ArticleProceedings of the National Academy of Sciences of the United States of America2004
Agonist-induced Ca2+ entry determined by inositol 1,4,5-trisphosphate recognition.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 66 citations in OpenAlex.
- The perspective of modern transplant science - transplant arteriosclerosis: inspiration derived from mitochondria associated endoplasmic reticulum membrane dysfunction in arterial diseases.International journal of surgery (London, England) · 2025Review
- THRA1/PGC-1α/SIRT3 pathway regulates oxidative stress and is implicated in hypertension of maternal hypothyroid rat offspring.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Binding of the erlin1/2 complex to the third intralumenal loop of IPThe Journal of biological chemistry · 2022Article
- Mitochondrial Calcium: Effects of Its Imbalance in Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Decoding the Phosphatase Code: Regulation of Cell Proliferation by Calcineurin.International journal of molecular sciences · 2022Review
- Tumor suppressor p53 regulates intestinal type 2 immunity.Nature communications · 2021Article
- Cartilage oligomeric matrix protein promotes prostate cancer progression by enhancing invasion and disrupting intracellular calcium homeostasis.Oncotarget · 2017Article
- Agonist-activated Ca2+ influx occurs at stable plasma membrane and endoplasmic reticulum junctions.Journal of cell science · 2010Article
- Linking structure to function: Recent lessons from inositol 1,4,5-trisphosphate receptor mutagenesis.Cell calcium · 2010Review
- Ca(2+) channels on the move.Biochemistry · 2009Review
- FcepsilonRI-mediated mast cell migration: signaling pathways and dependence on cytosolic free Ca2+ concentration.Cellular signalling · 2009Article
- B-lymphocyte calcium influx.Immunological reviews · 2009Review
- Cross-linking of FcepsilonRI causes Ca2+ mobilization via a sphingosine kinase pathway in a clathrin-dependent manner.Cell calcium · 2009Article
- Studying isoform-specific inositol 1,4,5-trisphosphate receptor function and regulation.Methods (San Diego, Calif.) · 2008Article
- Regulation of single inositol 1,4,5-trisphosphate receptor channel activity by protein kinase A phosphorylation.The Journal of physiology · 2008Article
- IP3 constricts cerebral arteries via IP3 receptor-mediated TRPC3 channel activation and independently of sarcoplasmic reticulum Ca2+ release.Circulation research · 2008Article
- Role of the store-operated calcium entry proteins Stim1 and Orai1 in muscarinic cholinergic receptor-stimulated calcium oscillations in human embryonic kidney cells.The Journal of physiology · 2007Article
- Native TRPC7 channel activation by an inositol trisphosphate receptor-dependent mechanism.The Journal of biological chemistry · 2006Article
- Calcium-dependent activation of T-lymphocytes.Pflugers Archiv : European journal of physiology · 2005Review
- RACK1 binds to inositol 1,4,5-trisphosphate receptors and mediates Ca2+ release.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
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 2 institutions in 1 country.
Funding
Abstract
It has been considered that Ca2+ release is the causal trigger for Ca2+ entry after receptor activation. In DT40 B cells devoid of inositol 1,4,5-trisphosphate receptors (IP3R), the lack of Ca2+ entry in response to receptor activation is attributed to the absence of Ca2+ release. We reveal in this article that IP3R recognition of IP3 determines agonist-induced Ca2+ entry (ACE), independent of its Ca2+ release activity. In DT40 IP3R(-/-) cells, endogenous ACE can be rescued with type 1 IP3R mutants (both a DeltaC-terminal truncation mutant and a D2550A pore mutant), which are defective in Ca2+ release channel activity. Thus, in response to B cell receptor activation, ACE is restored in an IP3R-dependent manner without Ca2+ store release. Conversely, ACE cannot be rescued with mutant IP3Rs lacking IP3 binding (both the Delta90-110 and R265Q IP3-binding site mutants). We conclude that an IP3-dependent conformational change in the IP3R, not endoplasmic reticulum Ca2+ pool release, triggers ACE.
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.