Maroof K. Zafar
Research Program Manager
staff
Biochemistry & Molecular Biology, College of Medicine
Research Areas
Biography and Research Information
OverviewAI-generated summary
Maroof K. Zafar's research focuses on molecular mechanisms underlying DNA damage, repair, and replication, with a particular emphasis on cancer biology. His work investigates the roles of specific enzymes, such as DNA polymerases and helicases, in cellular processes critical for maintaining genomic stability. Recent publications explore the involvement of DNA Polymerase Kappa in glioblastoma replication and how Dda helicase interacts with DNA. Additionally, his research has examined the impact of inhibiting tryptophan 2,3-dioxygenase on DNA damage tolerance in glioma cells and identified a rare SNP in the HELB gene affecting its cellular function. Zafar also contributes to multi-omics data integration for understanding triple-negative breast cancer and has explored immune system interactions in cancer treatment, as indicated by a publication on anti-PD-L1 induced vision loss. He collaborates with researchers at the University of Arkansas for Medical Sciences and Lyon College.
Metrics
- h-index: 15
- Publications: 33
- Citations: 697
Selected Publications
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Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB (2025)
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Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB (2024)
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Anti-Programmed Death Ligand-1 Induced Acute Vision Loss in a Patient With Cancer-Associated Retinopathy (2022)
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A structural feature of Dda helicase which enhances displacement of streptavidin and <i>trp</i> repressor from <scp>DNA</scp> (2021)
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Multi-omics data integration reveals correlated regulatory features of triple negative breast cancer (2021)
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DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma (2021)
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Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells (2021)
Collaboration Network
Top Collaborators
- Multi-omics data integration reveals correlated regulatory features of triple negative breast cancer
- A structural feature of Dda helicase which enhances displacement of streptavidin and <i>trp</i> repressor from <scp>DNA</scp>
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Multi-omics data integration reveals correlated regulatory features of triple negative breast cancer
- A structural feature of Dda helicase which enhances displacement of streptavidin and <i>trp</i> repressor from <scp>DNA</scp>
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- Multi-omics data integration reveals correlated regulatory features of triple negative breast cancer
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma
- DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Multi-omics data integration reveals correlated regulatory features of triple negative breast cancer
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Multi-omics data integration reveals correlated regulatory features of triple negative breast cancer
- A structural feature of Dda helicase which enhances displacement of streptavidin and <i>trp</i> repressor from <scp>DNA</scp>
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
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