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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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Meteorin-like facilitates skeletal muscle repair through a Stat3/IGF-1 mechanism

TL;DR: The myokine/cytokine Meteorin-like (Metrnl) is identified as an important regulator of muscle regeneration and a potential therapeutic target to enhance tissue repair in mice genetically lacking Metrnl.
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Partnership of PGC-1α and HNF4α in the Regulation of Lipoprotein Metabolism

TL;DR: A crucial role is pointed to for the PGC-1α/HNF4α partnership in hepatic lipoprotein metabolism, which is induced or activated under different stimuli in a highly tissue-specific manner and subsequently partners with certain transcription factors in those tissues to execute various biological programs.
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Behavioral assessment of c-fos mutant mice

TL;DR: The results suggest that c-fos mutants have some behavioral impairments that interfere with evaluation of complex learning on the Morris water task, but because all genotypes could perform a simple discrimination task, it is clear that c -fos is not essential for this simpler form of learning and memory.
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Identification of a fat cell enhancer: analysis of requirements for adipose tissue-specific gene expression.

TL;DR: A 520 bp enhancer at −5.4 kb of the aP2 gene can direct high levels of gene expression specifically to the adipose tissue of transgenic mice and also functions in a differentiation‐dependent manner in cultured adipocytes and cannot be transactivated in preadipocytes by C/EBP.
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Characterization of the novel brown adipocyte cell line HIB 1B. Adrenergic pathways involved in regulation of uncoupling protein gene expression

TL;DR: HIB 1B cells represent a functional system for the study of mechanisms related to brown adipose thermogenesis and beta 3-adrenergic receptors account for approximately 30-40% of catecholamine induced UCP gene stimulation, whereas about 60-70% is stimulated via the classical beta 1/2 adrenergic pathway.