排序方式: 共有55条查询结果,搜索用时 15 毫秒
51.
Braig M Lee S Loddenkemper C Rudolph C Peters AH Schlegelberger B Stein H Dörken B Jenuwein T Schmitt CA 《Nature》2005,436(7051):660-665
Acute induction of oncogenic Ras provokes cellular senescence involving the retinoblastoma (Rb) pathway, but the tumour suppressive potential of senescence in vivo remains elusive. Recently, Rb-mediated silencing of growth-promoting genes by heterochromatin formation associated with methylation of histone H3 lysine 9 (H3K9me) was identified as a critical feature of cellular senescence, which may depend on the histone methyltransferase Suv39h1. Here we show that Emicro-N-Ras transgenic mice harbouring targeted heterozygous lesions at the Suv39h1, or the p53 locus for comparison, succumb to invasive T-cell lymphomas that lack expression of Suv39h1 or p53, respectively. By contrast, most N-Ras-transgenic wild-type ('control') animals develop a non-lymphoid neoplasia significantly later. Proliferation of primary lymphocytes is directly stalled by a Suv39h1-dependent, H3K9me-related senescent growth arrest in response to oncogenic Ras, thereby cancelling lymphomagenesis at an initial step. Suv39h1-deficient lymphoma cells grow rapidly but, unlike p53-deficient cells, remain highly susceptible to adriamycin-induced apoptosis. In contrast, only control, but not Suv39h1-deficient or p53-deficient, lymphomas senesce after drug therapy when apoptosis is blocked. These results identify H3K9me-mediated senescence as a novel Suv39h1-dependent tumour suppressor mechanism whose inactivation permits the formation of aggressive but apoptosis-competent lymphomas in response to oncogenic Ras. 相似文献
52.
Myoneural junctions in larval ascidian tail 总被引:1,自引:0,他引:1
53.
Gilman AG Simon MI Bourne HR Harris BA Long R Ross EM Stull JT Taussig R Bourne HR Arkin AP Cobb MH Cyster JG Devreotes PN Ferrell JE Fruman D Gold M Weiss A Stull JT Berridge MJ Cantley LC Catterall WA Coughlin SR Olson EN Smith TF Brugge JS Botstein D Dixon JE Hunter T Lefkowitz RJ Pawson AJ Sternberg PW Varmus H Subramaniam S Sinkovits RS Li J Mock D Ning Y Saunders B Sternweis PC Hilgemann D Scheuermann RH DeCamp D Hsueh R Lin KM Ni Y Seaman WE Simpson PC O'Connell TD Roach T Simon MI 《Nature》2002,420(6916):703-706
The Alliance for Cellular Signaling is a large-scale collaboration designed to answer global questions about signalling networks. Pathways will be studied intensively in two cells--B lymphocytes (the cells of the immune system) and cardiac myocytes--to facilitate quantitative modelling. One goal is to catalyse complementary research in individual laboratories; to facilitate this, all alliance data are freely available for use by the entire research community. 相似文献
54.
A lentivirus-based system to functionally silence genes in primary mammalian cells,stem cells and transgenic mice by RNA interference 总被引:87,自引:0,他引:87
55.
S Seshagiri EW Stawiski S Durinck Z Modrusan EE Storm CB Conboy S Chaudhuri Y Guan V Janakiraman BS Jaiswal J Guillory C Ha GJ Dijkgraaf J Stinson F Gnad MA Huntley JD Degenhardt PM Haverty R Bourgon W Wang H Koeppen R Gentleman TK Starr Z Zhang DA Largaespada TD Wu FJ de Sauvage 《Nature》2012,488(7413):660-664