Arminja N. Kettenbach

Dartmouth College — United States

Biochemistry, Genetics and Molecular Biology · Life Sciences

38h-index6.2kcitations184works2.12yr avg

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Research Topics

Microtubule and mitosis dynamics(36), Cancer, Hypoxia, and Metabolism(27), Ubiquitin and proteasome pathways(26), Advanced Proteomics Techniques and Applications(18), Cellular transport and secretion(18)

Publications184 total

The clinical missense variant E282K in PPP3CA/calcineurin shifts substrate dephosphorylation by altering active site recruitment

Nature Communications·2026Open Access

Suppression of haptoglobin and loss of striatal neurons in mice chronically exposed to chlorpyrifos contaminated drinking water

Toxicological Sciences·2026

BPS2026 – The clinical missense variant E282K in PPP3CA/calcineurin shifts substrate dephosphorylation profiles by altering active site recruitment

Biophysical Journal·2026

MassIVE MSV000100567 - Characterization of Protein Phosphatase 1b substrate specificity

2026Open Access

Local Growth Hormone Facilitates Aging of the Colon Epithelial Microenvironment

Aging Cell·2025Open Access

Endocrine therapy induces oxidative stress in ER+ breast cancer that sensitizes persister cells to ferroptosis

2025Open Access

Interaction of IRS2 with PLK1 protects cells from mitotic stress

2025Open Access

The TRIP12 E3 ligase induces SWI/SNF component BRG1-β-catenin interaction to promote Wnt signaling

Nature Communications·2025Open Access

Spindle morphology changes between meiosis and mitosis driven by CK2 regulation of the Ran pathway

2 cited

The Journal of Cell Biology·2025· 2 cited

Quantitative proteomics analysis of triple-negative breast cancers

2 cited

npj Precision Oncology·2025· 2 citedOpen Access

Reply to: “Comments on the paper ‘Extensive epigenomic dysregulation is a hallmark of homologous recombination deficiency in triple‐negative breast cancer’ by Y. Chen et al.”

International Journal of Cancer·2025Open Access

Supplementary Table 7 from Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

2025Open Access

Suppl. Figure 2 from Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

2025Open Access

Suppl. Figure 8 from Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

2025Open Access

Supplementary Table 1 from Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

2025Open Access

Data from Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

2025Open Access

Suppl. Figure 4 from Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

2025Open Access

Supplementary Data Figure Legends from Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

2025Open Access

Suppl. Figure 7 from Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

2025Open Access

Supplementary Table 10 from Oxidative Phosphorylation Is a Metabolic Vulnerability of Endocrine Therapy–Tolerant Persister Cells in ER+ Breast Cancer

2025Open Access

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Frequent Co-authors

Scott A. Gerber(18), Isha Nasa(10), Scott Rusin(9), Mark E. Adamo(8), Jakob Nilsson(5), Lauren Cressey(5), Wolfgang Peti(5), Rebecca Page(5), Jennifer Loros(4), Jay Dunlap(4), Thomas Kruse(4), James B. Moseley(4), Nicole P. Jenkins(4), Dimitriya H. Garvanska(3), Meng S. Choy(3), Scott P. Lyons(3), Annie Yang(2), Zhou Zhu(2), Frank McKeon(2), Brendan K. Faherty(2)