Institution
Torrey Pines Institute for Molecular Studies
Nonprofit•San Diego, California, United States•
About: Torrey Pines Institute for Molecular Studies is a nonprofit organization based out in San Diego, California, United States. It is known for research contribution in the topics: Antigen & T cell. The organization has 2323 authors who have published 2217 publications receiving 112618 citations.
Topics: Antigen, T cell, Peptide, Solid-phase synthesis, Cytotoxic T cell
Papers published on a yearly basis
Papers
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TL;DR: HIV-1 envelope proteins are analyzed to determine if virus entry into highly permissive NP-2 cell lines expressing most known alternative CoRs differed by HIV-1 subtype and suggest that CCR3 may be used as a surrogate CoR by subtype B while FPRL1 may be use as a surrogates by subtypes A and C.
Abstract: Human immunodeficiency virus type 1 (HIV-1) infects target cells by binding to CD4 and a chemokine receptor, most commonly CCR5. CXCR4 is a frequent alternative coreceptor (CoR) in subtype B and D HIV-1 infection, but the importance of many other alternative CoRs remains elusive. We have analyzed HIV-1 envelope (Env) proteins from 66 individuals infected with the major subtypes of HIV-1 to determine if virus entry into highly permissive NP-2 cell lines expressing most known alternative CoRs differed by HIV-1 subtype. We also performed linear regression analysis to determine if virus entry via the major CoR CCR5 correlated with use of any alternative CoR and if this correlation differed by subtype. Virus pseudotyped with subtype B Env showed robust entry via CCR3 that was highly correlated with CCR5 entry efficiency. By contrast, viruses pseudotyped with subtype A and C Env proteins were able to use the recently described alternative CoR FPRL1 more efficiently than CCR3, and use of FPRL1 was correlated with CCR5 entry. Subtype D Env was unable to use either CCR3 or FPRL1 efficiently, a unique pattern of alternative CoR use. These results suggest that each subtype of circulating HIV-1 may be subject to somewhat different selective pressures for Env-mediated entry into target cells and suggest that CCR3 may be used as a surrogate CoR by subtype B while FPRL1 may be used as a surrogate CoR by subtypes A and C. These data may provide insight into development of resistance to CCR5-targeted entry inhibitors and alternative entry pathways for each HIV-1 subtype.
44 citations
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TL;DR: The structural, chemical and computational aspects of hypocholesterolemic drugs, both statins and non-statins, that target enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA) to block cholesterol biosynthesis are summarized.
Abstract: High levels of cholesterol are a primary risk factor in the development of cardiovascular diseases. In this review, we have summarized the structural, chemical and computational aspects of hypocholesterolemic drugs, both statins and non-statins, that target enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA) to block cholesterol biosynthesis.
44 citations
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TL;DR: These findings, coupled with a rapidly growing body of information regarding modulatory channel subunits and high resolution channel structures, are providing the critical information necessary for validation of K+ channels as drug targets.
43 citations
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TL;DR: The data suggest that DoA1 is the major source of ubiquitin for the DNA damage response and that Doa1 also plays an additional essential and more specific role in the monoubiquitination of histone H2B.
Abstract: The cellular response to DNA damage requires not only direct repair of the damage but also changes in the DNA replication machinery, chromatin, and transcription that facilitate survival. Here, we describe Saccharomyces cerevisiae Doa1, which helps to control the damage response by channeling ubiquitin from the proteosomal degradation pathway into pathways that mediate altered DNA replication and chromatin modification. DOA1 interacts with genes involved in PCNA ubiquitination, including RAD6, RAD18, RAD5, UBC13, and MMS2, as well as genes involved in histone H2B ubiquitination or deubiquitination, including RAD6, BRE1, LGE1, CDC73, UBP8, UBP10, and HTB2. In the absence of DOA1, damage-induced ubiquitination of PCNA does not occur. In addition, the level of ubiquitinated H2B is decreased under normal conditions and completely absent in the presence of DNA damage. In the case of PCNA, the defect associated with the doa1Δ mutant is alleviated by overexpression of ubiquitin, but in the case of H2B, it is not. The data suggest that Doa1 is the major source of ubiquitin for the DNA damage response and that Doa1 also plays an additional essential and more specific role in the monoubiquitination of histone H2B.
43 citations
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TL;DR: Using an SPCL composed in total of 52 128 400 nonacetylated hexapeptides, along with an iterative selection process based on competitive ELISA, the antigenic determinant of beta-endorphin recognized by monoclonal antibody (mAb) 3E7 is identified.
43 citations
Authors
Showing all 2327 results
Name | H-index | Papers | Citations |
---|---|---|---|
Eric J. Topol | 193 | 1373 | 151025 |
John R. Yates | 177 | 1036 | 129029 |
George F. Koob | 171 | 935 | 112521 |
Ian A. Wilson | 158 | 971 | 98221 |
Peter G. Schultz | 156 | 893 | 89716 |
Gerald M. Edelman | 147 | 545 | 69091 |
Floyd E. Bloom | 139 | 616 | 72641 |
Stuart A. Lipton | 134 | 488 | 71297 |
Benjamin F. Cravatt | 131 | 666 | 61932 |
Chi-Huey Wong | 129 | 1220 | 66349 |
Klaus Ley | 129 | 495 | 57964 |
Nicholas J. Schork | 125 | 587 | 62131 |
Michael Andreeff | 117 | 959 | 54734 |
Susan L. McElroy | 117 | 570 | 44992 |
Peter E. Wright | 115 | 444 | 55388 |