Kirk L. West

Post Doctoral Fellow

UAMS

Also affiliated: Arkansas Children's Hospital (2016–2017); University of Arkansas Medical Center (2015); Winthrop Rockefeller Foundation (2024–2025); Arkansas Department of Agriculture (2015)

Postdoc Researcher

9 h-index 28 pubs 351 cited

Research Areas

Biomedical Subjects

Links

ORCID Research Group

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: 351

Selected Publications

Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB (2025)

NAR Molecular Medicine DOI OpenAlex
Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction (2024)

Nucleic Acids Research 1 citation DOI OpenAlex
Nuclear F-actin assembly on damaged chromatin is regulated by DYRK1A and Spir1 phosphorylation (2024)

Nucleic Acids Research 7 citations DOI OpenAlex
Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction (2024)

bioRxiv (Cold Spring Harbor Laboratory) 1 citation DOI OpenAlex
Rare SNP in the <i>HELB</i> gene interferes with RPA interaction and cellular function of HELB (2024)

bioRxiv (Cold Spring Harbor Laboratory) DOI OpenAlex
Abstract PR011: Novel role of glycogen synthase kinase-3β in determining cancer cell response to PARPi through regulation of 53BP1 function (2024)

Cancer Research DOI OpenAlex
205 Targeting Homologous Repair to Overcome Genotoxic Therapy Resistance in Pancreatic Cancer (2022)

Journal of Clinical and Translational Science DOI OpenAlex
Screen identifies DYRK1B network as mediator of transcription repression on damaged chromatin (2020)

Proceedings of the National Academy of Sciences 45 citations DOI OpenAlex
Histone H2A variants alpha1-extension helix directs RNF168-mediated ubiquitination (2020)

Nature Communications 42 citations DOI OpenAlex
LC8/DYNLL1 is a 53BP1 effector and regulates checkpoint activation (2019)

Nucleic Acids Research 45 citations DOI OpenAlex
DEAD-box RNA helicases Dbp2, Ded1 and Mss116 bind to G-quadruplex nucleic acids and destabilize G-quadruplex RNA (2019)

Chemical Communications 39 citations DOI OpenAlex
Proteomic characterization of the arsenic response locus in S. cerevisiae (2019)

Epigenetics 8 citations DOI OpenAlex
Loss of E-Cadherin Inhibits CD103 Antitumor Activity and Reduces Checkpoint Blockade Responsiveness in Melanoma (2019)

Cancer Research 60 citations DOI OpenAlex
Framework for reanalysis of publicly available Affymetrix® GeneChip® data sets based on functional regions of interest (2017)

BMC Genomics 4 citations DOI OpenAlex
Trichloroethylene-induced alterations in DNA methylation were enriched in polycomb protein binding sites in effector/memory CD4+ T cells (2017)

Current Zoology 17 citations DOI OpenAlex