ArticleScience advances2022
Early SRC activation skews cell fate from apoptosis to senescence.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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
45 citing papers in PubMed, 64 citations in OpenAlex.
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- Expanding Synthetic Lethality in DNA Damage Response-Defective Cancers Through Stress Phenotype-Guided Kinase Targeting.International journal of molecular sciences · 2026Review
- The aging extracellular matrix as a missing link in senescent cell accumulation and persistence.Nature aging · 2026Article
- SenCat: Cataloging human cell senescence through multi-omic profiling of multiple senescent primary cell types.Molecular cell · 2026Article
- Computational Phosphosite-Specific Network Analysis of YES1 Y426 Reveals Cancer-Associated Phosphorylation Patterns.Proteomes · 2026Article
- Pseudo-senescence induced by palbociclib does not sensitise pleural mesothelioma cells to combinations with senolytics.Cell death & disease · 2026Article
- Discovery of potent kinase inhibitors with improved pharmacokinetics and safety potentials through structural optimization of dasatinib.Communications medicine · 2026Article
- DNA damage drives a unique, Alzheimer's disease-relevant senescent state in neurons.bioRxiv : the preprint server for biology · 2026Article
- Tryptophan metabolites 3-hydroxykynurenine (3HK) and 3-hydroxyanthranilic acid (3HAA) increase oxidative stress and impair osteoblastic bone formation.The Journal of biological chemistry · 2026Article
- Article
- SenCat: Cataloging human cell senescence through multiomic profiling of multiple senescent primary cell types.bioRxiv : the preprint server for biology · 2026Article
- Network pharmacology and molecular docking to explore the potential mechanism of Codonopsis pilosula delaying aging.Medicine · 2025Article
- A 'Spicy' Mechanotransduction Switch: Capsaicin-Activated TRPV1 Receptor Modulates Osteosarcoma Cell Behavior and Drug Sensitivity.International journal of molecular sciences · 2025Article
- Imbalanced chromatin distribution in cellular senescence specifies paraspeckle dynamics.Genome biology · 2025Article
- Lactate-Activated GPR132-Src Signal Induces Macrophage Senescence and Aggravates Atherosclerosis Under Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Network pharmacology and molecular docking to elucidate the mechanism of antiaging of Platycodon grandiflorus.Medicine · 2025Article
- Terpenes: natural compounds found in plants as potential senotherapeutics targeting senescent mesenchymal stromal cells and promoting apoptosis.Stem cell research & therapy · 2025Article
- Osalmid sensitizes clear cell renal cell carcinoma to navitoclax through a STAT3/BCL-XL pathway.Cancer letters · 2025Article
- Investigating the aging-modulatory mechanism of Rasayana Churna, an Ayurvedic herbal formulation, using a computational approach.Biogerontology · 2025Article
- Screening potential antileukemia ingredients from sweet potato: integration of metabolomics analysis, network pharmacology, and experimental validation.Frontiers in nutrition · 2025Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Cells responding to DNA damage implement complex adaptive programs that often culminate in one of two distinct outcomes: apoptosis or senescence. To systematically identify factors driving each response, we analyzed human IMR-90 fibroblasts exposed to increasing doses of the genotoxin etoposide and identified SRC as a key kinase contributing early to this dichotomous decision. SRC was activated by low but not high levels of etoposide. With low DNA damage, SRC-mediated activation of p38 critically promoted expression of cell survival and senescence proteins, while SRC-mediated repression of p53 prevented a rise in proapoptotic proteins. With high DNA damage, failure to activate SRC led to elevation of p53, inhibition of p38, and apoptosis. In mice exposed to DNA damage, pharmacologic inhibition of SRC prevented the accumulation of senescent cells in tissues. We propose that inhibiting SRC could be exploited to favor apoptosis over senescence in tissues to improve health outcomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.