ArticleNature communications2025
PIM2 inhibition promotes MCL1 dependency in plasma cells involving integrated stress response-driven NOXA expression.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Machine learning-driven identification of PIM2 kinase inhibitors through QSAR modeling and molecular dynamics simulations.Journal, genetic engineering & biotechnology · 2026Article
- In Silico Isomerization Produces Apt Negative Data for VHTS Validation.Journal of chemical information and modeling · 2026Article
- Recent Advances in Nanozymes Toward Diabetic Foot Ulcers.International journal of nanomedicine · 2026Review
- Knockdown of Gene Expression Following Activation of the NMD Pathway Using Splice-Switching Oligonucleotides.Methods in molecular biology (Clifton, N.J.) · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
Our study explores the complex dynamics of the integrated stress response (ISR) axis, highlighting PIM2 kinase's critical role and its interaction with the BCL2 protein family, uncovering key mechanisms of cell survival and tumor progression. Elevated PIM2 expression, a marker of various cancers, often correlates with disease aggressiveness. Using a model of normal and malignant plasma cells, we show that inhibiting PIM2 kinase inhibits phosphorylated BAD production and activates ISR-mediated NOXA expression. This shift towards MCL1 dependence underscores the synergy achieved through combined PIM/MCL1 inhibition, driven largely by ISR-mediated NOXA expression. In mouse xenograft models, dual targeting of PIM2 and MCL1 effectively controls tumor growth-a response reversed by ISR-specific inhibition and upregulation of genes linked to tumor cell dissemination. This work elucidates the molecular intricacies of PIM2 inhibition and its implications for cancer therapy, especially in tumors with elevated PIM2 expression.
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