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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: 342
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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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 <i>HELB</i> 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)
Collaboration Network
Top Collaborators
- 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
- 205 Targeting Homologous Repair to Overcome Genotoxic Therapy Resistance in Pancreatic Cancer
- Abstract PR011: Novel role of glycogen synthase kinase-3β in determining cancer cell response to PARPi through regulation of 53BP1 function
- Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB
Showing 5 of 6 shared publications
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Supplementary Figure S1 from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- Data from Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma
- 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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