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.
Papers published on a yearly basis
Papers
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TL;DR: It is shown that phosphorylation of STAT3 is prolonged in mouse Socs3-deficient macrophages after stimulation with interleukin-6 (IL-6) but not IL-10, indicating that SOCS3 specifically affects signaling mediated by IL-6 and gp130.
Abstract: Suppressor of cytokine signaling (SOCS) proteins are feedback inhibitors of the Janus kinase (JAK) and signal transducer and activator of transcription (STAT) signaling pathway. SOCS3 is upregulated by several signals in macrophages and has been implicated as a regulator of various signaling pathways. Here we show that phosphorylation of STAT3 is prolonged in mouse Socs3-deficient macrophages after stimulation with interleukin-6 (IL-6) but not IL-10, indicating that SOCS3 specifically affects signaling mediated by IL-6 and gp130. IL-6 induces a wider transcriptional response in Socs3-deficient macrophages than in wild-type cells; this response is dominated by interferon (IFN)-regulated genes owing to an excess of STAT1 phosphorylation. Thus, SOCS3 functions to control the quality of the response to IL-6 and prevents the activation of an IFN-induced program of gene expression.
432 citations
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University of Florida1, St. Jude Children's Research Hospital2, Stanford University3, Vanderbilt University4, Icahn School of Medicine at Mount Sinai5, Geisinger Health System6, Washington University in St. Louis7, University of Pennsylvania8, University of Chicago9, University of Utah10, University of Liverpool11, University of Alabama at Birmingham12, Science for Life Laboratory13
TL;DR: This document is an update to the 2011 Clinical Pharmacogenetics Implementation Consortium (CPIC) guideline for CYP2C9 and VKORC1 genotypes and warfarin dosing and incorporates recommendations for adult and pediatric patients that are specific to continental ancestry.
Abstract: This document is an update to the 2011 Clinical Pharmacogenetics Implementation Consortium (CPIC) guideline for CYP2C9 and VKORC1 genotypes and warfarin dosing. Evidence from the published literature is presented for CYP2C9, VKORC1, CYP4F2, and rs12777823 genotype-guided warfarin dosing to achieve a target international normalized ratio of 2-3 when clinical genotype results are available. In addition, this updated guideline incorporates recommendations for adult and pediatric patients that are specific to continental ancestry.
432 citations
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TL;DR: It is proposed that polymorphisms in susceptibility genes promote disease through defects in “sensing” protective signals from the microbiome, defining a potentially critical gene-environment etiology for IBD.
Abstract: Inflammatory bowel disease (IBD) is associated with risk variants in the human genome and dysbiosis of the gut microbiome, though unifying principles for these findings remain largely undescribed. The human commensal Bacteroides fragilis delivers immunomodulatory molecules to immune cells via secretion of outer membrane vesicles (OMVs). We reveal that OMVs require IBD-associated genes, ATG16L1 and NOD2, to activate a noncanonical autophagy pathway during protection from colitis. ATG16L1-deficient dendritic cells do not induce regulatory T cells (Tregs) to suppress mucosal inflammation. Immune cells from human subjects with a major risk variant in ATG16L1 are defective in Treg responses to OMVs. We propose that polymorphisms in susceptibility genes promote disease through defects in “sensing” protective signals from the microbiome, defining a potentially critical gene-environment etiology for IBD.
432 citations
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TL;DR: It is suggested that many of the abnormal stress responses seen in cells lacking ATM, NBS1, or BRCA1 result from a failure of ATM migration to sites of DNA breaks and a resultant lack of SMC1 phosphorylation.
Abstract: The ATM protein kinase is activated by intermolecular autophosphorylation in response to DNA damage and initiates cellular signaling pathways that facilitate cell survival and reduce chromosomal breakage. Here, we show that NBS1 and BRCA1 are required for the recruitment of previously activated ATM to the sites of DNA breaks after ionizing irradiation, and that this recruitment is required for the phosphorylation of SMC1 by ATM. To explore the functional importance of SMC1 phosphorylation, murine cells were generated, in which the two damage-induced phosphorylation sites in SMC1 are mutated. Although these cells demonstrate normal phosphorylation and focus formation of ATM, NBS1, and BRCA1 proteins after IR, they exhibit a defective S-phase checkpoint, decreased survival, and increased chromosomal aberrations after DNA damage. These observations suggest that many of the abnormal stress responses seen in cells lacking ATM, NBS1, or BRCA1 result from a failure of ATM migration to sites of DNA breaks and a resultant lack of SMC1 phosphorylation.
431 citations
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TL;DR: It is demonstrated that fertility is decreased among female Childhood Cancer Survivor Study participants, and the risk factors identified may be utilized for pretreatment counseling of patients and their parents.
Abstract: Purpose This study was undertaken to determine the effect, if any, of treatment for cancer diagnosed during childhood or adolescence on fertility. Patients and Methods We reviewed the fertility of female participants in the Childhood Cancer Survivor Study (CCSS), which consisted of 5-year survivors, and a cohort of randomly selected siblings who responded to a questionnaire. Medical records of all members of the cohort were abstracted to obtain chemotherapeutic agents administered; the cumulative dose of drug administered for several drugs of interest; and the doses, volumes, and dates of administration of all radiation therapy. Results There were 5,149 female CCSS participants, and there were 1,441 female siblings of CCSS participants who were age 15 to 44 years. The relative risk (RR) for survivors of ever being pregnant was 0.81 (95% CI, 0.73 to 0.90; P < .001) compared with female siblings. In multivariate models among survivors only, those who received a hypothalamic/pituitary radiation dose ≥ 30 Gy ...
430 citations
Authors
Showing all 9410 results
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 |