Kirk L. West
Assistant Professor
Also affiliated: Arkansas Children's Hospital (2016); University of Arkansas Medical Center (2015); Arkansas Children's Research Institute (2016–2017)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Kirk L. West's research focuses on understanding the molecular mechanisms underlying DNA damage response and repair. His work investigates the role of specific kinases, such as DYRK1A and Tousled-like kinases (TLKs), in orchestrating cellular responses to DNA breaks. West has published studies detailing how the phosphorylation status of these kinases influences their recruitment to damaged chromatin, often in conjunction with proteins like PCNA and Spir1.
His research also explores genetic variations impacting DNA repair pathways, as seen in investigations of rare single nucleotide polymorphisms (SNPs) in genes like HELB that can interfere with protein interactions and cellular function. Further contributions include examining the interplay between signaling pathways and DNA repair, such as the role of glycogen synthase kinase-3β in regulating 53BP1 function in response to PARP inhibitors. West collaborates with researchers at the University of Arkansas for Medical Sciences, including Brian Koss, Sara C. Shalin, and Erin M. Taylor.
Metrics
- h-index: 9
- Publications: 28
- Citations: 360
Positions
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Assistant Professor 2025–presentUniversity of Arkansas for Medical Sciences Biochemistry and Molecular Biology ORCID
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Post Doctoral Fellow 2018–2025University of Arkansas for Medical Sciences Radiation Oncology ORCID
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Ph.D. Candidate 2013–2018University of Arkansas for Medical Sciences Biochemistry and Molecular Biology ORCID
Selected Publications
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Rare SNP in the HELB gene interferes with RPA interaction and cellular function of HELB (2025)
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Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction (2024)
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Nuclear F-actin assembly on damaged chromatin is regulated by DYRK1A and Spir1 phosphorylation (2024)
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Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction (2024)
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Rare SNP in the HELB gene interferes with RPA interaction and cellular function of HELB (2024)
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Abstract PR011: Novel role of glycogen synthase kinase-3β in determining cancer cell response to PARPi through regulation of 53BP1 function (2024)
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205 Targeting Homologous Repair to Overcome Genotoxic Therapy Resistance in Pancreatic Cancer (2022)
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Screen identifies DYRK1B network as mediator of transcription repression on damaged chromatin (2020)
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Histone H2A variants alpha1-extension helix directs RNF168-mediated ubiquitination (2020)
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LC8/DYNLL1 is a 53BP1 effector and regulates checkpoint activation (2019)
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DEAD-box RNA helicases Dbp2, Ded1 and Mss116 bind to G-quadruplex nucleic acids and destabilize G-quadruplex RNA (2019)
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Proteomic characterization of the arsenic response locus in S. cerevisiae (2019)
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Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma (2019)
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Framework for reanalysis of publicly available Affymetrix® GeneChip® data sets based on functional regions of interest (2017)
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Trichloroethylene-induced alterations in DNA methylation were enriched in polycomb protein binding sites in effector/memory CD4+ T cells (2017)
Collaboration Network
Top Collaborators
- LC8/DYNLL1 is a 53BP1 effector and regulates checkpoint activation
- Screen identifies DYRK1B network as mediator of transcription repression on damaged chromatin
- Histone H2A variants alpha1-extension helix directs RNF168-mediated ubiquitination
- Nuclear F-actin assembly on damaged chromatin is regulated by DYRK1A and Spir1 phosphorylation
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction
Showing 5 of 9 shared publications
- Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 + T cells
- Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells
- Trichloroethylene-induced alterations in DNA methylation were enriched in polycomb protein binding sites in effector/memory CD4+ T cells
- Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 + T cells
- Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells
- Trichloroethylene-induced alterations in DNA methylation were enriched in polycomb protein binding sites in effector/memory CD4+ T cells
- Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 + T cells
- Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells
- Trichloroethylene-induced alterations in DNA methylation were enriched in polycomb protein binding sites in effector/memory CD4+ T cells
- Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 + T cells
- Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells
- Trichloroethylene-induced alterations in DNA methylation were enriched in polycomb protein binding sites in effector/memory CD4+ T cells
- Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 + T cells
- Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells
- Trichloroethylene-induced alterations in DNA methylation were enriched in polycomb protein binding sites in effector/memory CD4+ T cells
- Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 + T cells
- Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4+ T cells
- Trichloroethylene-induced alterations in DNA methylation were enriched in polycomb protein binding sites in effector/memory CD4+ T cells
- Framework for reanalysis of publicly available Affymetrix® GeneChip® data sets based on functional regions of interest
- Region-based custom chip description formats for reanalysis of publicly available affymetrix® genechip® data sets
- Framework for reanalysis of publicly available Affymetrix ® GeneChip ® data sets based on functional regions of interest
- Framework for reanalysis of publicly available Affymetrix® GeneChip® data sets based on functional regions of interest
- Region-based custom chip description formats for reanalysis of publicly available affymetrix® genechip® data sets
- Framework for reanalysis of publicly available Affymetrix ® GeneChip ® data sets based on functional regions of interest
- Framework for reanalysis of publicly available Affymetrix® GeneChip® data sets based on functional regions of interest
- Region-based custom chip description formats for reanalysis of publicly available affymetrix® genechip® data sets
- Framework for reanalysis of publicly available Affymetrix ® GeneChip ® data sets based on functional regions of interest
- Framework for reanalysis of publicly available Affymetrix® GeneChip® data sets based on functional regions of interest
- Region-based custom chip description formats for reanalysis of publicly available affymetrix® genechip® data sets
- Framework for reanalysis of publicly available Affymetrix ® GeneChip ® data sets based on functional regions of interest
- Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- DEAD-box RNA helicases Dbp2, Ded1 and Mss116 bind to G-quadruplex nucleic acids and destabilize G-quadruplex RNA
- Proteomic characterization of the arsenic response locus in S. cerevisiae
- DEAD-box RNA helicases Dbp2, Ded1 and Mss116 bind to G-quadruplex nucleic acids and destabilize G-quadruplex RNA
- Rare SNP in the HELB gene interferes with RPA interaction and cellular function of HELB
- Rare SNP in the HELB gene interferes with RPA interaction and cellular function of HELB
- DEAD-box RNA helicases Dbp2, Ded1 and Mss116 bind to G-quadruplex nucleic acids and destabilize G-quadruplex RNA
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction
- LC8/DYNLL1 is a 53BP1 effector and regulates checkpoint activation
- Screen identifies DYRK1B network as mediator of transcription repression on damaged chromatin
- Nuclear F-actin assembly on damaged chromatin is regulated by DYRK1A and Spir1 phosphorylation
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