Tudor Moldoveanu
Sourced from institutional research profiles (UAMS TRI or ARA).
Associate Professor
Faculty Researcher
COM | Biochemistry & Molecular Biology
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Tudor Moldoveanu's research focuses on understanding the structural mechanisms of mitochondrial outer membrane permeabilization during apoptosis, a process critical to programmed cell death. He has received funding from the National Institutes of Health (NIH) through the National Institute of General Medical Sciences for his work in this area. His federal grant, totaling $321,300, specifically aims to elucidate the structural basis of this cellular event.
As an Associate Professor in Biochemistry & Molecular Biology at the University of Arkansas for Medical Sciences, Moldoveanu leads a research group dedicated to these investigations. His scholarly contributions are reflected in a body of work that includes 79 publications, accumulating over 5,840 citations, and an h-index of 33. This metrics indicate a significant and widely recognized impact within his field.
Metrics
- h-index: 33
- Publications: 79
- Citations: 5,840
Selected Publications
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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
- Structural basis of BAK sequestration by MCL-1 in apoptosis
- 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
- 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
- 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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