Lilian Kabeche
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Lilian Kabeche has a total of 96 co-authors. Here are the top co-authors by number of shared publications:
- Chatchai Phoomak
Department of Biology, Faculty of Science, Chulalongkorn University
20 shared publications - Hannah Lea
Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut
20 shared publications - Hojin Lee
Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut
20 shared publications - Joseph N. Contessa
Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06510, USA; Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA
20 shared publications - Marta Baro
Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut
20 shared publications - Megan C. King
Yale School of Medicine
20 shared publications
Latest Publications
- Open Access
- 11 November 2026
- Published by Springer Nature in Nature Communications
ATR promotes genome instability via CENP-A eviction from centromeres after prolonged exposure to genotoxic stress
- 11 November 2026
- Published by Springer Nature in Nature Communications
Open AccessATR promotes genome instability via CENP-A eviction from centromeres after prolonged exposure to genotoxic stress
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S9 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 9: Inhibition of Wee1 is insufficient to abrogate JAK1 KO cell cycle changes despite sufficient dephosphorylation of CDK1 at Y15 and T14.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S9 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 9: Inhibition of Wee1 is insufficient to abrogate JAK1 KO cell cycle changes despite sufficient dephosphorylation of CDK1 at Y15 and T14.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Movie SM3 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplementary Movie SM3 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Movie SM3 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplementary Movie SM3 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S11 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 11: Combination of radiation and sovilnesib treatment increases phos-Ser10 Histone 3 staining in Detroit562 JAK1 KO tumor samples.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S11 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 11: Combination of radiation and sovilnesib treatment increases phos-Ser10 Histone 3 staining in Detroit562 JAK1 KO tumor samples.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S8 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 8: Hyperactivation of DNA damage signaling is unlikely to be responsible for JAK1 KO cell cycle phenotypes.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S8 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 8: Hyperactivation of DNA damage signaling is unlikely to be responsible for JAK1 KO cell cycle phenotypes.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S3 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 3: JAK1 KO clonogenic survival following treatment with DNA damaging agents in Cal27 control and JAK1 KO cells.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S3 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 3: JAK1 KO clonogenic survival following treatment with DNA damaging agents in Cal27 control and JAK1 KO cells.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S1 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 1. Sequencing of human kinome CRISPR KO library cloned into lentiGuide-Puro.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S1 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 1. Sequencing of human kinome CRISPR KO library cloned into lentiGuide-Puro.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S7 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 7: The canonical CDK1-dependent checkpoint is not responsible for JAK1 KO cell cycle phenotypes.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S7 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 7: The canonical CDK1-dependent checkpoint is not responsible for JAK1 KO cell cycle phenotypes.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Figure S5 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 5: Presence of 8N tetraploid cells and distribution of EdU-labeled population 8 hours following radiation or sham treatment.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessFigure S5 from Loss of JAK1 Function Causes G2–M Cell-Cycle Defects Vulnerable to KIF18A Inhibition
Supplemental Figure 5: Presence of 8N tetraploid cells and distribution of EdU-labeled population 8 hours following radiation or sham treatment.