ArticleCurrent biology : CB2012
A novel role for Bcl-2 in regulation of cellular calcium extrusion.
Article in Current biology : CB, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 45 citations in OpenAlex.
- BCL2 inhibition in acute and chronic pancreatitis - is there a therapeutic perspective?Cell death discovery · 2026Review
- Repurposing BCL2 inhibitors: Venetoclax protects against acinar cell necrosis in acute pancreatitis by promoting apoptosis.Cell death & disease · 2025Article
- The Impact of Calcium Overload on Cellular Processes: Exploring Calcicoptosis and Its Therapeutic Potential in Cancer.International journal of molecular sciences · 2024Review
- The role of CaCell calcium · 2023Review
- Driver Mutations of Pancreatic Cancer Affect CaFunction (Oxford, England) · 2023Article
- Activation of pancreatic stellate cells attenuates intracellular CaCell death & disease · 2022Article
- Astrocytes respond to a neurotoxic Aβ fragment with state-dependent CaActa neuropathologica communications · 2021Article
- Targeting the Calcium Signalling Machinery in Cancer.Cancers · 2020Review
- Primary Active CaCold Spring Harbor perspectives in biology · 2020Review
- ABT-199 (Venetoclax), a BH3-mimetic Bcl-2 inhibitor, does not cause CaBritish journal of pharmacology · 2019Article
- Research Progress on the Relationship Between Acute Pancreatitis and Calcium Overload in Acinar Cells.Digestive diseases and sciences · 2019Review
- Reduced SERCA activity underlies dysregulation of CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Metabolic regulation of the PMCA: Role in cell death and survival.Cell calcium · 2018Review
- BH4 domain peptides derived from Bcl-2/Bcl-XL as novel tools against acute pancreatitis.Cell death discovery · 2018Article
- Ryanodine Receptors in Autophagy: Implications for Neurodegenerative Diseases?Frontiers in cellular neuroscience · 2018Review
- On BH3 Mimetics and CaDrug development research · 2017Article
- Non-apoptotic functions of BCL-2 family proteins.Cell death and differentiation · 2017Review
- BH3 mimetic-elicited CaCell death & disease · 2017Article
- Protein Lipidation As a Regulator of Apoptotic Calcium Release: Relevance to Cancer.Frontiers in oncology · 2017Review
- Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The antiapoptotic protein Bcl-2 plays important roles in Ca(2+) signaling by influencing inositol triphosphate receptors and regulating Ca(2+)-induced Ca(2+) release. Here we investigated whether Bcl-2 affects Ca(2+) extrusion in pancreatic acinar cells. We specifically blocked the Ca(2+) pumps in the endoplasmic reticulum and assessed the rate at which the cells reduced an elevated cytosolic Ca(2+) concentration after a period of enhanced Ca(2+) entry. Because external Ca(2+) was removed and endoplasmic reticulum Ca(2+) pumps were blocked, Ca(2+) extrusion was the only process responsible for recovery. Cells lacking Bcl-2 restored the basal cytosolic Ca(2+) level much faster than control cells. The enhanced Ca(2+) extrusion in cells from Bcl-2 knockout (Bcl-2 KO) mice was not due to increased Na(+)/Ca(2+) exchange activity, because removal of external Na(+) did not influence the Ca(2+) extrusion rate. Overexpression of Bcl-2 in the pancreatic acinar cell line AR42J decreased Ca(2+) extrusion, whereas silencing Bcl-2 expression (siRNA) had the opposite effect. Loss of Bcl-2, while increasing Ca(2+) extrusion, dramatically decreased necrosis and promoted apoptosis induced by oxidative stress, whereas specific inhibition of Ca(2+) pumps in the plasma membrane (PMCA) with caloxin 3A1 reduced Ca(2+) extrusion and increased necrosis. Bcl-2 regulates PMCA function in pancreatic acinar cells and thereby influences cell fate.
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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.