR.
 
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 - (Wy14643 = PPARα agonist)