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Institution

St. Jude Children's Research Hospital

HealthcareMemphis, 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
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Journal ArticleDOI
TL;DR: Evidence from the literature supporting a single coding single‐nucleotide polymorphism in SLCO1B1 increases systemic exposure to simvastatin and the risk of muscle toxicity and therapeutic recommendations are provided.
Abstract: Simvastatin is among the most commonly used prescription medications for cholesterol reduction. A single coding single-nucleotide polymorphism, rs4149056T>C, in SLCO1B1 increases systemic exposure to simvastatin and the risk of muscle toxicity. We summarize evidence from the literature supporting this association and provide therapeutic recommendations for simvastatin based on SLCO1B1 genotype. This article is an update to the 2012 Clinical Pharmacogenetics Implementation Consortium guideline for SLCO1B1 and simvastatin-induced myopathy.

354 citations

Journal ArticleDOI
TL;DR: A mouse model of Seckel syndrome characterized by a severe deficiency in ATR supports a model whereby replicative stress, particularly in utero, contributes to the onset of aging in postnatal life, and this is balanced by the replicative Stress–limiting role of the checkpoint proteins ATR and p53.
Abstract: Although DNA damage is considered a driving force for aging, the nature of the damage that arises endogenously remains unclear. Replicative stress, a source of endogenous DNA damage, is prevented primarily by the ATR kinase. We have developed a mouse model of Seckel syndrome characterized by a severe deficiency in ATR. Seckel mice show high levels of replicative stress during embryogenesis, when proliferation is widespread, but this is reduced to marginal amounts in postnatal life. In spite of this decrease, adult Seckel mice show accelerated aging, which is further aggravated in the absence of p53. Together, these results support a model whereby replicative stress, particularly in utero, contributes to the onset of aging in postnatal life, and this is balanced by the replicative stress-limiting role of the checkpoint proteins ATR and p53.

352 citations

Journal ArticleDOI
TL;DR: Results suggest that the active form of the activator is a Ca2+-activator complex, in agreement with the findings of Teo and Wang.

352 citations

Journal ArticleDOI
08 May 2008-Neuron
TL;DR: This work studies a mouse model without alteration to outer hair cell and organ of Corti mechanics or to mechanoelectric transduction, but with diminished prestin function, demonstrating that prestin-based electromotility is required for cochlear amplification.

352 citations

Journal ArticleDOI
TL;DR: Prophylaxis with thrombolytic flushes might prevent CVC infections and catheter-related thromboses, but confirmatory studies and cost-effectiveness analysis of this approach are needed.

351 citations


Authors

Showing all 9410 results

NameH-indexPapersCitations
Richard A. Flavell2311328205119
David Baltimore203876162955
John C. Reed190891164382
Joan Massagué189408149951
Stuart H. Orkin186715112182
Douglas R. Green182661145944
Richard K. Wilson173463260000
Todd R. Golub164422201457
Robert G. Webster15884390776
Elaine R. Mardis156485226700
David Cella1561258106402
Rafi Ahmed14663393190
Ching-Hon Pui14580572146
Yoshihiro Kawaoka13988375087
Seth M. Steinberg13793680148
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202333
2022108
20211,277
20201,136
2019965
2018877