Institution
Howard Hughes Medical Institute
Nonprofit•Chevy 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.
Topics: Gene, RNA, Population, Receptor, Cellular differentiation
Papers published on a yearly basis
Papers
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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
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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
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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
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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
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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
Name | H-index | Papers | Citations |
---|---|---|---|
Bert Vogelstein | 247 | 757 | 332094 |
Richard A. Flavell | 231 | 1328 | 205119 |
Steven A. Rosenberg | 218 | 1204 | 199262 |
Kenneth W. Kinzler | 215 | 640 | 243944 |
Robert J. Lefkowitz | 214 | 860 | 147995 |
Rob Knight | 201 | 1061 | 253207 |
Irving L. Weissman | 201 | 1141 | 172504 |
Ronald M. Evans | 199 | 708 | 166722 |
Francis S. Collins | 196 | 743 | 250787 |
Craig B. Thompson | 195 | 557 | 173172 |
Thomas C. Südhof | 191 | 653 | 118007 |
Joan Massagué | 189 | 408 | 149951 |
Stuart H. Orkin | 186 | 715 | 112182 |
John P. A. Ioannidis | 185 | 1311 | 193612 |
Eric R. Kandel | 184 | 603 | 113560 |