Tudor Moldoveanu
Sourced from institutional research profiles (UAMS TRI or ARA).
Associate Professor
COM | Biochemistry & Molecular Biology
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Tudor Moldoveanu leads a research group at the University of Arkansas for Medical Sciences, focusing on the molecular mechanisms of apoptosis, particularly the BCL-2 protein family. His work investigates how these proteins regulate cell death, a critical process in development and disease. Moldoveanu has received federal funding from the NIH/National Institute of General Medical Sciences for research aimed at elucidating the structural basis of mitochondrial outer membrane permeabilization in apoptosis. His publications explore the interactions within the BCL-2 family, the role of specific proteins like BOK and BAK, and the structural dynamics of these molecules, including a study on the Ca2+ switch aligning the active site of Calpain.
His research has contributed to understanding programmed cell death pathways, with implications for various physiological and pathological conditions. Moldoveanu's scholarship metrics include an h-index of 33, with 79 total publications and over 5,840 citations. He is recognized as a federal grant principal investigator, underscoring his role in securing and managing research funding. His group's recent activity and publication record indicate ongoing contributions to the field of cell death research.
Metrics
- h-index: 33
- Publications: 79
- Citations: 5,840
Positions
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Associate Professor 2022–presentUniversity of Arkansas for Medical Sciences COM | Biochemistry & Molecular Biology Institutional directory
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Assistant Member 2017–2022St. Jude Children's Research Hospital Structural Biology ORCID
Selected Publications
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A safety pin against BAX (2026)
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Making zombies to kill cancer (2026)
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A peptide-based screen for cell death inhibitors identifies the cytoprotective compound CDL36 (2026)
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Structural basis of BAK sequestration by MCL-1 in apoptosis (2025)
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Abstract A010: Proteasome inhibitors induce a BAX and BAK independent, non-canonical apoptosis (2024)
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Abstract 5731: Apoptosis Inducing Agent 1 enhances cancer therapy-induced apoptosis by direct interaction with BAX and BAK (2023)
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Apoptotic mitochondrial poration by a growing list of pore‐forming BCL‐2 family proteins (2023)
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Alzheimer’s disease-associated U1 snRNP splicing dysfunction causes neuronal hyperexcitability and cognitive impairment (2022)
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Small molecule SJ572946 activates BAK to initiate apoptosis (2022)
Federal Grants 1 $321,300 total
Elucidating the structural basis of mitochondrial outer membrane permeabilization in apoptosis
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- GLP-1 Based Therapies on Lymphedema in Overweight or Obese Breast Cancer Patients State of Arkansas via Arkansas Breast Cancer Research Program Principal Investigator
Collaboration Network
Top Collaborators
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Abstract 5731: Apoptosis Inducing Agent 1 enhances cancer therapy-induced apoptosis by direct interaction with BAX and BAK
- A peptide-based screen for cell death inhibitors identifies the cytoprotective compound CDL36
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Structural basis of BAK sequestration by MCL-1 in apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Abstract 5731: Apoptosis Inducing Agent 1 enhances cancer therapy-induced apoptosis by direct interaction with BAX and BAK
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Structural basis of BAK sequestration by MCL-1 in apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- A peptide-based screen for cell death inhibitors identifies the cytoprotective compound CDL36
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Structural basis of BAK sequestration by MCL-1 in apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Small molecule SJ572946 activates BAK to initiate apoptosis
- Alzheimer’s disease-associated U1 snRNP splicing dysfunction causes neuronal hyperexcitability and cognitive impairment
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