S
Scott Ribich
Researcher at Harvard University
Publications - 12
Citations - 1718
Scott Ribich is an academic researcher from Harvard University. The author has contributed to research in topics: Deiodinase & Triiodothyronine. The author has an hindex of 10, co-authored 11 publications receiving 1601 citations. Previous affiliations of Scott Ribich include Brigham and Women's Hospital & University of Miami.
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Journal ArticleDOI
Cellular and Molecular Basis of Deiodinase-Regulated Thyroid Hormone Signaling
Balázs Gereben,Ann Marie Zavacki,Scott Ribich,Brian W. Kim,Stephen A. Huang,Warner S. Simonides,Anikó Zeöld,Antonio C. Bianco,Antonio C. Bianco +8 more
TL;DR: It seems clear that deiodinases play a much broader role than once thought, with great ramifications for the control of thyroid hormone signaling during vertebrate development and metamorphosis, as well as injury response, tissue repair, hypothalamic function, and energy homeostasis in adults.
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Promoter Choice Determines Splice Site Selection in Protocadherin α and γ Pre-mRNA Splicing
Bosiljka Tasic,Christoph E. Nabholz,Kristin K. Baldwin,Youngwook Kim,Erroll H. Rueckert,Scott Ribich,Paula Cramer,Qiang Wu,Richard Axel,Tom Maniatis +9 more
TL;DR: It is shown that each Pcdh variableExon is preceded by a promoter and that promoter choice determines which variable exon is included in a PCDh mRNA, providing evidence that alternative splicing of variable exons within a gene cluster occurs via a cis-splicing mechanism.
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Membrane Association and Protein Conformation of α-Synuclein in Intact Neurons: EFFECT OF PARKINSON′S DISEASE-LINKED MUTATIONS *
TL;DR: The Parkinson's disease-associated mutations have no effect on membrane interaction; however, the Ala-30 --> Pro mutation alters the three-dimensional conformation of alpha-synuclein, as measured by significantly increased fluorescence resonance energy transfer between the N and C termini.
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Identification of long-range regulatory elements in the protocadherin-α gene cluster
TL;DR: It is shown that HS5–1 is required for maximal levels of expression from the PCDh α1–12 and αC1 promoters, but not the Pcdh-αC2 promoter, which is consistent with the possibility that the monoallelic expression of PcdH-α V exons is a consequence of competition between individual V exon promoters for the two regulatory elements.
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Absence of thyroid hormone activation during development underlies a permanent defect in adaptive thermogenesis.
Jessica A. Hall,Scott Ribich,Marcelo A. Christoffolete,Marcelo A. Christoffolete,Gordana Simovic,Mayrin Correa-Medina,Mary-Elizabeth Patti,Antonio C. Bianco +7 more
TL;DR: It is reported that the adult D2KO BAT has a permanent thermogenic defect that stems from impaired embryonic BAT development and highlights the importance of deiodinase-controlled thyroid hormone signaling in BAT development, where it has important metabolic repercussions for energy homeostasis in adulthood.