Jinglan Wang
Yale University
5 Papers
83 Citations
Jinglan Wang is an academic researcher from Yale University. The author has contributed to research in topics: Fusion protein & SUZ12. The author has an hindex of 5, co-authored 5 publications.
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Papers
A neoplastic gene fusion mimics trans-splicing of RNAs in normal human cells.
TL;DR: It is shown that normal endometrial stromal cells contain a specific chimeric RNA joining 5′ exons of the JAZF1 gene on chromosome 7p15 to 3′ exon of the Polycomb group gene JJAZ1/SUZ12 on chromosome 17q11 and that this RNA is translated into J AZF1-JJAZ1, a protein with anti-apoptotic activity.
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Malat1 as an evolutionarily conserved lncRNA, plays a positive role in regulating proliferation and maintaining undifferentiated status of early-stage hematopoietic cells
TL;DR: Malat1 plays a critical role in maintaining the proliferation potential of early-stage hematopoietic cells and is shed a light on exploring the Malat1 biological role including therapeutic significance to inhibit the proliferation Potential of malignant cells.
Effects of rearrangement and allelic exclusion of JJAZ1/SUZ12 on cell proliferation and survival
TL;DR: It is shown that both benign and malignant forms of this tumor have theJAZF1–JJAZ1 fusion but only the malignant form also exhibits exclusion of the unrearranged JJAZ1 allele, indicating the likely functional importance of allelic exclusion of genes disrupted by chromosomal translocations, as seen in a variety of other cancers.
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Gene fusions and RNA trans-splicing in normal and neoplastic human cells
TL;DR: Observations are consistent with the conclusion that chromosomal rearrangements and gene fusions in neoplastic cells may represent mechanisms for the deregulated expression of chimeric gene products that are generated at specific stages in cell development and have physiologic functions in normal cells.
The JAZF1-SUZ12 Fusion Protein Disrupts PRC2 Complexes and Impairs Chromatin Repression During Human Endometrial Stromal Tumorogenesis
TL;DR: The studies reveal that JAZF1-SUZ12 fusion protein disrupts the PRC2 complex, abolishes HMT activity and subsequently activates chromatin/genes normally repressed by PRC3, which inhibits normal neural differentiation of ES cell and increases cell proliferation.