T
Theresa Alenghat
Researcher at Cincinnati Children's Hospital Medical Center
Publications - 49
Citations - 6739
Theresa Alenghat is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: HDAC3 & Innate lymphoid cell. The author has an hindex of 26, co-authored 39 publications receiving 5623 citations. Previous affiliations of Theresa Alenghat include University of Pennsylvania & University of Cincinnati Academic Health Center.
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Journal ArticleDOI
HDAC3 Is a Critical Negative Regulator of Long-Term Memory Formation
Susan C. McQuown,Ruth M. Barrett,Dina P. Matheos,Rebecca J. Post,George A. Rogge,Theresa Alenghat,Shannon E. Mullican,Steven W. Jones,James R. Rusche,Mitchell A. Lazar,Marcelo A. Wood +10 more
TL;DR: A critical role is demonstrated for HDAC3 in the molecular mechanisms underlying long-term memory formation in mice modified with adeno-associated virus-expressing Cre recombinase and a selective inhibitor ofHDAC3 via RGFP136.
Journal ArticleDOI
Nuclear receptor corepressor and histone deacetylase 3 govern circadian metabolic physiology
Theresa Alenghat,Katherine Meyers,Shannon E. Mullican,Kirstin Leitner,Adetoun Adeniji-Adele,Jacqueline Avila,Maja Bucan,Rexford S. Ahima,Klaus H. Kaestner,Mitchell A. Lazar +9 more
TL;DR: It is shown that specific, genetic disruption of the Ncor1–Hdac3 interaction in mice causes aberrant regulation of clock genes and results in abnormal circadian behaviour, demonstrating that circadian regulation of metabolism is critical for normal energy balance.
Journal ArticleDOI
Histone deacetylase 3 is an epigenomic brake in macrophage alternative activation
Shannon E. Mullican,Christine A. Gaddis,Theresa Alenghat,Meera G. Nair,Paul R. Giacomin,Logan J. Everett,Dan Feng,David J. Steger,Jonathan Schug,David Artis,Mitchell A. Lazar +10 more
TL;DR: It is reported that macrophages lacking histone deacetylase 3 (HDAC3) display a polarization phenotype similar to IL-4-induced alternative activation and, furthermore, are hyperresponsive to IL (IL-4) stimulation.
Journal ArticleDOI
Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis
Theresa Alenghat,Lisa C. Osborne,Steven A. Saenz,Dmytro Kobuley,Carly G. K. Ziegler,Shannon E. Mullican,Inchan Choi,Stephanie Grunberg,Rohini Sinha,Meghan A. Wynosky-Dolfi,Annelise G. Snyder,Paul R. Giacomin,Karen L. Joyce,Tram B. Hoang,Meenakshi Bewtra,Igor E. Brodsky,Gregory F. Sonnenberg,Frederic D. Bushman,Kyoung-Jae Won,Mitchell A. Lazar,David Artis +20 more
TL;DR: Re-derivation of HDAC3ΔIEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis and intestinal barrier function were largely restored in the absence of commensal bacteria.
Journal ArticleDOI
Commensal Fungi Recapitulate the Protective Benefits of Intestinal Bacteria
Tony T. Jiang,Tzu-Yu Shao,W.X. Gladys Ang,Jeremy M. Kinder,Lucien H. Turner,Giang Pham,Jordan Whitt,Theresa Alenghat,Sing Sing Way +8 more
TL;DR: It is shown that commensal fungi can functionally replace intestinal bacteria by conferring protection against injury to mucosal tissues and positively calibrating the responsiveness of circulating immune cells.