Downregulation of repressive CUP/AP-2 isoforms during adipocyte differentiation.
Holt EH., Lane MD.
Animal Study, published in Biochem Biophys Res Commun (2001) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Biochem Biophys Res Commun (2001)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 11688971
- DOI
- 10.1006/bbrc.2001.5846
Abstract (original English)
Activation of transcription of the C/EBPalpha (CCAAT/enhancer binding protein alpha) gene is a critical event in the differentiation of 3T3-L1 preadipocytes into adipocytes. The kinetics of this process parallels a decline of AP-2alpha protein (also referred to as CUP, C/EBP undifferentiated protein) and decreased binding of CUP/AP-2alpha to the C/EBPalpha promoter. Mutation of the CUP/AP-2 binding sites in the C/EBPalpha promoter results in increased C/EBPalpha expression. Based on these findings, it appears that decline in AP-2alpha expression is an important early event in the adipocyte differentiation program. In the studies presented here, we identify three mRNAs that encode the repressive CUP/AP-2alpha isoforms expressed in undifferentiated 3T3-L1 preadipocytes. We demonstrate that the kinetics of the decline of these isoforms' expression over the course of differentiation parallels both the decrease in CUP/AP-2alpha DNA binding activity and the increase in C/EBPalpha protein observed in previous studies.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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