Yangjin Bae
Baylor College of Medicine
26 Papers
143 Citations
Yangjin Bae is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Notch signaling pathway & Osteoclast. The author has an hindex of 17, co-authored 26 publications. Previous affiliations of Yangjin Bae include University of Illinois at Urbana–Champaign.
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Papers
The transcriptional repressor JHDM3A demethylates trimethyl histone H3 lysine 9 and lysine 36.
Robert J. Klose,Kenichi Yamane,Kenichi Yamane,Yangjin Bae,Dianzheng Zhang,Hediye Erdjument-Bromage,Paul Tempst,Jiemin Wong,Yi Zhang,Yi Zhang +9 more
TL;DR: It is demonstrated that JHDM3A (jumonji C (JmjC)-domain-containing histone demethylase 3A) is capable of removing the me3 group from modified H3 lysine 9 (H3K9) and H3Lysine 36 (H2K36), indicating that J HDD3A may function in euchromatin to remove histone methylation marks that are associated with active transcription.
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miRNA-34c regulates Notch signaling during bone development
Yangjin Bae,Tao Yang,Huan-Chang Zeng,Philippe M. Campeau,Yuqing Chen,Terry Bertin,Brian Dawson,Elda Munivez,Jianning Tao,Brendan Lee,Brendan Lee +10 more
TL;DR: The results demonstrate that miR-34c is critical during osteoblastogenesis in part by regulating Notch signaling in bone homeostasis and one possible mechanism to modulate the proliferative effect of Notch in the committed osteoblasts progenitors which may be important in the pathogenesis of osteosarcomas.
Therapeutic Antibody Targeting Tumor- and Osteoblastic Niche-Derived Jagged1 Sensitizes Bone Metastasis to Chemotherapy
Hanqiu Zheng,Yangjin Bae,Sabine Kasimir-Bauer,Rebecca Tang,Jin Chen,Guangwen Ren,Min Yuan,Mark Esposito,Wenyang Li,Yong Wei,Minhong Shen,Lanjing Zhang,Nikolai Tupitsyn,Klaus Pantel,Chadwick T. King,Jan Sun,Jodi Moriguchi,Helen Toni Jun,Angela Coxon,Brendan Lee,Yibin Kang,Yibin Kang +21 more
TL;DR: 15D11 dramatically sensitizes bone metastasis to chemotherapy, which induces Jagged1 expression in osteoblasts to provide a survival niche for cancer cells, establishing 15D11 as a potential therapeutic agent for the prevention or treatment ofBone metastasis.
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Yunis-Varón Syndrome Is Caused by Mutations in FIG4, Encoding a Phosphoinositide Phosphatase
Philippe M. Campeau,Guy M. Lenk,James T. Lu,Yangjin Bae,Lindsay C. Burrage,Peter D. Turnpenny,Jorge Román Corona-Rivera,Lucia Morandi,Marina Mora,Heiko Reutter,Anneke T. Vulto-van Silfhout,Laurence Faivre,Eric Haan,Richard A. Gibbs,Miriam H. Meisler,Brendan Lee,Brendan Lee +16 more
TL;DR: This genotype-phenotype correlation demonstrates that absence of FIG4 activity leads to central nervous system dysfunction and extensive skeletal anomalies, and a role for PI(3,5)P(2) signaling in skeletal development and maintenance is described.
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Role of an mSin3A-Swi/Snf chromatin remodeling complex in the feedback repression of bile acid biosynthesis by SHP.
TL;DR: It is suggested that SHP mediates recruitment of mSin3A-Swi/Snf to the CYP7A1 promoter, resulting in chromatin remodeling and gene repression, which may also be a mechanism for the repression by SHP of genes activated by many nuclear receptors.
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