Institution
St. Jude Children's Research Hospital
Healthcare•Memphis, Tennessee, United States•
About: St. Jude Children's Research Hospital is a healthcare organization based out in Memphis, Tennessee, United States. It is known for research contribution in the topics: Population & Virus. The organization has 9344 authors who have published 19233 publications receiving 1233399 citations. The organization is also known as: St. Jude Children's Hospital & St. Jude Hospital.
Topics: Population, Virus, Cancer, Influenza A virus, Leukemia
Papers published on a yearly basis
Papers
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TL;DR: This review is focused on how CRLs are dynamically controlled with an emphasis on how cullin neddylation cycles are integrated with receptor exchange.
Abstract: Cullin–RING E3 ubiquitin ligases (CRLs) control a plethora of biological pathways through targeted ubiquitylation of signalling proteins. These modular assemblies use substrate receptor modules to recruit specific targets. Recent efforts have focused on understanding the mechanisms that control the activity state of CRLs through dynamic alterations in CRL architecture. Central to these processes are cycles of cullin neddylation and deneddylation, as well as exchange of substrate receptor modules to re-sculpt the CRL landscape, thereby responding to the cellular requirements to turn over distinct proteins in different contexts. This review is focused on how CRLs are dynamically controlled with an emphasis on how cullin neddylation cycles are integrated with receptor exchange.
278 citations
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TL;DR: These new markers should allow MRD studies in all B-lineage ALL patients, and substantially improve their sensitivity, when incorporated in 6-marker combinations.
278 citations
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TL;DR: The study was designed to determine the effectiveness of hyperfractionated radiation for the treatment of children and young adults with brain stem gliomas.
Abstract: CHILDREN'S CANCER GROUP Protocol CCG-9882 was designed to determine the effectiveness of hyperfractionated radiation for the treatment of children and young adults with brain stem gliomas. The study opened for the accrual of patients on September 21, 1988, and was closed on June 30, 1991. Th
277 citations
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TL;DR: AML relapse after transplantation was not associated with the acquisition of previously unknown AML‐specific mutations or structural variations in immune‐related genes, but it was associated with dysregulation of pathways that may influence immune function, including down‐regulation of MHC class II genes, which are involved in antigen presentation.
Abstract: Background As consolidation therapy for acute myeloid leukemia (AML), allogeneic hematopoietic stem-cell transplantation provides a benefit in part by means of an immune-mediated graft-versus-leukemia effect. We hypothesized that the immune-mediated selective pressure imposed by allogeneic transplantation may cause distinct patterns of tumor evolution in relapsed disease. Methods We performed enhanced exome sequencing on paired samples obtained at initial presentation with AML and at relapse from 15 patients who had a relapse after hematopoietic stem-cell transplantation (with transplants from an HLA-matched sibling, HLA-matched unrelated donor, or HLA-mismatched unrelated donor) and from 20 patients who had a relapse after chemotherapy. We performed RNA sequencing and flow cytometry on a subgroup of these samples and on additional samples for validation. Results On exome sequencing, the spectrum of gained and lost mutations observed with relapse after transplantation was similar to the spectrum ...
277 citations
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TL;DR: A unique triclosan-resistant flavoprotein, FabK, is described that can also catalyse this reaction in Streptococcus pneumoniae, and has implications for the development of FabI-specific inhibitors as antibacterial agents.
Abstract: Triclosan is an antimicrobial agent that is widely used in a variety of consumer products and acts by inhibiting one of the highly conserved enzymes (enoyl-ACP reductase, or FabI) of bacterial fatty-acid biosynthesis. But several key pathogenic bacteria do not possess FabI, and here we describe a unique triclosan-resistant flavoprotein, FabK, that can also catalyse this reaction in Streptococcus pneumoniae. Our finding has implications for the development of FabI-specific inhibitors as antibacterial agents.
277 citations
Authors
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Name | H-index | Papers | Citations |
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Richard A. Flavell | 231 | 1328 | 205119 |
David Baltimore | 203 | 876 | 162955 |
John C. Reed | 190 | 891 | 164382 |
Joan Massagué | 189 | 408 | 149951 |
Stuart H. Orkin | 186 | 715 | 112182 |
Douglas R. Green | 182 | 661 | 145944 |
Richard K. Wilson | 173 | 463 | 260000 |
Todd R. Golub | 164 | 422 | 201457 |
Robert G. Webster | 158 | 843 | 90776 |
Elaine R. Mardis | 156 | 485 | 226700 |
David Cella | 156 | 1258 | 106402 |
Rafi Ahmed | 146 | 633 | 93190 |
Ching-Hon Pui | 145 | 805 | 72146 |
Yoshihiro Kawaoka | 139 | 883 | 75087 |
Seth M. Steinberg | 137 | 936 | 80148 |