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Yokoyama S Woods SL Boyle GM Aoude LG MacGregor S Zismann V Gartside M Cust AE Haq R Harland M Taylor JC Duffy DL Holohan K Dutton-Regester K Palmer JM Bonazzi V Stark MS Symmons J Law MH Schmidt C Lanagan C O'Connor L Holland EA Schmid H Maskiell JA Jetann J Ferguson M Jenkins MA Kefford RF Giles GG Armstrong BK Aitken JF Hopper JL Whiteman DC Pharoah PD Easton DF Dunning AM Newton-Bishop JA Montgomery GW Martin NG Mann GJ Bishop DT Tsao H Trent JM Fisher DE Hayward NK Brown KM 《Nature》2011,480(7375):99-103
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Frequent somatic mutations in MAP3K5 and MAP3K9 in metastatic melanoma identified by exome sequencing 总被引:1,自引:0,他引:1
Stark MS Woods SL Gartside MG Bonazzi VF Dutton-Regester K Aoude LG Chow D Sereduk C Niemi NM Tang N Ellis JJ Reid J Zismann V Tyagi S Muzny D Newsham I Wu Y Palmer JM Pollak T Youngkin D Brooks BR Lanagan C Schmidt CW Kobe B MacKeigan JP Yin H Brown KM Gibbs R Trent J Hayward NK 《Nature genetics》2012,44(2):165-169
We sequenced eight melanoma exomes to identify new somatic mutations in metastatic melanoma. Focusing on the mitogen-activated protein (MAP) kinase kinase kinase (MAP3K) family, we found that 24% of melanoma cell lines have mutations in the protein-coding regions of either MAP3K5 or MAP3K9. Structural modeling predicted that mutations in the kinase domain may affect the activity and regulation of these protein kinases. The position of the mutations and the loss of heterozygosity of MAP3K5 and MAP3K9 in 85% and 67% of melanoma samples, respectively, together suggest that the mutations are likely to be inactivating. In in vitro kinase assays, MAP3K5 I780F and MAP3K9 W333* variants had reduced kinase activity. Overexpression of MAP3K5 or MAP3K9 mutants in HEK293T cells reduced the phosphorylation of downstream MAP kinases. Attenuation of MAP3K9 function in melanoma cells using siRNA led to increased cell viability after temozolomide treatment, suggesting that decreased MAP3K pathway activity can lead to chemoresistance in melanoma. 相似文献
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Corda D Hidalgo Carcedo C Bonazzi M Luini A Spanò S 《Cellular and molecular life sciences : CMLS》2002,59(11):1819-1832
Membrane fission is essential in various intracellular dissociative transport steps. The molecular mechanisms by which endocytic
vesicles detach from the plasma membrane are being rapidly elucidated. Much less is known about the fission mechanisms operating
at Golgi tubular networks; these include the Golgi transport and sorting stations, the trans-Golgi and cis-Golgi networks,
where the geometry and physical properties of the membranes differ from those at the cell surface. Here we discuss the lipid
and protein machineries that have so far been related to the fission process, with emphasis on those acting in the Golgi complex.
Received 10 May 2002; received after revision 20 June 2002; accepted 26 June 2002
RID="*"
ID="*"Corresponding author. 相似文献
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