H
Hungwen Chen
Researcher at Academia Sinica
Publications - 39
Citations - 1908
Hungwen Chen is an academic researcher from Academia Sinica. The author has contributed to research in topics: Syncytiotrophoblast & Transcription factor. The author has an hindex of 22, co-authored 37 publications receiving 1712 citations. Previous affiliations of Hungwen Chen include National Taiwan University & National Institutes of Health.
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Journal ArticleDOI
GCMa regulates the syncytin-mediated trophoblastic fusion.
Chenchou Yu,Kuofeng Shen,Mei-Yao Lin,Porchun Chen,Chenchen Lin,Geen-Dong Chang,Hungwen Chen,Hungwen Chen +7 more
TL;DR: GCMa was able to regulatesyncytin gene expression via two GCMa-binding sites upstream of the 5′-long terminal repeat of thesyncytin-harboring HERV-W family member in BeWo and JEG3 cells but not in HeLa cells, which may help to explain the mechanism underlying the cell fusion event specific for syncytiotrophoblast formation.
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Glucose-6-phosphatase dependent substrate transport in the glycogen storage disease type-1a mouse.
Ke-Jian Lei,Hungwen Chen,Chi-Jiunn Pan,Jerrold M. Ward,Bedrich Mosinger,Eric J. Lee,Heiner Westphal,Brian C. Mansfield,Janice Yang Chou +8 more
TL;DR: It is demonstrated that glucose–6–P transport and hydrolysis are performed by separate proteins which are tightly coupled, and a modified translocase catalytic unit model for G6Pase catalysis is proposed.
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Functional Characterization of the Placental Fusogenic Membrane Protein Syncytin
Chie-Pein Chen,Liang-Fu Chen,Su-Ray Yang,Chia-Yu Chen,Chun-Chuan Ko,Geen-Dong Chang,Hungwen Chen,Hungwen Chen +7 more
TL;DR: The results suggest that syncytin 2 may function as a second fusogenic protein for placental cell fusion, and it is demonstrated that the disulfide bridge-forming CX2C and CX7C motifs found in syncytins 1 and 2 are essential for theirfusogenic activities.
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Decreased Placental GCM1 (Glial Cells Missing) Gene Expression in Pre-eclampsia
TL;DR: It is suggested that GCM1 is a distinct transcription factor involved in placental disease and altered expression of theGCM1 gene may contribute to the etiology of pre-eclampsia.
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Stimulation of GCMa Transcriptional Activity by Cyclic AMP/Protein Kinase A Signaling Is Attributed to CBP-Mediated Acetylation of GCMa
TL;DR: The results reveal a novel regulation of GCMa activity by cAMP-dependent protein acetylation and provide a molecular mechanism by which cAMP signaling regulates trophoblastic fusion.