Jin Wang
Columbia University
6 Papers
Jin Wang is an academic researcher from Columbia University. The author has contributed to research in topics: SR protein & Alternative splicing. The author has an hindex of 4, co-authored 4 publications.
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Papers
Loss of splicing factor ASF/SF2 induces G2 cell cycle arrest and apoptosis, but inhibits internucleosomal DNA fragmentation
TL;DR: Results indicate that loss of an SR protein splicing factor can induce cell cycle arrest and apoptosis, and illustrate the important role of ICAD and its regulation by alternative splicing in the process of apoptotic DNA fragmentation.
U1 snRNP-ASF/SF2 interaction and 5′ splice site recognition: characterization of required elements
Sharon F. Jamison,Zvi Pasman,Jin Wang,Cindy L. Will,Reinhard Lührmann,James L. Manley,Mariano A. Garcia-Blanco +6 more
TL;DR: The requirements for the formation of a ternary complex with pre-mRNA, domains in ASF/SF2 and components of the U1 snRNP particle are shown to be required for complex formation and it is shown that sequences at the 5' splice site of PIP7.
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Genetic analysis of the SR protein ASF/SF2: interchangeability of RS domains and negative control of splicing
TL;DR: The results provide the first demonstration that an SR protein can influence splicing of specific pre-mRNAs in vivo, and the DT40 system is used to show that depletion of ASF/SF2 affects spliced transcripts in vivo.
Exploring the effect of Er miao San-containing serum on macrophage polarization through miR-33/NLRP3 pathway.
Min Liu,Jin Wang,Si Jin Chen,Xiangwen Meng,Zhi-Jiao Cheng,Jiayu Wang,Yanan Tan,Wen-Ling Su,Zhiyuan Lu,Min Zhang,Xiaoyi Jia +10 more
TL;DR: EMS-containing serum inhibits the activation of the NLRP3 inflammasome by downregulating miRNA-33, thus preventing the polarization of M1-type macrophages.
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NEK7: a new target for the treatment of multiple tumors and chronic inflammatory diseases
TL;DR: The mechanism of NEK7 participates in the process of mitosis and regulates the activation of NLRP3 inflammasome, the aberrant expression ofNEK7 in a variety of tumors and chronic inflammatory diseases, and some potential inhibitors, which may provide some new ideas for the treatment of diverse tumors and Chronic inflammatory diseases associated with NEK8.
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