ArticleThe EMBO journal2001
The death substrate Gas2 binds m-calpain and increases susceptibility to p53-dependent apoptosis.
Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
The trial behind it
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Who cites it
36 citing papers in PubMed, 112 citations in OpenAlex.
- Myogenic IGFBP5 levels in rhabdomyosarcoma are nourished by mesenchymal stromal cells and regulate growth arrest and apoptosis.Cell communication and signaling : CCS · 2025Article
- Insights into Structure and Function of Growth Arrest Specific 2 (GAS2).Journal of Cancer · 2025Review
- A novel variant in GAS2 is associated with autosomal dominant nonsyndromic hearing impairment in a Chinese family.Human genomics · 2024Article
- Changes in calpain-2 expression during glioblastoma progression predisposes tumor cells to temozolomide resistance by minimizing DNA damage and p53-dependent apoptosis.Cancer cell international · 2023Article
- Growth arrest-specific protein 2 (GAS2) interacts with CXCR4 to promote T-cell leukemogenesis partially via c-MYC.Molecular oncology · 2022Article
- Growth arrest-specific 2 protein family: Structure and function.Cell proliferation · 2021Review
- Array-based Western-blotting reveals spatial differences in hepatic signaling and metabolism following CAR activation.Archives of toxicology · 2020Article
- GAS2 Promotes Cell Proliferation and Invasion and Suppresses Apoptosis in Pediatric T-Cell Acute Lymphoblastic Leukemia and Activates Wnt/β-Catenin Pathway.OncoTargets and therapy · 2020Article
- Growth arrest-specific gene 2 suppresses hepatocarcinogenesis by intervention of cell cycle and p53-dependent apoptosis.World journal of gastroenterology · 2019Article
- CRTH2 promotes endoplasmic reticulum stress-induced cardiomyocyte apoptosis through m-calpain.EMBO molecular medicine · 2018Article
- Global gene expression profiles of hematopoietic stem and progenitor cells from patients with chronic myeloid leukemia: the effect of in vitro culture with or without imatinib.Cancer medicine · 2017Article
- Review
- Article
- Growth arrest specific gene 2 in tilapia (Oreochromis niloticus): molecular characterization and functional analysis under low-temperature stress.BMC molecular biology · 2017Article
- Bcr-abl regulates Stat5 through Shp2, the interferon consensus sequence binding protein (Icsbp/Irf8), growth arrest specific 2 (Gas2) and calpain.Oncotarget · 2016Article
- Growth arrest specific 2 is up-regulated in chronic myeloid leukemia cells and required for their growth.PloS one · 2014Article
- Hypoxia-triggered m-calpain activation evokes endoplasmic reticulum stress and neuropathogenesis in a transgenic mouse model of Alzheimer's disease.CNS neuroscience & therapeutics · 2013Article
- Article
- Serum and antibodies of glaucoma patients lead to changes in the proteome, especially cell regulatory proteins, in retinal cells.PloS one · 2012Article
- The global transcriptional response of isolated human islets of langerhans to glucagon-like Peptide-1 receptor agonist liraglutide.ISRN endocrinology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gas2 is a caspase-3 substrate that plays a role in regulating microfilament and cell shape changes during apoptosis. Here we provide evidence that overexpression of Gas2 efficiently increases cell susceptibility to apoptosis following UV irradiation, etoposide and methyl methanesulfonate treatments, and that these effects are dependent on increased p53 stability and transcription activity. To investigate possible pathways linking Gas2 to p53, a yeast two-hybrid screen swas performed, indicating m-calpain as a strong Gas2- interacting protein. Moreover, we demonstrate that Gas2 physically interacts with m-calpain in vivo and that recombinant Gas2 inhibits calpain-dependent processing of p53. Importantly, the Gas2 dominant-negative form (Gas2171-314) that binds calpain but is unable to inhibit its activity abrogates Gas2's ability to stabilize p53, to enhance p53 transcriptional activity and to induce p53-dependent apoptosis. Finally, we show that Gas2 is able to regulate the levels of p53 independently of Mdm2 status, suggesting that, like calpastatin, it may enhance p53 stability by inhibiting calpain activity.
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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.