Jocelyn Duen-Ya Jea

ORCID: 0000-0003-3264-2529
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About
Contact & Profiles
Research Areas
  • RNA modifications and cancer
  • RNA Research and Splicing
  • CRISPR and Genetic Engineering
  • RNA Interference and Gene Delivery
  • Mitochondrial Function and Pathology
  • Virus-based gene therapy research
  • Cancer, Hypoxia, and Metabolism
  • RNA and protein synthesis mechanisms
  • Genomics and Chromatin Dynamics
  • DNA Repair Mechanisms
  • Metabolism, Diabetes, and Cancer
  • Cancer-related molecular mechanisms research

Baylor College of Medicine
2019-2024

Children's Cancer Center
2021-2024

The University of Texas Southwestern Medical Center
2016

Oncogenic fusion genes as the result of chromosomal rearrangements are important for understanding genome instability in cancer cells and developing useful therapies. To date, mechanisms that create such oncogenic poorly understood. Previously we reported an unappreciated RNA-driven mechanism human prostate which expression chimeric RNA induces specified gene fusions a sequence-dependent manner. One fundamental question yet to be addressed is whether generalizable, or rather, special case...

10.1371/journal.pgen.1009985 article EN cc-by PLoS Genetics 2021-12-20

Abstract The ability to control the expression of a therapeutic gene or transgene in mammalian cells is crucial for safe and efficacious cell therapy, as well elucidating function specific product. Yet current regulation systems either evoke harmful immune responses hosts lack required regulatory efficiency. Here we describe highly responsive RNA-based molecular switch, pA regulator, that harnesses power polyA signal cleavage within 5’ UTR expression. regulator governed by ‘dual mechanism’...

10.1101/2023.01.27.525935 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-01-28

10.1007/978-1-4939-9904-0_15 article EN Methods in molecular biology 2019-11-14

Cancer cells frequently display high rates of aerobic glycolysis (the Warburg effect) in comparison to their nontransformed counterparts. Activated oncogenes and loss tumor suppressors turn alter metabolism induce glycolysis. Here we report that DOC-2/DAB2 interactive protein (DAB2IP), a suppressor gene, decreases the glycolytic activity prostate cancer cell. In addition, DAB2IP inhibits expression hexokinase 2 (HK-II) which catalyzes phosphorylation glucose first step Although molecular...

10.1096/fasebj.30.1_supplement.1099.22 article EN The FASEB Journal 2016-04-01
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