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RewiringofGeneticNetworksinResponsetoDNADamageouravBandyopadhyay,MonikaMehta,DwightKu...
Rewiring of Genetic Networks inResponse to DNA Damage
ourav Bandyopadhyay, Monika Mehta, Dwight Kuo, Min-Kyung Sung, Ryan Chuang,
ric J. Jaehnig, Bernd Bodenmiller, Katherine Licon, Wilbert Copeland, Michael Shales,Dorothea Fiedler, Janusz Dutkowski, Aude Guénolé, Haico van Attikum,
Kevan M. Shokat, Richard D. Kolodner, Won-Ki Huh, Ruedi Aebersold,Michael-Christopher Keogh, * Nevan J. Krogan, * Trey Ideker *
Although cellular behaviors are dynamic, the networks that govern these behaviors have been mapped primarily as static snapshots. Using an approach called differential epistasis mapping,we have discovered widespread changes in genetic interaction among yeast kinases, phosphatases,and transcription factors as the cell responds to DNA damage. Differential interactions uncover many gene functions that go undetected in static conditions. They are very effective at identifying DNA repair pathways, highlighting new damage-dependent roles for the Slt2 kinase, Pph3
hosphatase, and histone variant Htz1. The data also reveal that protein complexes are generally table in response to perturbation, but the functional relations between these complexes are ubstantially reorganized. Differential networks chart a new type of genetic landscape that is nvaluable for mapping cellular responses to stimuli.
one of the mostbasic approaches to under-standing gene function relies on the identification of genetic interactions, which occur when the phenotypic effects of one gene depend on the presence of a second. Recently, a number of technologies have been developed to systematically map genetic interaction networks over large sets of genes in budding yeast (1–3and other model organisms(4,5).Thus far,these networks have been constructed only under nor-mal laboratory conditions.However,cells are constantly bombarded by signals and stresses, such as ligands, drugs, hormones, toxins, or other environmental conditions. Although it is clear that some genetic interactions are conditiondependent (6, 7), to what extent environmentalstresses can affect genetic interaction networks,and the pathways they represent,is still unknown. 展开
ourav Bandyopadhyay, Monika Mehta, Dwight Kuo, Min-Kyung Sung, Ryan Chuang,
ric J. Jaehnig, Bernd Bodenmiller, Katherine Licon, Wilbert Copeland, Michael Shales,Dorothea Fiedler, Janusz Dutkowski, Aude Guénolé, Haico van Attikum,
Kevan M. Shokat, Richard D. Kolodner, Won-Ki Huh, Ruedi Aebersold,Michael-Christopher Keogh, * Nevan J. Krogan, * Trey Ideker *
Although cellular behaviors are dynamic, the networks that govern these behaviors have been mapped primarily as static snapshots. Using an approach called differential epistasis mapping,we have discovered widespread changes in genetic interaction among yeast kinases, phosphatases,and transcription factors as the cell responds to DNA damage. Differential interactions uncover many gene functions that go undetected in static conditions. They are very effective at identifying DNA repair pathways, highlighting new damage-dependent roles for the Slt2 kinase, Pph3
hosphatase, and histone variant Htz1. The data also reveal that protein complexes are generally table in response to perturbation, but the functional relations between these complexes are ubstantially reorganized. Differential networks chart a new type of genetic landscape that is nvaluable for mapping cellular responses to stimuli.
one of the mostbasic approaches to under-standing gene function relies on the identification of genetic interactions, which occur when the phenotypic effects of one gene depend on the presence of a second. Recently, a number of technologies have been developed to systematically map genetic interaction networks over large sets of genes in budding yeast (1–3and other model organisms(4,5).Thus far,these networks have been constructed only under nor-mal laboratory conditions.However,cells are constantly bombarded by signals and stresses, such as ligands, drugs, hormones, toxins, or other environmental conditions. Although it is clear that some genetic interactions are conditiondependent (6, 7), to what extent environmentalstresses can affect genetic interaction networks,and the pathways they represent,is still unknown. 展开
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基因网路的电路重组DNA破坏响应
ourav Bandyopadhyay,莫妮卡的一名小小郭、怀特梅宋、瑞恩庄奕琦;
瑞克Jaehnig本《Bodenmiller,凯瑟琳·Licon科普伊,迈克尔的页岩,桃乐丝菲德勒,Janusz Dutkowski Guenole,Haico货车,奥德Attikum,
Kevan m . Shokat,理查德·d·Kolodner,Won-Ki哈,Ruedi Aebersold,Michael-Christopher Keogh,* * Krogan Trey《妮娃Ideker *
虽然细胞行为都是动态的,网络管理这些行为已在地图上,主要是作为静态快照。用这种方式称为“微分epistasis地图,我们发现了广泛的变化之间的交互的遗传,蛋白激酶、酵母转录因子像细胞对DNA损伤。微分互动去揭开的许多基因功能没有在静态条件。可以非常有效的确认DNA修复途径,突出新damage-dependent Slt2激酶作用反应
hosphatase,和组蛋白Htz1变种。数据还表明,蛋白质复合物摄动响应一般表间的函数关系,但这种复合体ubstantially改组。微分网络图的一种新型遗传景观,虚实映射nvaluable刺激细胞反应。
mostbasic之一与以往方法依赖于基因功能的基因鉴定,其中发生相互作用的一个基因表型效应的存在取决于第二。最近,许多技术已经发展到系统相互作用对大的网络遗传地图在组的基因(1-3and殖酵母模式生物(4、5)工作远,这些网络已经建成nor-mal只有在实验室条件下然而,细胞不断被广告信号和应力,如配体、药品、激素、毒素,或其他环境条件。尽管很明显,一些基因相互作用conditiond
ourav Bandyopadhyay,莫妮卡的一名小小郭、怀特梅宋、瑞恩庄奕琦;
瑞克Jaehnig本《Bodenmiller,凯瑟琳·Licon科普伊,迈克尔的页岩,桃乐丝菲德勒,Janusz Dutkowski Guenole,Haico货车,奥德Attikum,
Kevan m . Shokat,理查德·d·Kolodner,Won-Ki哈,Ruedi Aebersold,Michael-Christopher Keogh,* * Krogan Trey《妮娃Ideker *
虽然细胞行为都是动态的,网络管理这些行为已在地图上,主要是作为静态快照。用这种方式称为“微分epistasis地图,我们发现了广泛的变化之间的交互的遗传,蛋白激酶、酵母转录因子像细胞对DNA损伤。微分互动去揭开的许多基因功能没有在静态条件。可以非常有效的确认DNA修复途径,突出新damage-dependent Slt2激酶作用反应
hosphatase,和组蛋白Htz1变种。数据还表明,蛋白质复合物摄动响应一般表间的函数关系,但这种复合体ubstantially改组。微分网络图的一种新型遗传景观,虚实映射nvaluable刺激细胞反应。
mostbasic之一与以往方法依赖于基因功能的基因鉴定,其中发生相互作用的一个基因表型效应的存在取决于第二。最近,许多技术已经发展到系统相互作用对大的网络遗传地图在组的基因(1-3and殖酵母模式生物(4、5)工作远,这些网络已经建成nor-mal只有在实验室条件下然而,细胞不断被广告信号和应力,如配体、药品、激素、毒素,或其他环境条件。尽管很明显,一些基因相互作用conditiond
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2011-01-01
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基因网路的电路重组DNA破坏响应
ourav Bandyopadhyay,莫妮卡的一名小小郭、怀特梅宋、瑞恩庄奕琦;
瑞克Jaehnig本《Bodenmiller,凯瑟琳·Licon科普伊,迈克尔的页岩,桃乐丝菲德勒,Janusz Dutkowski Guenole,Haico货车,奥德Attikum,
Kevan m . Shokat,理查德·d·Kolodner,Won-Ki哈,Ruedi Aebersold,Michael-Christopher Keogh,* * Krogan Trey《妮娃Ideker *
虽然细胞行为都是动态的,网络管理这些行为已在地图上,主要是作为静态快照。用这种方式称为“微分epistasis地图,我们发现了广泛的变化之间的交互的遗传,蛋白激酶、酵母转录因子像细胞对DNA损伤。微分互动去揭开的许多基因功能没有在静态条件。可以非常有效的确认DNA修复途径,突出新damage-dependent Slt2激酶作用反应
hosphatase,和组蛋白Htz1变种。数据还表明,蛋白质复合物摄动响应一般表间的函数关系,但这种复合体ubstantially改组。微分网络图的一种新型遗传景观,虚实映射nvaluable刺激细胞反应。
mostbasic之一与以往方法依赖于基因功能的基因鉴定,其中发生相互作用的一个基因表型效应的存在取决于第二。最近,许多技术已经发展到系统相互作用对大的网络遗传地图在组的基因(1-3and殖酵母模式生物(4、5)工作远,这些网络已经建成nor-mal只有在实验室条件下然而,细胞不断被广告信号和应力,如配体、药品、激素、毒素,或其他环境条件。尽管很明显,一些基因相互作用conditiondependent(6、7个),在什么程度上environmentalstresses会影响遗传互动网络,的过程以及他们所代表的仍是一个谜。
ourav Bandyopadhyay,莫妮卡的一名小小郭、怀特梅宋、瑞恩庄奕琦;
瑞克Jaehnig本《Bodenmiller,凯瑟琳·Licon科普伊,迈克尔的页岩,桃乐丝菲德勒,Janusz Dutkowski Guenole,Haico货车,奥德Attikum,
Kevan m . Shokat,理查德·d·Kolodner,Won-Ki哈,Ruedi Aebersold,Michael-Christopher Keogh,* * Krogan Trey《妮娃Ideker *
虽然细胞行为都是动态的,网络管理这些行为已在地图上,主要是作为静态快照。用这种方式称为“微分epistasis地图,我们发现了广泛的变化之间的交互的遗传,蛋白激酶、酵母转录因子像细胞对DNA损伤。微分互动去揭开的许多基因功能没有在静态条件。可以非常有效的确认DNA修复途径,突出新damage-dependent Slt2激酶作用反应
hosphatase,和组蛋白Htz1变种。数据还表明,蛋白质复合物摄动响应一般表间的函数关系,但这种复合体ubstantially改组。微分网络图的一种新型遗传景观,虚实映射nvaluable刺激细胞反应。
mostbasic之一与以往方法依赖于基因功能的基因鉴定,其中发生相互作用的一个基因表型效应的存在取决于第二。最近,许多技术已经发展到系统相互作用对大的网络遗传地图在组的基因(1-3and殖酵母模式生物(4、5)工作远,这些网络已经建成nor-mal只有在实验室条件下然而,细胞不断被广告信号和应力,如配体、药品、激素、毒素,或其他环境条件。尽管很明显,一些基因相互作用conditiondependent(6、7个),在什么程度上environmentalstresses会影响遗传互动网络,的过程以及他们所代表的仍是一个谜。
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基因网路的电路重组DNA破坏响应
ourav Bandyopadhyay,莫妮卡的一名小小郭、怀特梅宋、瑞恩庄奕琦;
瑞克Jaehnig本《Bodenmiller,凯瑟琳·Licon科普伊,迈克尔的页岩,桃乐丝菲德勒,Janusz Dutkowski Guenole,Haico货车,奥德Attikum,
Kevan m . Shokat,理查德·d·Kolodner,Won-Ki哈,Ruedi Aebersold,Michael-Christopher Keogh,* * Krogan Trey《妮娃Ideker *
虽然细胞行为都是动态的,网络管理这些行为已经文学硕士学位
ourav Bandyopadhyay,莫妮卡的一名小小郭、怀特梅宋、瑞恩庄奕琦;
瑞克Jaehnig本《Bodenmiller,凯瑟琳·Licon科普伊,迈克尔的页岩,桃乐丝菲德勒,Janusz Dutkowski Guenole,Haico货车,奥德Attikum,
Kevan m . Shokat,理查德·d·Kolodner,Won-Ki哈,Ruedi Aebersold,Michael-Christopher Keogh,* * Krogan Trey《妮娃Ideker *
虽然细胞行为都是动态的,网络管理这些行为已经文学硕士学位
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