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Biography and Research Information
OverviewAI-generated summary
Leena Maddukuri's research focuses on DNA repair mechanisms and their role in cancer, particularly glioblastoma. She investigates the function of specific DNA polymerases, such as Rev1 and DNA Polymerase Kappa, in managing DNA damage and replication stress. Her work examines how these polymerases interact with complex DNA structures like G-quadruplexes and how their activity impacts genomic stability in cancer cells.
Maddukuri's publications explore the functional consequences of genetic alterations in DNA polymerases, including the deletion of putative xenobiotic response elements in DNA Polymerase Kappa, and its effect on the replication stress response. She also studies the role of enzymes like tryptophan 2,3-dioxygenase in DNA damage tolerance and repair within glioma cells. Her research network includes collaborators at the University of Arkansas for Medical Sciences, with whom she has co-authored multiple publications.
Metrics
- h-index: 18
- Publications: 39
- Citations: 668
Selected Publications
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A Functional Precision Medicine Pipeline Combines Comparative Transcriptomics and Tumor Organoid Modeling to Identify Bespoke Treatment Strategies for Glioblastoma (2021)
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Deletion of putative xenobiotic response elements (XREs) in hpol κ alters the replication stress response and overall genomic instability in glioblastoma cells (2021)
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Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes (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)
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Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs (2021)
Collaboration Network
Top Collaborators
- A Functional Precision Medicine Pipeline Combines Comparative Transcriptomics and Tumor Organoid Modeling to Identify Bespoke Treatment Strategies for Glioblastoma
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- 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
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
Showing 5 of 6 shared publications
- A Functional Precision Medicine Pipeline Combines Comparative Transcriptomics and Tumor Organoid Modeling to Identify Bespoke Treatment Strategies for Glioblastoma
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- 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
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
Showing 5 of 6 shared publications
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- 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
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
- Deletion of putative xenobiotic response elements (XREs) in hpol κ alters the replication stress response and overall genomic instability in glioblastoma cells
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- DNA Polymerase Kappa Acts as a Barrier to Unrestrained Replication in Glioblastoma
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
- Deletion of putative xenobiotic response elements (XREs) in hpol κ alters the replication stress response and overall genomic instability in glioblastoma cells
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs
- Selective Binding Of Human Rev1 With G‐Quadruplex DNA Is Determined By A Region Unique to Higher Eukaryotes
- 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
- A Functional Precision Medicine Pipeline Combines Comparative Transcriptomics and Tumor Organoid Modeling to Identify Bespoke Treatment Strategies for Glioblastoma
- 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
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
- Inhibition of tryptophan 2,3-dioxygenase impairs DNA damage tolerance and repair in glioma cells
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