ReviewCell calcium2015
Ca²⁺ microdomains organized by junctophilins.
Review in Cell calcium, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 90 citations in OpenAlex.
- JP2 and JCN Crosstalk Abrogate MURF1-Mediated JCN Ubiquitination and Degradation in Cardiomyocytes.JACC. Basic to translational science · 2026Article
- Mechanistic Insights into Glucocorticoid-Induced Ocular Hypertension Using Differences in Mouse Strain Responsiveness.The American journal of pathology · 2026Article
- S165F mutation-induced Junctophilin-2 autoinhibition impairs CaCommunications biology · 2025Article
- Stabilizing the retromer complex rescues synaptic dysfunction and endosomal trafficking deficits in an Alzheimer's disease mouse model.Acta neuropathologica communications · 2025Article
- Junctophilin-2 Regulates Store-Operated Calcium Entry to Drive Cardiac Fibroblast Activation, Fibrotic Repair, and Angiogenesis After Myocardial Infarction.Circulation · 2025Article
- Tmem45b modulates itch via endoplasmic reticulum calcium regulation.Frontiers in physiology · 2025Article
- Electrophysical cardiac remodeling at the molecular level: Insights into ryanodine receptor activation and calcium-induced calcium release from a stochastic explicit-particle model.Biophysical journal · 2024Article
- Structure, Function, and Regulation of the Junctophilin Family.Annual review of physiology · 2024Review
- Huntington disease-like 2: insight into neurodegeneration from an African disease.Nature reviews. Neurology · 2024Review
- CaPhysiological reviews · 2024Review
- Speg interactions that regulate the stability of excitation-contraction coupling protein complexes in triads and dyads.Communications biology · 2023Article
- Article
- Searching for Mechanisms Underlying the Assembly of Calcium Entry Units: The Role of Temperature and pH.International journal of molecular sciences · 2023Article
- ER-PM Junctions on GABAergic Interneurons Are Organized by Neuregulin 2/VAP Interactions and Regulated by NMDA Receptors.International journal of molecular sciences · 2023Article
- Article
- NMR resonance assignments of the DNA binding domain of mouse Junctophilin-2.Biomolecular NMR assignments · 2022Article
- Junctophilins 1, 2, and 3 all support voltage-induced Ca2+ release despite considerable divergence.The Journal of general physiology · 2022Article
- The role of junctophilin proteins in cellular function.Physiological reviews · 2022Review
- The Sarcoplasmic Reticulum of Skeletal Muscle Cells: A Labyrinth of Membrane Contact Sites.Biomolecules · 2022Review
- Calpain-2 specifically cleaves Junctophilin-2 at the same site as Calpain-1 but with less efficacy.The Biochemical journal · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Excitable cells typically possess junctional membrane complexes (JMCs) constructed by the plasma membrane and the endo/sarcoplasmic reticulum (ER/SR) for channel crosstalk. These JMCs are termed triads in skeletal muscle, dyads in cardiac muscle, peripheral couplings in smooth and developing striated muscles, and subsurface cisterns in neurons. Junctophilin subtypes contribute to the formation and maintenance of JMCs by serving as a physical bridge between the plasma membrane and ER/SR membrane in different cell types. In muscle cells, junctophilin deficiency prevents JMC formation and functional crosstalk between cell-surface Ca(2+) channels and ER/SR Ca(2+) release channels. Human genetic mutations in junctophilin subtypes are linked to congenital hypertrophic cardiomyopathy and neurodegenerative diseases. Furthermore, growing evidence suggests that dysregulation of junctophilins induces pathological alterations in skeletal and cardiac muscle.
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.