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Leah N Huiting
Researcher at Boston University
Publications - 6
Citations - 74
Leah N Huiting is an academic researcher from Boston University. The author has contributed to research in topics: Unfolded protein response & Endoplasmic reticulum. The author has an hindex of 3, co-authored 5 publications receiving 55 citations.
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The Zebrafish as a Tool to Cancer Drug Discovery.
TL;DR: The advantages of in vivo imaging, large progeny, and rapid development that the zebrafish provides make it an attractive model to promote novel cancer drug discovery and reduce the hurdles and cost of clinical trials.
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UFD1 contributes to MYC-mediated leukemia aggressiveness through suppression of the proapoptotic unfolded protein response
Leah N Huiting,Y. Samaha,Guang Lan Zhang,Guang Lan Zhang,Justine E. Roderick,B. Li,Nicole M. Anderson,Y. W. Wang,Y. W. Wang,L. Wang,Fabrice Laroche,Jae Won Choi,Ching-Ti Liu,Michelle A. Kelliher,Hui Feng +14 more
TL;DR: These studies identify UFD1 as a critical regulator of the ER stress response and a novel contributor to MyC-mediated leukemia aggressiveness, with implications for targeted therapy in T-ALL and likely other MYC-driven cancers.
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Cross organelle stress response disruption promotes gentamicin-induced proteotoxicity
Chinaemere Igwebuike,Julia A. Yaglom,Julia A. Yaglom,Leah N Huiting,Hui Feng,Joshua D. Campbell,Zhiyong Wang,Andrea Havasi,David R. Pimentel,Michael Y. Sherman,Michael Y. Sherman,Steven C. Borkan +11 more
TL;DR: CORE disruption is identified as an early and remediable cause of gentamicin proteotoxicity that precedes downstream UPR activation and cell death, and preserved the CORE significantly improves renal cell survival likely by reducing organelle-specific proteot toxicity during gentamicIn exposure.
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α-Ketoglutarate-Mediated DNA Demethylation Sustains T-Acute Lymphoblastic Leukemia upon TCA Cycle Targeting
Yanwu Wang,Ning Shen,Gervase Spurlin,Sovannarith Korm,Sarah Huang,Nicole M. Anderson,Leah N Huiting,Hudan Liu,Hui Feng +8 more
TL;DR: This research seeks to understand how T acute lymphoblastic leukemia (T-ALL) escapes disruption of the tricarboxylic acid (TCA) cycle, a biochemical pathway critical for T-ALL survival, and shows that leukemic cells modify their DNA to increase the activity of other pathways to compensate for diminished TCA cycle function.
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Unraveling the regulatory role of endoplasmic-reticulum-associated degradation in tumor immunity.
TL;DR: Current knowledge on how ERAD promotes protein degradation, regulates immune cell development and function, participates in antigen presentation, exerts paradoxical roles on tumorigenesis and immunity, and thus impacts current cancer therapy are summarized.