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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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Book ChapterDOI

Transcriptional Control of Mitochondrial Energy Metabolism through the PGC1 Coactivators

TL;DR: The data show that the PGC1s are key modulators of mitochondrial biology and important protective molecules against ROS generation and damage and the implications for diabetes and neurodegenerative diseases are discussed.
Journal ArticleDOI

Targeted disruption of the c-fos gene demonstrates c-fos-dependent and -independent pathways for gene expression stimulated by growth factors or oncogenes.

TL;DR: The results clearly demonstrate that some AP‐1‐dependent genes require c‐fos for full expression while others do not; oncogenes may activate expression of metalloproteases via either fos‐dependent orfos‐independent mechanisms; and imply that c‐ fos may play an important regulatory role in the invasive behavior of malignant tumors.
Journal ArticleDOI

A direct role for C/EBP and the AP-I-binding site in gene expression linked to adipocyte differentiation.

TL;DR: Results indicate that sequences that bind C/EBP and the Fos-Jun complex play major roles in the expression of the aP2 gene during adipocyte differentiation and demonstrate that C/ EBP can directly regulate cellular gene expression.
Journal ArticleDOI

Mitochondrial Patch Clamp of Beige Adipocytes Reveals UCP1-Positive and UCP1-Negative Cells Both Exhibiting Futile Creatine Cycling

TL;DR: Patch clamped the inner mitochondrial membrane of beige and brown fat to provide a direct comparison of their thermogenic H+ leak (IH) and found all inguinal beige adipocytes had robust UCP1-dependent IH comparable to brown fat, but it was about three times less sensitive to purine nucleotide inhibition.
Journal ArticleDOI

Elevated PGC-1α Activity Sustains Mitochondrial Biogenesis and Muscle Function without Extending Survival in a Mouse Model of Inherited ALS

TL;DR: It is reported that elevation of P GC-1α levels in muscles of mice that develop fatal paralysis from an ALS-causing SOD1 mutant elevates PGC-1 α-dependent pathways throughout disease course, and drugs increasing PGC -1α activity in muscle represent an attractive therapy for maintaining muscle function during progression of ALS.