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Institution

Howard Hughes Medical Institute

NonprofitChevy Chase, Maryland, United States
About: Howard Hughes Medical Institute is a nonprofit organization based out in Chevy Chase, Maryland, United States. It is known for research contribution in the topics: Gene & RNA. The organization has 20371 authors who have published 34677 publications receiving 5247143 citations. The organization is also known as: HHMI & hhmi.org.


Papers
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Journal ArticleDOI
TL;DR: The role of crystal packing in determining the observed conformations of amino acid side-chains in protein crystals is investigated by analysis of a database of proteins that have been crystallized in different unit cells and theoretical predictions of side-chain conformations with the crystal environment explicitly represented.

968 citations

Journal ArticleDOI
TL;DR: A modification of the polymerase chain reaction has been used to establish the fact that a collection of Staphylococcus aureus toxins are "superantigens," each of which interacts with the T-cell alpha beta receptor of human T cells by means of a specific set of V beta elements.
Abstract: A modification of the polymerase chain reaction has been used to establish the fact that a collection of Staphylococcus aureus toxins are "superantigens," each of which interacts with the T-cell alpha beta receptor of human T cells by means of a specific set of V beta elements.

968 citations

Journal ArticleDOI
25 Aug 2016-Cell
TL;DR: This work provides a systematic methodology for achieving comprehensive molecular classification of neurons, identifies novel neuronal types, and uncovers transcriptional differences that distinguish types within a class.

967 citations

Journal ArticleDOI
17 Sep 2004-Cell
TL;DR: It is shown that acidosis activates Ca2+ -permeable acid-sensing ion channels (ASICs), inducing glutamate receptor-independent, Ca2-dependent, neuronal injury inhibited by ASIC blockers, and disclosing new potential therapeutic targets for stroke.

966 citations

Journal ArticleDOI
02 Feb 1995-Nature
TL;DR: It is shown by targeted gene disruption in mice that tal-1 is essential for embryonic blood formation in vivo and resembles loss of the erythroid transcription factor GATA-113,14 or the LIM protein rbtn215 .
Abstract: CHROMOSOMAL translocations associated with malignancies often result in deregulated expression of genes encoding transcription factors1. In human T-cell leukaemias such regulators belong to diverse protein families and may normally be expressed widely (for example, Ttg-1/rbtnl, Ttg-2/rbtn2) 2,3, exclusively outside the haematopoietic system (for example, Hoxll) 4, or specifically in haematopoietic cells and other selected sites (for example, tal-1/ SCL, lyl-1) 5,6. Aberrant expression within T cells is thought to interfere with programmes of normal maturation. The most frequently activated gene in acute T-cell leukaemias, tal-1 (also called SCL) 7,8, encodes a candidate regulator of haematopoietic development9, a basic-helix-loop-helix protein5, related to critical myogenic10 and neurogenic11 factors. Here we show by targeted gene disruption in mice12 that tal-1 is essential for embryonic blood formation in vivo. With respect to embryonic erythropoiesis, tal-1 deficiency resembles loss of the erythroid transcription factor GATA-113,14 or the LIM protein rbtn215 .Profound reduction in myeloid cells cultured in vivo from tal-1 null yolk sacs suggests a broader defect manifest at the myelo-erythroid or multipotential progenitor cell level.

966 citations


Authors

Showing all 20486 results

NameH-indexPapersCitations
Bert Vogelstein247757332094
Richard A. Flavell2311328205119
Steven A. Rosenberg2181204199262
Kenneth W. Kinzler215640243944
Robert J. Lefkowitz214860147995
Rob Knight2011061253207
Irving L. Weissman2011141172504
Ronald M. Evans199708166722
Francis S. Collins196743250787
Craig B. Thompson195557173172
Thomas C. Südhof191653118007
Joan Massagué189408149951
Stuart H. Orkin186715112182
John P. A. Ioannidis1851311193612
Eric R. Kandel184603113560
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202330
2022228
20211,583
20201,587
20191,591
20181,394