Institution
University of Massachusetts Medical School
Education•Worcester, Massachusetts, United States•
About: University of Massachusetts Medical School is a education organization based out in Worcester, Massachusetts, United States. It is known for research contribution in the topics: Population & Health care. The organization has 16161 authors who have published 31822 publications receiving 1909739 citations. The organization is also known as: UMass Medical School.
Topics: Population, Health care, Immune system, Gene, Signal transduction
Papers published on a yearly basis
Papers
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TL;DR: TNF-induced programmed necrosis is facilitated by TNFR-2 signaling and caspase inhibition and may play a role in controlling viral infection.
440 citations
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TL;DR: The comprehensive characterization of homeodomain DNA-binding specificities from a metazoan genome reveals the breadth of DNA sequences that can be specified by this recognition motif.
439 citations
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TL;DR: The role of autophagy in cell death is reviewed and howAutophagy interfaces with other forms of cell death including apoptosis and necrosis is examined, as well as engulfment and inflammation.
Abstract: Autophagy influences cell survival through maintenance of cell bioenergetics and clearance of protein aggregates and damaged organelles Several lines of evidence indicate that autophagy is a multifaceted regulator of cell death, but controversy exists over whether autophagy alone can drive cell death under physiologically relevant circumstances Here, we review the role of autophagy in cell death and examine how autophagy interfaces with other forms of cell death including apoptosis and necrosis
439 citations
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TL;DR: It is shown that JNK mediated feedback inhibition of the insulin signal in mouse embryo fibroblasts, 3T3-L1 adipocytes, and 32DIR cells supports the hypothesis that J NK is a negative feedback regulator of insulin action by phosphorylating Ser307 in Irs1.
439 citations
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TL;DR: It is shown that kinase-independent scaffolding RIPK1 functions regulate homeostasis and prevent inflammation in barrier tissues by inhibiting epithelial cell apoptosis and necroptosis, and is identified as a more potent trigger of inflammation compared with apoptosis.
Abstract: Necroptosis has emerged as an important pathway of programmed cell death in embryonic development, tissue homeostasis, immunity and inflammation. RIPK1 is implicated in inflammatory and cell death signalling and its kinase activity is believed to drive RIPK3-mediated necroptosis. Here we show that kinase-independent scaffolding RIPK1 functions regulate homeostasis and prevent inflammation in barrier tissues by inhibiting epithelial cell apoptosis and necroptosis. Intestinal epithelial cell (IEC)-specific RIPK1 knockout caused IEC apoptosis, villus atrophy, loss of goblet and Paneth cells and premature death in mice. This pathology developed independently of the microbiota and of MyD88 signalling but was partly rescued by TNFR1 (also known as TNFRSF1A) deficiency. Epithelial FADD ablation inhibited IEC apoptosis and prevented the premature death of mice with IEC-specific RIPK1 knockout. However, mice lacking both RIPK1 and FADD in IECs displayed RIPK3-dependent IEC necroptosis, Paneth cell loss and focal erosive inflammatory lesions in the colon. Moreover, a RIPK1 kinase inactive knock-in delayed but did not prevent inflammation caused by FADD deficiency in IECs or keratinocytes, showing that RIPK3-dependent necroptosis of FADD-deficient epithelial cells only partly requires RIPK1 kinase activity. Epidermis-specific RIPK1 knockout triggered keratinocyte apoptosis and necroptosis and caused severe skin inflammation that was prevented by RIPK3 but not FADD deficiency. These findings revealed that RIPK1 inhibits RIPK3-mediated necroptosis in keratinocytes in vivo and identified necroptosis as a more potent trigger of inflammation compared with apoptosis. Therefore, RIPK1 is a master regulator of epithelial cell survival, homeostasis and inflammation in the intestine and the skin.
438 citations
Authors
Showing all 16331 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Karin | 236 | 704 | 226485 |
Richard A. Flavell | 231 | 1328 | 205119 |
Robert M. Califf | 196 | 1561 | 167961 |
Eric J. Topol | 193 | 1373 | 151025 |
Joan Massagué | 189 | 408 | 149951 |
Stuart H. Orkin | 186 | 715 | 112182 |
Ramachandran S. Vasan | 172 | 1100 | 138108 |
Mark Gerstein | 168 | 751 | 149578 |
David R. Jacobs | 165 | 1262 | 113892 |
Bruce L. Miller | 163 | 1153 | 115975 |
Yuh Nung Jan | 162 | 460 | 74818 |
Christopher J. O'Donnell | 159 | 869 | 126278 |
David W. Bates | 159 | 1239 | 116698 |
Adi F. Gazdar | 157 | 776 | 104116 |
John E. Morley | 154 | 1377 | 97021 |