ArticleCell death & disease2012
Selective modulation of subtype III IP₃R by Akt regulates ER Ca²⁺ release and apoptosis.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.
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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
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.
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Who cites it
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.
- MAM kinases: physiological roles, related diseases, and therapeutic perspectives-a systematic review.Cellular & molecular biology letters · 2025Pooled it
- A PRK-armed oncolytic adenovirus drives calreticulin exposure for dendritic cell licensing to prime antitumor CD8⁺ T cells and synergizes with anti-PD-1 or CAR-T therapy in colorectal cancer.Journal of gastroenterology · 2026Article
- Metabolic Kinases as Regulators of Inter-Organelle Communication in Aging and Age-Related Diseases.Aging cell · 2026Review
- Mitochondria-ER crosstalk via MAMS: Bridging cellular homeostasis and cancer progression.Apoptosis : an international journal on programmed cell death · 2026Review
- USP1-TRAF2 axis-regulated mortalin stability mediates chemoresistance by disrupting calcium transport in peripheral T-cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanisms underlying the estradiol mediated protection of yak oviduct epithelial cells against ER-CaBMC genomics · 2025Article
- Endoplasmic reticulum-mitochondria crosstalk: new mechanisms in the development of atherosclerosis.Frontiers in endocrinology · 2025Review
- Thermodynamic Considerations on the Biophysical Interaction between Low-Energy Electromagnetic Fields and Biosystems.Membranes · 2024Article
- IPAntioxidants (Basel, Switzerland) · 2024Article
- Genome-wide kinase-MAM interactome screening reveals the role of CK2A1 in MAM CaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Phosphoinositides and intracellular calcium signaling: novel insights into phosphoinositides and calcium coupling as negative regulators of cellular signaling.Experimental & molecular medicine · 2023Review
- Endoplasmic reticulum homeostasis: a potential target for diabetic nephropathy.Frontiers in endocrinology · 2023Review
- Inositol 1,4,5-trisphosphate receptors in cardiomyocyte physiology and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Article
- Sodium para-aminosalicylic acid ameliorates lead-induced hippocampal neuronal apoptosis by suppressing the activation of the IPEcotoxicology and environmental safety · 2022Article
- TRPC3 shapes the ER-mitochondria CaNature communications · 2022Article
- Put in a "CaCells · 2022Review
- Mitochondria inter-organelle relationships in cancer protein aggregation.Frontiers in cell and developmental biology · 2022Review
- Aberrant calcium signalling downstream of mutations in TP53 and the PI3K/AKT pathway genes promotes disease progression and therapy resistance in triple negative breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2022Review
- Calcium Signaling Is Impaired in PTEN-Deficient T Cell Acute Lymphoblastic Leukemia.Frontiers in immunology · 2022Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Ca²⁺ transfer from endoplasmic reticulum (ER) to mitochondria can trigger apoptotic pathways by inducing release of mitochondrial pro-apoptotic factors. Three different types of inositol 1,4,5-trisphosphate receptor (IP₃R) serve to discharge Ca²⁺ from ER, but possess some peculiarities, especially in apoptosis induction. The anti-apoptotic protein Akt can phosphorylate all IP₃R isoforms and protect cells from apoptosis, reducing ER Ca²⁺ release. However, it has not been elucidated which IP₃R subtypes mediate these effects. Here, we show that Akt activation in COS7 cells, which lack of IP₃R I, strongly suppresses IP₃-mediated Ca²⁺ release and apoptosis. Conversely, in SH-SY 5Y cells, which are type III-deficient, Akt is unable to modulate ER Ca²⁺ flux, losing its anti-apoptotic activity. In SH-SY 5Y-expressing subtype III, Akt recovers its protective function on cell death, by reduction of Ca²⁺ release. Moreover, regulating Ca²⁺ flux to mitochondria, Akt maintains the mitochondrial integrity and delays the trigger of apoptosis, in a type III-dependent mechanism. These results demonstrate a specific activity of Akt on IP₃R III, leading to diminished Ca²⁺ transfer to mitochondria and protection from apoptosis, suggesting an additional level of cell death regulation mediated by Akt.
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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.