http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
SEC31A-ALKFusion Gene in Lung Adenocarcinoma
김룡남,최윤라,이미숙,Maruja E. Lira,Mao Mao,Derrick Mann,Joshua Stahl,Abel Licon,최소정,Michael Van Vrancken,한종호,Iwona Wlodarska,김진국 대한암학회 2016 Cancer Research and Treatment Vol.48 No.1
Anaplastic lymphoma kinase (ALK) fusion is a common mechanism underlying patho- genesis of non-small cell lung carcinoma (NSCLC) where these rearrangements represent important diagnostic and therapeutic targets. In this study, we found a new ALK fusion gene, SEC31A-ALK, in lung carcinoma from a 53-year-old Korean man. The conjoined region in the fusion transcript was generated by the fusion of SEC31A exon 21 and ALK exon 20 by genomic rearrangement, which contributed to genera- tion of an intact, in-frame open reading frame. SEC31A-ALK encodes a predicted fusion protein of 1,438 amino acids comprising the WD40 domain of SEC31A at the N-terminus and ALK kinase domain at the C-terminus. Fluorescence in situ hybridiza- tion studies suggested that SEC31A-ALK was generated by an unbalanced genomic rearrangement associated with loss of the 3!-end of SEC31A. This is the first report of SEC31A-ALK fusion transcript in clinical NSCLC, which could be a novel diagnostic and therapeutic target for patients with NSCLC.
Rewiring of Genetic Networks in Response to DNA Damage
Bandyopadhyay, S.,Mehta, M.,Kuo, D.,Sung, M.-K.,Chuang, R.,Jaehnig, E. J.,Bodenmiller, B.,Licon, K.,Copeland, W.,Shales, M.,Fiedler, D.,Dutkowski, J.,Guenole, A.,van Attikum, H.,Shokat, K. M.,Kolodner American Association for the Advancement of Scienc 2010 Science Vol.330 No.6009
<P>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 phosphatase, and histone variant Htz1. The data also reveal that protein complexes are generally stable in response to perturbation, but the functional relations between these complexes are substantially reorganized. Differential networks chart a new type of genetic landscape that is invaluable for mapping cellular responses to stimuli.</P>