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: FGFR-3 appears to regulate endochondral ossification by an essentially negative mechanism, limiting rather than promoting osteogenesis, and certain human disorders, such as achondroplasia, can be interpreted as gain-of-function mutations that activate the fundamentally negative growth control exerted by the FGFR- 3 kinase.
1,045 citations
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TL;DR: It is found that B cell division is restricted to the DZ, with a net vector of B cell movement from the D Z to the LZ, and T cell help, and not direct competition for antigen, is the limiting factor in GC selection.
1,045 citations
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TL;DR: Data indicate that recombinant selenomethionyl proteins analyzed by MAD phasing offer a rather general means for the elucidation of atomic structures.
Abstract: An expression system has been established for the incorporation of selenomethionine into recombinant proteins produced from plasmids in Escherichia coli. Replacement of methionine by selenomethionine is demonstrated at the level of 100% for both T4 and E. coli thioredoxins. The natural recombinant proteins and the selenomethionyl variants of both thioredoxins crystallize isomorphously. Anomalous scattering factors were deduced from synchrotron X-ray absorption measurements of crystals of the selenomethionyl proteins. Taken with reference to experience in the structural analysis of selenobiotinyl streptavidin by the method of multiwavelength anomalous diffraction (MAD), these data indicate that recombinant selenomethionyl proteins analyzed by MAD phasing offer a rather general means for the elucidation of atomic structures.
1,042 citations
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TL;DR: Observations indicate that cleavage of p35 to p25 by calpain may be involved in the pathogenesis of Alzheimer's disease.
Abstract: Cyclin-dependent kinase 5 (cdk5) and its neuron-specific activator p35 are required for neurite outgrowth and cortical lamination. Proteolytic cleavage of p35 produces p25, which accumulates in the brains of patients with Alzheimer's disease. Conversion of p35 to p25 causes prolonged activation and mislocalization of cdk5. Consequently, the p25/cdk5 kinase hyperphosphorylates tau, disrupts the cytoskeleton and promotes the death (apoptosis) of primary neurons. Here we describe the mechanism of conversion of p35 to p25. In cultured primary cortical neurons, excitotoxins, hypoxic stress and calcium influx induce the production of p25. In fresh brain lysates, addition of calcium can stimulate cleavage of p35 to p25. Specific inhibitors of calpain, a calcium-dependent cysteine protease, effectively inhibit the calcium-induced cleavage of p35. In vitro, calpain directly cleaves p35 to release a fragment with relative molecular mass 25,000. The sequence of the calpain cleavage product corresponds precisely to that of p25. Application of the amyloid beta-peptide A beta(1-42) induces the conversion of p35 to p25 in primary cortical neurons. Furthermore, inhibition of cdk5 or calpain activity reduces cell death in A beta-treated cortical neurons. These observations indicate that cleavage of p35 to p25 by calpain may be involved in the pathogenesis of Alzheimer's disease.
1,042 citations
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TL;DR: The procedures used to develop 17 lines of human embryonic stem cells from the inner cell masses of blastocysts are discussed.
Abstract: This report, first published online on March 3, 2004, discusses the procedures used to develop 17 lines of human embryonic stem cells from the inner cell masses of blastocysts. These cell lines are available to researchers under a Material Transfer Agreement; according to current regulations, the cells cannot be used for research supported by federal funds. These cells are expected to facilitate research on a variety of serious chronic diseases.
1,041 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 |