Institution
Cold Spring Harbor Laboratory
Nonprofit•Cold Spring Harbor, New York, United States•
About: Cold Spring Harbor Laboratory is a nonprofit organization based out in Cold Spring Harbor, New York, United States. It is known for research contribution in the topics: Gene & Genome. The organization has 3772 authors who have published 6603 publications receiving 1010873 citations. The organization is also known as: CSHL.
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Papers
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TL;DR: The polyoma virus middle-T and the T24 Harvey ras1 genes are individually unable to transform primary baby rat kidney cells and separate establishment and transforming functions are required for oncogenic transformation of primary cells in culture.
Abstract: The polyoma virus middle-T and the T24 Harvey ras1 genes are individually unable to transform primary baby rat kidney cells. Adenovirus early region 1A provides functions required by these genes to transform primary cells following DNA-mediated gene transfer. These results suggest that separate establishment and transforming functions are required for oncogenic transformation of primary cells in culture.
1,245 citations
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TL;DR: It is proposed that the origin recognition complex acts as the initiator protein for S. cerevisiae origins of DNA replication, and specific DNA binding by theorigin recognition complex is dependent upon the addition of ATP.
Abstract: A multiprotein complex that specifically recognizes cellular origins of DNA replication has been identified and purified from the yeast Saccharomyces cerevisiae. We observe a strong correlation between origin function and origin recognition by this activity. Interestingly, specific DNA binding by the origin recognition complex is dependent upon the addition of ATP. We propose that the origin recognition complex acts as the initiator protein for S. cerevisiae origins of DNA replication.
1,243 citations
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TL;DR: Using microarray analysis, it is shown that heterochromatin in Arabidopsis is determined by transposable elements and related tandem repeats, under the control of the chromatin remodelling ATPase DDM1 (Decrease in DNA Methylation 1).
Abstract: Heterochromatin has been defined as deeply staining chromosomal material that remains condensed in interphase, whereas euchromatin undergoes de-condensation. Heterochromatin is found near centromeres and telomeres, but interstitial sites of heterochromatin (knobs) are common in plant genomes and were first described in maize. These regions are repetitive and late-replicating. In Drosophila, heterochromatin influences gene expression, a heterochromatin phenomenon called position effect variegation. Similarities between position effect variegation in Drosophila and gene silencing in maize mediated by "controlling elements" (that is, transposable elements) led in part to the proposal that heterochromatin is composed of transposable elements, and that such elements scattered throughout the genome might regulate development. Using microarray analysis, we show that heterochromatin in Arabidopsis is determined by transposable elements and related tandem repeats, under the control of the chromatin remodelling ATPase DDM1 (Decrease in DNA Methylation 1). Small interfering RNAs (siRNAs) correspond to these sequences, suggesting a role in guiding DDM1. We also show that transposable elements can regulate genes epigenetically, but only when inserted within or very close to them. This probably accounts for the regulation by DDM1 and the DNA methyltransferase MET1 of the euchromatic, imprinted gene FWA, as its promoter is provided by transposable-element-derived tandem repeats that are associated with siRNAs.
1,199 citations
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TL;DR: It is reported that a missense mutation in PTEN, PTEN-G129E, which is observed in two Cowden disease kindreds, specifically ablates the ability of PTEN to recognize inositol phospholipids as a substrate, suggesting that loss of the lipid phosphatase activity is responsible for the etiology of the disease.
Abstract: Since their discovery, protein tyrosine phosphatases have been speculated to play a role in tumor suppression because of their ability to antagonize the growth-promoting protein tyrosine kinases. Recently, a tumor suppressor from human chromosome 10q23, called PTEN or MMAC1, has been identified that shares homology with the protein tyrosine phosphatase family. Germ-line mutations in PTEN give rise to several related neoplastic disorders, including Cowden disease. A key step in understanding the function of PTEN as a tumor suppressor is to identify its physiological substrates. Here we report that a missense mutation in PTEN, PTEN-G129E, which is observed in two Cowden disease kindreds, specifically ablates the ability of PTEN to recognize inositol phospholipids as a substrate, suggesting that loss of the lipid phosphatase activity is responsible for the etiology of the disease. Furthermore, expression of wild-type or substrate-trapping forms of PTEN in HEK293 cells altered the levels of the phospholipid products of phosphatidylinositol 3-kinase and ectopic expression of the phosphatase in PTEN-deficient tumor cell lines resulted in the inhibition of protein kinase (PK) B/Akt and regulation of cell survival.
1,197 citations
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TL;DR: Statistical analysis of plasmid rescue frequencies has revealed that the MDRS loci detect differential modifications of the transgene insertions among mouse lines that show distinctive patterns of transgenes expression.
Abstract: Plasmids comprising transgene insertions in four lines of transgenic mice have been retrieved by plasmid rescue into a set of Escherichia coli strains with mutations in different members of the methylation-dependent restriction system (MDRS). Statistical analysis of plasmid rescue frequencies has revealed that the MDRS loci detect differential modifications of the transgene insertions among mouse lines that show distinctive patterns of transgene expression. Plasmids in mice that express hybrid insulin transgenes during development can be readily cloned into E. coli strains carrying mutations in two of the MDRS loci, mcrA and mcrB. In mice in which transgene expression is inappropriately delayed into adulthood, plasmids can only be cloned into E. coli that carry mutations in all known MDRS activities. Differential cloning frequencies in the presence or absence of the various methylation-dependent restriction genes represent a further way to distinguish regions of mammalian chromosomes. These multiply deficient E. coli strains will also facilitate the molecular cloning of modified chromosomal DNA.
1,187 citations
Authors
Showing all 3800 results
Name | H-index | Papers | Citations |
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Phillip A. Sharp | 172 | 614 | 117126 |
Gregory J. Hannon | 165 | 421 | 140456 |
Ian A. Wilson | 158 | 971 | 98221 |
Marco A. Marra | 153 | 620 | 184684 |
Michael E. Greenberg | 148 | 316 | 114317 |
Tom Maniatis | 143 | 318 | 299495 |
Detlef Weigel | 142 | 516 | 84670 |
Kim Nasmyth | 142 | 294 | 59231 |
Arnold J. Levine | 139 | 485 | 116005 |
Joseph E. LeDoux | 139 | 478 | 91500 |
Gerald R. Fink | 138 | 316 | 70868 |
Ramnik J. Xavier | 138 | 597 | 101879 |
Harold E. Varmus | 137 | 496 | 76320 |
David A. Jackson | 136 | 1095 | 68352 |
Scott W. Lowe | 134 | 396 | 89376 |