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Institution

Rockefeller University

EducationNew York, New York, United States
About: Rockefeller University is a education organization based out in New York, New York, United States. It is known for research contribution in the topics: Population & Gene. The organization has 15867 authors who have published 32938 publications receiving 2940261 citations. The organization is also known as: Rockefeller University & Rockefeller Institute.
Topics: Population, Gene, Virus, RNA, Antigen


Papers
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Journal ArticleDOI
TL;DR: It is concluded that basal cells represent an alternative multipotent progenitor cell population of bronchial airways and that progenitors cell selection is dictated by the type of airway injury.
Abstract: Commitment of the pulmonary epithelium to bronchial and bronchiolar airway lineages occurs during the transition from pseudoglandular to cannalicular phases of lung development, suggesting that regional differences exist with respect to the identity of stem and progenitor cells that contribute to epithelial maintenance in adulthood. We previously defined a critical role for Clara cell secretory protein-expressing (CE) cells in renewal of bronchiolar airway epithelium following injury. Even though CE cells are also the principal progenitor for maintenance of the bronchial airway epithelium, CE cell injury is resolved through a mechanism involving recruitment of a second progenitor cell population that we now identify as a GSI-B4 reactive, cytokeratin-14-expressing basal cell. These cells exhibit multipotent differentiation capacity as assessed by analysis of cellular phenotype within clones of LacZ-tagged cells. Clones were derived from K14-expressing cells tagged in a cell-type-specific fashion by ligand-regulable Cre recombinase-mediated genomic rearrangement of the ROSA26 recombination substrate allele. We conclude that basal cells represent an alternative multipotent progenitor cell population of bronchial airways and that progenitor cell selection is dictated by the type of airway injury.

523 citations

Journal ArticleDOI
31 Jan 2008-Nature
TL;DR: A novel thermodynamic model is described that computes expression patterns as a function of cis-regulatory sequence and of the binding-site preferences and expression of participating transcription factors and is applied to the segmentation gene network of Drosophila melanogaster.
Abstract: The establishment of complex expression patterns at precise times and locations is key to metazoan development, yet a mechanistic understanding of the underlying transcription control networks is still missing. Here we describe a novel thermodynamic model that computes expression patterns as a function of cis-regulatory sequence and of the binding-site preferences and expression of participating transcription factors. We apply this model to the segmentation gene network of Drosophila melanogaster and find that it predicts expression patterns of cis-regulatory modules with remarkable accuracy, demonstrating that positional information is encoded in the regulatory sequence and input factor distribution. Our analysis reveals that both strong and weaker binding sites contribute, leading to high occupancy of the module DNA, and conferring robustness against mutation; short-range homotypic clustering of weaker sites facilitates cooperative binding, which is necessary to sharpen the patterns. Our computational framework is generally applicable to most protein-DNA interaction systems.

523 citations

Journal ArticleDOI
TL;DR: Sign-R1 has been shown to preferentially bind to 2,6-sialylated glycoproteins as discussed by the authors, which suggests that a specific binding site is created by the sialylation of IgG Fc.
Abstract: The anti-inflammatory activity of intravenous Ig (IVIG) results from a minor population of the pooled IgG molecules that contains terminal α2,6-sialic acid linkages on their Fc-linked glycans. These anti-inflammatory properties can be recapitulated with a fully recombinant preparation of appropriately sialylated IgG Fc fragments. We now demonstrate that these sialylated Fcs require a specific C-type lectin, SIGN-R1, (specific ICAM-3 grabbing non-integrin-related 1) expressed on macrophages in the splenic marginal zone. Splenectomy, loss of SIGN-R1+ cells in the splenic marginal zone, blockade of the carbohydrate recognition domain (CRD) of SIGN-R1, or genetic deletion of SIGN-R1 abrogated the anti-inflammatory activity of IVIG or sialylated Fc fragments. Although SIGN-R1 has not previously been shown to bind to sialylated glycans, we demonstrate that it preferentially binds to 2,6-sialylated Fc compared with similarly sialylated, biantennary glycoproteins, thus suggesting that a specific binding site is created by the sialylation of IgG Fc. A human orthologue of SIGN-R1, DC-SIGN, displays a similar binding specificity to SIGN-R1 but differs in its cellular distribution, potentially accounting for some of the species differences observed in IVIG protection. These studies thus identify an antibody receptor specific for sialylated Fc, and present the initial step that is triggered by IVIG to suppress inflammation.

522 citations

Journal ArticleDOI
19 Oct 2006-Neuron
TL;DR: It is demonstrated that ovulation is driven by estrogen actions upon ERalpha-expressing neuronal afferents to GnRH neurons, located within rostral periventricular regions of the hypothalamus.

522 citations

Journal ArticleDOI
TL;DR: In this paper, a quantitative, genome-wide analysis of 5hmC, 5-methylcytosine (5mC), and gene expression in differentiated CNS cell types in vivo is presented.
Abstract: SUMMARY The high level of 5-hydroxymethylcytosine (5hmC) present in neuronal genomes suggests that mechanisms interpreting 5hmC in the CNS may differ from those present in embryonic stem cells. Here, we present quantitative, genome-wide analysis of 5hmC, 5-methylcytosine (5mC), and gene expression in differentiated CNS cell types in vivo. We report that 5hmC is enriched in active genes and that, surprisingly, strong depletion of 5mC is observed over these regions. The contribution of these epigenetic marks to gene expression depends critically on cell type. We identify methyl-CpG-binding protein 2 (MeCP2) as the major 5hmC-binding protein in the brain and demonstrate that MeCP2 binds 5hmC- and 5mC-containing DNA with similar high affinities. The Rett-syndrome-causing mutation R133C preferentially inhibits 5hmC binding. These findings support a model in which 5hmC and MeCP2 constitute a cell-specific epigenetic mechanism for regulation of chromatin structure and gene expression.

521 citations


Authors

Showing all 15925 results

NameH-indexPapersCitations
Bruce S. McEwen2151163200638
David Baltimore203876162955
Ronald M. Evans199708166722
Lewis C. Cantley196748169037
Ronald Klein1941305149140
Scott M. Grundy187841231821
Jie Zhang1784857221720
Andrea Bocci1722402176461
Ralph M. Steinman171453121518
Masayuki Yamamoto1711576123028
Zena Werb168473122629
Nahum Sonenberg167647104053
Michel C. Nussenzweig16551687665
Harvey F. Lodish165782101124
Dennis R. Burton16468390959
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202314
202284
2021873
2020792
2019716
2018767