ArticleBiochemical pharmacology2008
Modulation of intracellular Ca2+ signalling in HeLa cells by the apoptotic cell death enhancer PK11195.
Article in Biochemical pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 23 citations in OpenAlex.
- Tanycytic TSPO inhibition induces lipophagy to regulate lipid metabolism and improve energy balance.Autophagy · 2020Article
- Article
- VDAC1 and the TSPO: Expression, Interactions, and Associated Functions in Health and Disease States.International journal of molecular sciences · 2019Review
- A role for TSPO in mitochondrial CaCell death & disease · 2017Article
- Translocator Protein (TSPO) Affects Mitochondrial Fatty Acid Oxidation in Steroidogenic Cells.Endocrinology · 2016Article
- Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress.Integrative medicine research · 2015Article
- Molecular mechanisms of cell death: central implication of ATP synthase in mitochondrial permeability transition.Oncogene · 2015Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
1-(2-Chlorophenyl-N-methylpropyl)-3-isoquinolinecarboxamide (PK11195) is a proven enhancer of apoptotic cell death in a variety of cellular models. This effect is independent of its established cellular target, the mitochondrial benzodiazepine receptor (mBzR), since it is able to promote cell death also in mBzR knockout cells. Thus recently it was suggested that PK11195 might exert its effect by modulating the expression and function of the oncogene Bcl-2. We have previously demonstrated that Bcl-2 modulates cellular Ca2+ homeostasis as its overexpression reduces the Ca2+ concentration in the endoplasmic reticulum (ER) ([Ca2+](er)), impairing mitochondrial and cytosolic Ca2+ overload during cellular stress and therefore inhibiting the induction of the apoptotic cascade. Here, using ER, mitochondria and cytosolic targeted aequorin probes, we show that cellular treatment with PK11195 induces opposite changes in cellular Ca2+ homeostasis, increasing the [Ca2+](er) and amplifying IP(3) induced Ca2+ transients in mitochondria ([Ca2+](m)) and cytosol ([Ca2+](c)). This work provides evidence for a novel pharmacological effect of PK11195 on Ca2+ signalling which may be linked to its effect on Bcl-2 and account for its role in apoptotic cell death.
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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.