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Bruce M. Spiegelman

Researcher at Harvard University

Publications -  443
Citations -  172265

Bruce M. Spiegelman is an academic researcher from Harvard University. The author has contributed to research in topics: Adipose tissue & Transcription factor. The author has an hindex of 179, co-authored 434 publications receiving 158009 citations. Previous affiliations of Bruce M. Spiegelman include University of California, San Francisco & Vassar College.

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Thrap3 docks on phosphoserine 273 of PPARγ and controls diabetic gene programming

TL;DR: Reduced expression of Thrap3 in fat tissue by antisense oligonucleotides regulates a specific set of genes, including the key adipokines adiponectin and adipsin, and effectively improves hyperglycemia and insulin resistance in high-fat-fed mice without affecting body weight.
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Yeast GCN4 as a probe for oncogenesis by AP-1 transcription factors: transcriptional activation through AP-1 sites is not sufficient for cellular transformation.

TL;DR: The properties of an autonomous and heterologous AP-1 protein, yeast GCN4, in rat embryo fibroblasts are examined, indicating that the amino-terminal regions of Jun and Fos each contain regulatory functions that are required for oncogenesis but are distinct from generic transcriptional activation domains.
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Adrenal glucocorticoids regulate adipsin gene expression in genetically obese mice.

TL;DR: It is shown here that the adipsin structural gene is located on chromosome 10 and hence is physically distinct from any obesity genes so far identified in the mouse and strongly suggest that the hyperglucocorticoid state seen in certain obese models plays a significant role in lowering adipin mRNA and protein levels.
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Heparin potentiation of 3T3-adipocyte stimulated angiogenesis: Mechanisms of action on endothelial cells

TL;DR: The data suggest that heparin potentiates angiogenesis in vivo by stimulating endothelial cell plasminogen activator, motility, or both, and that for adipocyte‐induced blood vessel formation, hepar in does not appear to affect the mitogenic activity.