ArticleJournal of molecular neuroscience : MN2001
Roles of BCL-2 and caspase 3 in the adenosine A3 receptor-induced apoptosis.
Article in Journal of molecular neuroscience : MN, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 43 citations in OpenAlex.
- Targeting the A3 adenosine receptor to treat hepatocellular carcinoma: anti-cancer and hepatoprotective effects.Purinergic signalling · 2023Review
- Antitumoral Action of Resveratrol Through Adenosinergic Signaling in C6 Glioma Cells.Frontiers in neuroscience · 2021Article
- Modulation of Adenosine Receptors and Antioxidative Effect of Beer Extracts in in Vitro Models.Nutrients · 2019Article
- Effects of synthetic A3 adenosine receptor agonists on cell proliferation and viability are receptor independent at micromolar concentrations.Journal of physiology and biochemistry · 2013Article
- Adenosine induces cell cycle arrest and apoptosis via cyclinD1/Cdk4 and Bcl-2/Bax pathways in human ovarian cancer cell line OVCAR-3.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- Molecular mechanisms of A3 adenosine receptor-induced G1 cell cycle arrest and apoptosis in androgen-dependent and independent prostate cancer cell lines: involvement of intrinsic pathway.Journal of cancer research and clinical oncology · 2011Article
- Impact of disrupting adenosine A₃ receptors (A₃⁻/⁻ AR) on colonic motility or progression of colitis in the mouse.Inflammatory bowel diseases · 2011Article
- Investigational A₃ adenosine receptor targeting agents.Expert opinion on investigational drugs · 2011Review
- RNAi-mediated CD73 suppression induces apoptosis and cell-cycle arrest in human breast cancer cells.Cancer science · 2010Article
- Purinoceptors on neuroglia.Molecular neurobiology · 2009Review
- The Anti-Cancer Effect of AImmunology, endocrine & metabolic agents in medicinal chemistry · 2007Article
- Modulation of the Akt/Ras/Raf/MEK/ERK pathway by A₃ adenosine receptor.Purinergic signalling · 2006Article
- Overexpression of von Hippel-Lindau tumor suppressor protein and antisense HIF-1alpha eradicates gliomas.Cancer gene therapy · 2006Article
- Adenosine and deoxyadenosine induces apoptosis in oestrogen receptor-positive and -negative human breast cancer cells via the intrinsic pathway.Cell proliferation · 2005Article
- Adenosine receptor signaling in the brain immune system.Trends in pharmacological sciences · 2005Review
- Behavioral characterization of mice lacking the A3 adenosine receptor: sensitivity to hypoxic neurodegeneration.Cellular and molecular neurobiology · 2003Article
- A3 adenosine receptors in human astrocytoma cells: agonist-mediated desensitization, internalization, and down-regulation.Molecular pharmacology · 2002Article
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 3 institutions in 2 countries.
Funding
Abstract
Selective A3 adenosine receptor agonists have been shown to induce apoptosis in a variety of cell types. In this study we examined the effects of adenosine receptor agonists selective for A1, A2A, or A3 receptors on the induction of apoptosis in primary cultures of rat astrocytes and in C6 glial cells. Treatment of the cells with the A3 receptor agonist Cl-IB-MECA (10 microM) induced apoptosis in both cell types. The effects of Cl-IB-MECA were partially antagonized by the A3 receptor-selective antagonist MRS 1191. In contrast, the A1 and A2A receptor agonists, CPA and CGS 21680, respectively, did not have significant effects on apoptosis in these cells. Cl-IB-MECA reduced the expression of endogenous Bcl-2, whereas it did not affect the expression of Bax. Overexpression of Bcl-2 in C6 cells abrogated the induction of apoptosis induced by the A3 agonist. Cl-IB-MECA also induced an increase in caspase 3 activity and caspase inhibitors decreased the apoptosis induced by the A3 agonist. These findings suggest that intense activation of the A3 receptor is pro-apoptotic in glial cells via bcl2 and caspase-3 dependent pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.