1 美国普林斯顿大学教授David Botstein
2 美国哈佛大学教授Eric S. Lander 获基因组学奖
3 美国康奈尔大学教授Lewis C. Cantley
4 荷兰皇家艺术与科学学院Hubrecht研究所教授Hans Clevers
5 美国加州大学圣地亚哥分校教授Napoleone Ferrara
6 美国纪念斯隆•凯特林癌症中心教授Charles L. Sawyers
7 美国约翰•霍普金斯大学教授Bert Vogelstein
8 美国麻省理工学院教授Robert A. Weinberg 获癌症奖
9 美国洛克菲勒大学教授Titia de Lange 获端粒奖
10 日本京都大学山中伸弥Shinya Yamanaka 获干细胞奖
11 美国洛克菲勒大学教授Cornelia I. Bargmann 获神经生物学奖
3 美国康奈尔大学教授Lewis C. Cantley
找到的结果数: |
492 |
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被引频次总计: |
63409 |
去除自引的被引频次总计: |
61829 |
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施引文献: |
43395 |
去除自引的施引文献: |
43033 |
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每项平均引用次数: |
128.88 |
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h-index : |
127 |
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L. C. Cantley
Journal: Science , vol. 296, no. 5573, pp. 1655-1657, 2002
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L CANTLEY
Journal: Cell , vol. 64, no. 2, pp. 281-302, 1991
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L. C. Cantley
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Brendan D. Manning, Lewis C. Cantley
Journal: Cell , vol. 129, no. 7, pp. 1261-1274, 2007
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Jeffrey A. Engelman, Kreshnik Zejnullahu, Tetsuya Mitsudomi, Youngchul Song, Courtney Hyland, Joon Oh Park, Neal Lindeman, Christopher-Michael Gale, Xiaojun Zhao, James Christensen, Takayuki Kosaka, Alison J. HolmesLewis C. Cantleyhttp://academic.research.microsoft.com/io.ashx?type=5&id=15082659&selfId1=17942531&selfId2=-1&maxNumber=12&query=
The epidermal growth factor receptor (EGFR) kinase inhibitors gefitinib and erlotinib are effective treatments for lung cancers with EGFR activating mutations, but these tumors invariably develop drug resistance. Here, we describe a gefitinib-sensitive lung cancer cell line that developed resistance to gefitinib as a result of focal amplification of the MET proto-oncogene. inhibition of MET signaling in these ...
Journal: Science , vol. 316, no. 5827, pp. 1039-1043, 2007
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The 14-3-3 family of proteins mediates signal transduction by binding to phosphoserine-containing proteins. Using phosphoserine-oriented peptide libraries to probe all mammalian and yeast 14-3-3s, we identified two different binding motifs, RSXpSXP and RXY/FXpSXP, present in nearly all known 14-3-3 binding proteins. The crystal structure of 14-3-3ζ complexed with the ...
Journal: Cell , vol. 91, no. 7, pp. 961-971, 1997
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Scansite identifies short protein sequence motifs that are recognized bymodular signaling domains, phosphorylated by protein Ser/Thr- or Tyr-kinases or mediate specific interactions with protein or phos- pholipid ligands. Each sequence motif is repre- sented as a position-specific scoring matrix (PSSM) based on results from oriented peptide libraryand phage displayexperiments. Predicted domain-motif interactions from Scansite can be ...
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Alex Toker, Lewis C. Cantley
When a stimulatory agonist molecule binds at the exterior of the cell membrane, a second messenger transduces the signal to the interior of the cell. Second messengers can be derived from phospholipids in the membrane by the action of the enzymes phospholipase C or phosphoinositide-3-OH kinase (PI(3)K). PI(3)K is a key player in many ...
Journal: Nature , vol. 387, no. 6634, pp. 673-676, 1997
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The S/T-protein kinases activated by phosphoinositide 3-kinase (PI3K) regulate a myriad of cellular processes. Here, we show that an approach using a combination of biochemistry and bioinformatics can identify substrates of these kinases. This approach identifies the tuberous sclerosis complex-2 gene product, tuberin, as a potential target of Akt/PKB. We demonstrate that, upon activation of ...
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The binding of erythropoietin (EPO) to its receptor (EPO-R) activates the protein tyrosine kinase JAK2. The mechanism of JAK2 inactivation has been unclear. We show that the hematopoietic protein tyrosine phosphatase SH-PTP1 (also called HCP and PTPIC) associates via its SH2 domains with the tyrosine-phosphorylated EPO-R. In vitro binding studies suggest that Y429 in the cytoplasmic ...
Journal: Cell , vol. 80, no. 5, pp. 729-738, 1995
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Phosphatidylinositol 3-kinases (PI3Ks) evolved from a single enzyme that regulates vesicle trafficking in unicellular eukaryotes into a family of enzymes that regulate cellular metabolism and growth in multicellular organisms. In this review, we examine how the PI3K pathway has evolved to control these fundamental processes, and how this pathway is in turn regulated by intricate feedback and crosstalk mechanisms. ...
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Reuben J. Shaw, Lewis C. Cantley
All eukaryotic cells coordinate cell growth with the availability of nutrients in their environment. The mTOR protein kinase has emerged as a critical growth-control node, receiving stimulatory signals from Ras and phosphatidylinositol-3-OH kinase (PI(3)K) downstream from growth factors, as well as nutrient inputs in the form of amino-acid, glucose and oxygen availability. Notably, components ...
Journal: Nature , vol. 441, no. 7092, pp. 424-430, 2006
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Recently, a number of cDNA clones with homology to the catalytic subunit of phosphoinositide 3-kinase have been identified, and the sequence of the first cDNA clone encoding a phosphatidylinositol 4-phosphate 5-kinase has been published. Use of both dominant-negative mutants of phosphoinositide 3-kinase and the inhibitors wortmannin and LY294002 has identified a number of processes in ...
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In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes, most cancer cells instead rely on aerobic glycolysis, a phenomenon termed "the Warburg effect." Aerobic glycolysis is an inefficient way to generate adenosine 5´-triphosphate (ATP), however, and the advantage it confers to cancer cells has been unclear. Here ...
Journal: Science , vol. 324, no. 5930, pp. 1029-1033, 2009
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Miikka Vikkula, Laurence M Boon, Kermit L. Carraway Iii, Jennifer T Calvert, A. John Diamonti, Boyan Goumnerov, Krystyna A Pasyk, Douglas A. Marchuk, Matthew L. Warman, Lewis C. Cantley, John B. Mulliken, Bjorn R. Olsen
Venous malformations (VMs), the most common errors of vascular morphogenesis in humans, are composed of dilated, serpiginous channels. The walls of the channels have a variable thickness of smooth muscle; some mural regions lack smooth muscle altogether. A missense mutation resulting in an arginine-to-tryptophan substitution at position 849 in the kinase domain of the receptor tyrosine kinase TIE2 ...
Journal: Cell , vol. 87, no. 7, pp. 1181-1190, 1996
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Germline mutations in LKB1, TSC2, or PTEN tumor suppressor genes result in hamartomatous syndromes with shared tumor biological features. The recent observations of LKB1-mediated activation of AMP-activated protein kinase (AMPK) and AMPK inhibition of mTOR through TSC2 prompted us to examine the biochemical and biological relationship between LKB1 and mTOR regulation. Here, we report that LKB1 is required ...
Zhou Songyang, Kermit L. Carraway, Michael J. Eck, Stephen C. Harrison, Ricardo A. Feldman, Moosa Mohammadi, Joseph Schlessinger, Stevan R. Hubbard, Darrin P. Smith, Charis Eng, Marla J. Lorenzo, Bruce A. J. PonderLewis C. Cantleyhttp://academic.research.microsoft.com/io.ashx?type=5&id=14869855&selfId1=17942531&selfId2=-1&maxNumber=12&query=
HOW do distinct protein-tyrosine kinases activate specific downstream events? Src-homology-2 (SH2) domains on tyrosine kinases or targets of tyrosine kinases recognize phosphotyrosine in a specific sequence context and thereby provide some specificity1-3. The role of the catalytic site of tyrosine kinases in determining target specificity has not been fully investigated. Here we use a degenerate peptide ...
Journal: Nature , vol. 373, no. 6514, pp. 536-539, 1995
http://academic.research.microsoft.com/Detail?entitytype=2&searchtype=2&id=17942531&orderBy=1