Tudor Moldoveanu, PhD

Research Program: Cancer Therapeutics Faculty Rank: Associate Professor Campus: University of Arkansas for Medical Sciences College: College of Medicine Department: Biochemistry & Molecular Biology

Cancer Research Interest

• Disease Site Focus: No Specific Disease Site, Multiple Myeloma, Breast, Gynecology, Hematologic Malignancies, Leukemia/ Lymphoma
• Research Focus Area: Carcinogenesis, Treatment, Informatics
• Type of Research: Basic, Translational
• Research Keywords: Programmed cell death; apoptosis; necroptosis; ferroptosis; structural and chemical biology; membrane and signaling proteins
• Research Interest Statement: Programmed cell death plays a central role in normal biology and cancer pathogenesis. Our laboratory uses structural and chemical biology to explore the mechanisms underlying cell death. We are interested in identifying and understanding how programmed cell death pathways can be targeted as a therapeutic approach. The mechanisms that manipulate programmed cell death play critical roles in regulating homeostasis but are often deregulated in cancer, which leads to chemotherapy resistance. Our research encompasses elucidation of the regulatory mechanisms responsible for apoptosis initiation as well as necroptosis and ferroptosis execution, all of which involve membrane permeabilization events. Additionally, we are designing small molecule chemical probes for key targets in these pathways for use in preclinical cancer research broadly applicable to many types of cancer.

Contact Information

• Email Address: TMoldoveanu@uams.edu
• Profiles Research Networking Software: View Profile

Active Grants

• NIH/Nat. Inst. of General Medical Sciences – 5R01GM129470
  “Elucidating the structural basis of mitochondrial outer membrane permeabilization in apoptosis”
  Principal Investigator
  8/1/2022 – 7/31/2025

Recent Publications

• Rühl S, Li Z, Srivastava S, [et al., including Moldoveanu T]. Inhibition of BAK-mediated apoptosis by the BH3-only protein BNIP5. Cell death and differentiation. 2024. PMID: 39406920.
• Wright T, Turnis ME, Grace CR, [et al., including Moldoveanu T]. Anti-apoptotic MCL-1 promotes long-chain fatty acid oxidation through interaction with ACSL1. Molecular cell. 2024 84(7):1338-1353.e8. PMID: 38503284. PMCID: PMC11017322.
• Moldoveanu T. Apoptotic mitochondrial poration by a growing list of pore-forming BCL-2 family proteins. BioEssays : news and reviews in molecular, cellular and developmental biology. 2023:e2200221. PMID: 36650950. PMCID: PMC9975053.
• Sekar G, Singh G, Qin X, [et al., including Moldoveanu T]. Small molecule SJ572946 activates BAK to initiate apoptosis. iScience. 2022 25(10):105064. PMID: 36147946. PMCID: PMC9485059.
• Chen PC, Han X, Shaw TI, [et al., including Moldoveanu T]. Alzheimer's disease-associated U1 snRNP splicing dysfunction causes neuronal hyperexcitability and cognitive impairment. Nature aging. 2022 2(10):923-940. PMID: 36636325. PMCID: PMC9833817.
• Sekar G, Ojoawo A, Moldoveanu T. Protein-protein and protein-lipid interactions of pore-forming BCL-2 family proteins in apoptosis initiation. Biochemical Society transactions. 2022 50(3):1091-1103. PMID: 35521828. PMCID: PMC9310348.
• Singh G, Guibao CD, Seetharaman J, [et al., including Moldoveanu T]. Structural basis of BAK activation in mitochondrial apoptosis initiation. Nature communications. 2022 13(1):250. PMID: 35017502. PMCID: PMC8752837.
• Ojoawo AM, Moldoveanu T. A killer metamorphosis: catching BAK in action at the membrane. The EMBO journal. 2021 40(20):e109529. PMID: 34542920. PMCID: PMC8521302.
• Schnetler R, Fanucchi S, Moldoveanu T, Koorsen G. Linker Histone H1.2 Directly Activates BAK through the K/RVVKP Motif on the C-Terminal Domain. Biochemistry. 2020 59(36):3332-3346. PMID: 32786407.
• Moldoveanu T, Czabotar PE. BAX, BAK, and BOK: A Coming of Age for the BCL-2 Family Effector Proteins. Cold Spring Harbor perspectives in biology. 2020 12(4). PMID: 31570337. PMCID: PMC7111251.