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.
Papers published on a yearly basis
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TL;DR: The proposed method for determining intracellular free calcium concentration from single-wavelength fluorescence signals does not require independent estimates of resting [Ca(2+)] but relies on the measurement of fluorescence close to indicator saturation during an experiment, which makes it well suited to [ Ca( 2+)] indicators for which saturation can be achieved under physiological conditions.
404 citations
TL;DR: The differential antagonism between a negative and two positive regulators exemplifies how inclusion of an alternative exon can be modulated.
404 citations
TL;DR: The results implicate p63 as a key regulator of cellular adhesion and survival in basal cells of the mammary gland and other stratified epithelial tissues.
Abstract: p63 is critical for epithelial development yet little is known about the transcriptional programmes it regulates. By characterising transcriptional changes and cellular effects following modulation of p63 expression, we have defined a vital role for p63 in cellular adhesion. Knockdown of p63 expression caused downregulation of cell adhesion-associated genes, cell detachment and anoikis in mammary epithelial cells and keratinocytes. Conversely, overexpression of the TAp63gamma or deltaNp63alpha isoforms of p63 upregulated cell adhesion molecules, increased cellular adhesion and conferred resistance to anoikis. Apoptosis induced by loss of p63 was rescued by signalling downstream of beta4 integrin. Our results implicate p63 as a key regulator of cellular adhesion and survival in basal cells of the mammary gland and other stratified epithelial tissues.
402 citations
TL;DR: Results show that 11q13.3 amplification could be an effective biomarker for patients most likely to respond to anti-FGF19 therapy, and forward-transformation assays and RNAi-mediated inhibition in human HCC cells established that FGF19 is an equally important driver gene in HCC.
402 citations
TL;DR: From the order of the fragments formed by EcoRI and Hpa I on the adenovirus 2 map, it is concluded that these cell lines contain only the segment of viral DNA that stretches from the left-hand end to a point about 14% along the viral genome, which must be coded by any viral function expressed in transformed cells.
400 citations
Authors
Showing all 3800 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| 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 |