The DOI matches its Crossref record.
Ca2+ microdomains organized by junctophilins
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Of Ryr2-associated regulators, only Jph4 showed a weak response to R55.
“Of Ryr2-associated regulators [38], only Jph4 showed a weak response to R55”
From Stabilizing the retromer complex rescues synaptic dysfunction and endosomal trafficking deficits in an Alzheimer’s disease mouse model (2025) · cites this paper as [38]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
No references could be resolved yet.
Research works printed but not linked: 86
- Porter, 1957, Studies on the endoplasmic reticulum. III. Its form and distribution in striated muscle cells, J. Biophys. Biochem. Cytol., 3, 269, 10.1083/jcb.3.2.269 · DOI
- Friedman, 2011, The ER in 3D: a multifunctional dynamic membrane network, Trends Cell Biol., 21, 709, 10.1016/j.tcb.2011.07.004 · DOI
- Rosenbluth, 1962, Subsurface cisterns and their relationship to the neuronal plasma membrane, J. Cell Biol., 13, 405, 10.1083/jcb.13.3.405 · DOI
- Franzini-Armstrong, 1997, Ryanodine receptors of striated muscles: a complex channel capable of multiple interactions, Physiol. Rev., 77, 699, 10.1152/physrev.1997.77.3.699 · DOI
- Bers, 2002, Cardiac excitation–contraction coupling, Nature, 415, 198, 10.1038/415198a · DOI
- Shen, 2011, Remodelling of the endoplasmic reticulum during store-operated calcium entry, Biol. Cell, 103, 365, 10.1042/BC20100152 · DOI
- Franzini-Armstrong, 2009, Architecture and regulation of the Ca2+ delivery system in muscle cells, Appl. Physiol. Nutr. Metab., 34, 323, 10.1139/H09-017 · DOI
- Hayashi, 2009, Three-dimensional electron microscopy reveals new details of membrane systems for Ca2+ signaling in the heart, J. Cell Sci., 122, 1005, 10.1242/jcs.028175 · DOI
- Soeller, 1999, Examination of the transverse tubular system in living cardiac rat myocytes by 2-photon microscopy and digital image-processing techniques, Circ. Res., 84, 266, 10.1161/01.RES.84.3.266 · DOI
- Wagner, 2012, Stimulated emission depletion live-cell super-resolution imaging shows proliferative remodeling of T-tubule membrane structures after myocardial infarction, Circ. Res., 111, 402, 10.1161/CIRCRESAHA.112.274530 · DOI
- Pinali, 2013, Three-dimensional reconstruction of cardiac sarcoplasmic reticulum reveals a continuous network linking transverse-tubules: this organization is perturbed in heart failure, Circ. Res., 113, 1219, 10.1161/CIRCRESAHA.113.301348 · DOI
- Huxley, 1958, Local activation of striated muscle fibres, J. Physiol., 144, 426, 10.1113/jphysiol.1958.sp006111 · DOI
- Ziman, 2010, Excitation–contraction coupling changes during postnatal cardiac development, J. Mol. Cell. Cardiol., 48, 379, 10.1016/j.yjmcc.2009.09.016 · DOI
- Di Maio, 2007, T-tubule formation in cardiacmyocytes: two possible mechanisms, J. Muscle Res. Cell Motil., 28, 231, 10.1007/s10974-007-9121-x · DOI
- Das, 2013, Adding a new dimension to cardiac nano-architecture using electron microscopy: coupling membrane excitation to calcium signaling, J. Mol. Cell. Cardiol., 58, 5, 10.1016/j.yjmcc.2012.11.009 · DOI
- Stern, 1992, Theory of excitation–contraction coupling in cardiac muscle, Biophys. J., 63, 497, 10.1016/S0006-3495(92)81615-6 · DOI
- Stern, 1997, Local control model of excitation–contraction coupling in skeletal muscle, J. Gen. Physiol., 110, 415, 10.1085/jgp.110.4.415 · DOI
- Fabiato, 1978, Calcium-induced release of calcium from the sarcoplasmic reticulum of skinned cells from adult human, dog, cat, rabbit, rat, and frog hearts and from fetal and new-born rat ventricles, Ann. N. Y. Acad. Sci., 307, 491, 10.1111/j.1749-6632.1978.tb41979.x · DOI
- Felder, 2002, Morphology and molecular composition of sarcoplasmic reticulum surface junctions in the absence of DHPR and RyR in mouse skeletal muscle, Biophys. J., 82, 3144, 10.1016/S0006-3495(02)75656-7 · DOI
- Paolini, 2007, Reorganized stores and impaired calcium handling in skeletal muscle of mice lacking calsequestrin-1, J. Physiol., 583, 767, 10.1113/jphysiol.2007.138024 · DOI
- Knollmann, 2006, Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia, J. Clin. Investig., 116, 2510
- Chopra, 2009, Ablation of triadin causes loss of cardiac Ca2+ release units, impaired excitation–contraction coupling, and cardiac arrhythmias, Proc. Natl. Acad. Sci. U. S. A., 106, 7636, 10.1073/pnas.0902919106 · DOI
- Shen, 2007, Triadins modulate intracellular Ca(2+) homeostasis but are not essential for excitation–contraction coupling in skeletal muscle, J. Biol. Chem., 282, 37864, 10.1074/jbc.M705702200 · DOI
- Wong, 2013, Nanoscale distribution of ryanodine receptors and caveolin-3 in mouse ventricular myocytes: dilation of T-tubules near junctions, Biophys. J., 104, L22, 10.1016/j.bpj.2013.02.059 · DOI
- Galbiati, 2001, Caveolin-3 null mice show a loss of caveolae, changes in the microdomain distribution of the dystrophin–glycoprotein complex, and T-tubule abnormalities, J. Biol. Chem., 276, 21425, 10.1074/jbc.M100828200 · DOI
- Woodman, 2002, Caveolin-3 knock-out mice develop a progressive cardiomyopathy and show hyperactivation of the p42/44 MAPK cascade, J. Biol. Chem., 277, 38988, 10.1074/jbc.M205511200 · DOI
- Prokic, 2014, Amphiphysin 2 (BIN1) in physiology and diseases, J. Mol. Med., 92, 453, 10.1007/s00109-014-1138-1 · DOI · Paper page
- Hong, 2012, BIN1 is reduced and Cav1.2 trafficking is impaired in human failing cardiomyocytes, Heart Rhythm, 9, 812, 10.1016/j.hrthm.2011.11.055 · DOI
- Lee, 2002, Amphiphysin 2 (Bin1) and T-tubule biogenesis in muscle, Science, 297, 1193, 10.1126/science.1071362 · DOI
- Hong, 2014, Cardiac BIN1 folds T-tubule membrane, controlling ion flux and limiting arrhythmia, Nat. Med., 20, 624, 10.1038/nm.3543 · DOI
- Takeshima, 1998, Mitsugumin29, a novel synaptophysin family member from the triad junction in skeletal muscle, Biochem. J., 331, 317, 10.1042/bj3310317 · DOI
- M. Nishi, S. Komazaki, N. Kurebayashi, Y. Ogawa, T. Noda, M. Iino, H. Takeshima, Abnormal features in skeletal muscle from mice lacking mitsugumin29, J. Cell Biol. 147 (1999), 1473-1480. · DOI
- Takeshima, 2000, Junctophilins: a novel family of junctional membrane complex proteins, Mol. Cell, 6, 11
- Nishi, 2003, Coexpression of junctophilin type 3 and type 4 in brain, Brain Res. Mol. Brain Res., 118, 102, 10.1016/S0169-328X(03)00341-3 · DOI
- S. Kakizawa, S. Moriguchi, A. Ikeda, M. Iino and H. Takeshima, Functional crosstalk between cell-surface and intracellular channels mediated by junctophilins essential for neuronal functions, Cerebellum7, 2008, 385–391. · DOI
- Bennett, 2013, Human junctophilin-2 undergoes a structural rearrangement upon binding PtdIns(3,4,5)P3 and the S101R mutation identified in hypertrophic cardiomyopathy obviates this response, Biochem. J., 456, 205, 10.1042/BJ20130591 · DOI
- Ma, 2006, MORN motifs in plant PIPKs are involved in the regulation of subcellular localization and phospholipid binding, Cell Res., 16, 466, 10.1038/sj.cr.7310058 · DOI
- Minamisawa, 2004, Junctophilin type 2 is associated with caveolin-3 and is down-regulated in the hypertrophic and dilated cardiomyopathies, Biochem. Biophys. Res. Commun., 325, 852, 10.1016/j.bbrc.2004.10.107 · DOI
- Golini, 2011, Junctophilin 1 and 2 proteins interact with the l-type Ca2+ channel dihydropyridine receptors (DHPRs) in skeletal muscle, J. Biol. Chem., 286, 43717, 10.1074/jbc.M111.292755 · DOI
- Phimister, 2007, Conformation-dependent stability of junctophilin 1 (JP1) and ryanodine receptor type 1 (RyR1) channel complex is mediated by their hyper-reactive thiols, J. Biol. Chem., 282, 8667, 10.1074/jbc.M609936200 · DOI
- Beavers, 2013, Mutation E169K in junctophilin-2 causes atrial fibrillation due to impaired RyR2 stabilization, J. Am. Coll. Cardiol., 62, 2010, 10.1016/j.jacc.2013.06.052 · DOI
- Chen, 2013, Critical roles of junctophilin-2 in T-tubule and excitation–contraction coupling maturation during postnatal development, Cardiovasc. Res., 100, 54, 10.1093/cvr/cvt180 · DOI
- Reynolds, 2013, Junctophilin-2 is necessary for T-tubule maturation during mouse heart development, Cardiovasc. Res., 100, 44, 10.1093/cvr/cvt133 · DOI
- Ito, 2001, Deficiency of triad junction and contraction in mutant skeletal muscle lacking junctophilin type 1, J. Cell Biol., 154, 1059, 10.1083/jcb.200105040 · DOI
- Komazaki, 2002, Deficiency of triad formation in developing skeletal muscle cells lacking junctophilin type 1, FEBS Lett., 524, 225, 10.1016/S0014-5793(02)03042-9 · DOI
- Komazaki, 2003, Abnormal junctional membrane structures in cardiac myocytes expressing ectopic junctophilin type 1, FEBS Lett., 542, 69, 10.1016/S0014-5793(03)00340-5 · DOI
- Moriguchi, 2006, Functional uncoupling between Ca2+ release and after hyperpolarization in mutant hippocampal neurons lacking junctophilins, Proc. Natl. Acad. Sci. U. S. A., 103, 10811, 10.1073/pnas.0509863103 · DOI
- S. Kakizawa, Y. Kishimoto, K. Hashimoto, T. Miyazaki, K. Furutani, H. Shimizu, M. Fukaya, M. Nishi, H. Sakagami, A. Ikeda, H. Kondo, M. Kano, M. Watanabe, M. Iino and H. Takeshima, Junctophilin-mediated channel crosstalk essential for cerebellar synaptic plasticity, EMBO J.26, 2007, 1924–1933. · DOI
- Moriguchi, 2014, Aberrant behavioral sensitization by methamphetamine in junctophilin-deficient mice, Mol. Neurobiol.
- Yamazaki, 2011, TRIC-A channels in vascular smooth muscle contribute to blood pressure maintenance, Cell Metab., 14, 231, 10.1016/j.cmet.2011.05.011 · DOI
- Fahrner, 2013, The STIM1/Orai signaling machinery, Channels, 7, 330, 10.4161/chan.26742 · DOI
- Hogan, 2010, Molecular basis of calcium signaling in lymphocytes: STIM and ORAI, Annu. Rev. Immunol., 28, 491, 10.1146/annurev.immunol.021908.132550 · DOI
- Uehara, 2002, Store-operated Ca2+ entry uncoupled with ryanodine receptor and junctional membrane complex in heart muscle cells, Cell Calcium, 31, 89, 10.1054/ceca.2001.0257 · DOI
- Hirata, 2006, Uncoupling store-operated Ca2+ entry and altered Ca2+ release from sarcoplasmic reticulum through silencing of junctophilin genes, Biophys. J., 90, 4418, 10.1529/biophysj.105.076570 · DOI
- Li, 2010, Impaired Orai1-mediated resting Ca2+ entry reduces the cytosolic [Ca2+] and sarcoplasmic reticulum Ca2+ loading in quiescent junctophilin 1 knock-out myotubes, J. Biol. Chem., 285, 39171, 10.1074/jbc.M110.149690 · DOI
- Pla-Martin, 2014, Junctophilin-1 is a modifier gene of GDAP1-related Charcot-Marie-Tooth disease, Hum. Mol. Genet.
- Zhang, 2013, Ultrastructural uncoupling between T-tubules and sarcoplasmic reticulum in human heart failure, Cardiovasc. Res., 98, 269, 10.1093/cvr/cvt030 · DOI
- Landstrom, 2011, Junctophilin-2 expression silencing causes cardiocyte hypertrophy and abnormal intracellular calcium-handling, Circ. Heart Fail, 4, 214, 10.1161/CIRCHEARTFAILURE.110.958694 · DOI
- Xu, 2007, Intermolecular failure of l-type Ca2+ channel and ryanodine receptor signaling in hypertrophy, PLoS Biol., 5, e21, 10.1371/journal.pbio.0050021 · DOI
- Wei, 2010, T-tubule remodeling during transition from hypertrophy to heart failure, Circ. Res., 107, 520, 10.1161/CIRCRESAHA.109.212324 · DOI
- Xu, 2012, Mir-24 regulates junctophilin-2 expression in cardiomyocytes, Circ. Res., 111, 837, 10.1161/CIRCRESAHA.112.277418 · DOI
- Chen, 2012, β-Adrenergic receptor antagonists ameliorate myocyte T-tubule remodeling following myocardial infarction, FASEB J., 26, 2531, 10.1096/fj.11-199505 · DOI
- Xie, 2012, Sildenafil prevents and reverses transverse-tubule remodeling and Ca(2+) handling dysfunction in right ventricle failure induced by pulmonary artery hypertension, Hypertension, 59, 355, 10.1161/HYPERTENSIONAHA.111.180968 · DOI
- Wu, 2014, Calpain-dependent cleavage of junctophilin-2 and T-tubule remodeling in a mouse model of reversible heart failure, J. Am. Heart Assoc., 3, e000527, 10.1161/JAHA.113.000527 · DOI
- Zhang, 2014, Microtubule-mediated defects in junctophilin-2 trafficking contribute to myocyte transverse-tubule remodeling and Ca2+ handling dysfunction in heart failure, Circulation, 129, 1742, 10.1161/CIRCULATIONAHA.113.008452 · DOI
- Wu, 2012, Ultrastructural remodelling of Ca(2+) signalling apparatus in failing heart cells, Cardiovasc. Res., 95, 430, 10.1093/cvr/cvs195 · DOI
- Han, 2013, Morphogenesis of T-tubules in heart cells: the role of junctophilin-2, Sci. China Life Sci., 56, 647, 10.1007/s11427-013-4490-4 · DOI
- Guo, 2013, Emerging mechanisms of T-tubule remodelling in heart failure, Cardiovasc. Res., 98, 204, 10.1093/cvr/cvt020 · DOI
- van Oort, 2011, Disrupted junctional membrane complexes and hyperactive ryanodine receptors after acute junctophilin knockdown in mice, Circulation, 123, 979, 10.1161/CIRCULATIONAHA.110.006437 · DOI
- Wu, 2011, PI3Ks maintain the structural integrity of T-tubules in cardiac myocytes, PLoS One, 6, e24404, 10.1371/journal.pone.0024404 · DOI
- Guo, 2014, Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress, Proc. Natl. Acad. Sci. U. S. A., 111, 12240, 10.1073/pnas.1412729111 · DOI
- Matsushita, 2007, Mutation of junctophilin type 2 associated with hypertrophic cardiomyopathy, J. Hum. Genet., 52, 543, 10.1007/s10038-007-0149-y · DOI
- Landstrom, 2007, Mutations in JPH2-encoded junctophilin-2 associated with hypertrophic cardiomyopathy in humans, J. Mol. Cell. Cardiol., 42, 1026, 10.1016/j.yjmcc.2007.04.006 · DOI
- Woo, 2010, S165F mutation of junctophilin 2 affects Ca2+ signalling in skeletal muscle, Biochem. J., 427, 125, 10.1042/BJ20091225 · DOI
- Woo, 2012, Hypertrophy in skeletal myotubes induced by junctophilin-2 mutant, Y141H, involves an increase in store-operated Ca2+ entry via Orai1, J. Biol. Chem., 287, 14336, 10.1074/jbc.M111.304808 · DOI
- van Rooij, 2006, A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure, Proc. Natl. Acad. Sci. U. S. A., 103, 18255, 10.1073/pnas.0608791103 · DOI
- Li, 2013, In vivo suppression of microRNA-24 prevents the transition toward decompensated hypertrophy in aortic-constricted mice, Circ. Res., 112, 601, 10.1161/CIRCRESAHA.112.300806 · DOI
- Zatz, 2005, Calpains and disease, N. Engl. J. Med., 352, 2413, 10.1056/NEJMra043361 · DOI
- Patterson, 2011, Tear me down: role of calpain in the development of cardiac ventricular hypertrophy, Circ. Res., 109, 453, 10.1161/CIRCRESAHA.110.239749 · DOI
- Murphy, 2013, Ca2+-dependent proteolysis of junctophilin-1 and junctophilin-2 in skeletal and cardiac muscle, J. Physiol., 591, 719, 10.1113/jphysiol.2012.243279 · DOI
- Cooper, 2006, Cytoskeletal networks and the regulation of cardiac contractility: microtubules, hypertrophy, and cardiac dysfunction, Am. J. Physiol. Heart Circ. Physiol., 291, H1003, 10.1152/ajpheart.00132.2006 · DOI
- Webster, 2002, Microtubules in cardiac toxicity and disease, Cardiovasc. Toxicol., 2, 75, 10.1385/CT:2:2:075 · DOI
- Holmes, 2001, A repeat expansion in the gene encoding junctophilin-3 is associated with Huntington disease-like 2, Nat. Genet., 29, 377, 10.1038/ng760 · DOI
- Govert, 2013, Huntington's disease and Huntington's disease-like syndromes: an overview, Curr. Opin. Neurol., 26, 420, 10.1097/WCO.0b013e3283632d90 · DOI
- Seixas, 2012, Loss of junctophilin-3 contributes to Huntington disease-like 2 pathogenesis, Ann. Neurol., 71, 245, 10.1002/ana.22598 · DOI
- Garbino, 2010, Emerging role of junctophilin-2 as a regulator of calcium handling in the heart, Acta Pharmacol. Sin., 31, 1019, 10.1038/aps.2010.116 · DOI
Cited by
Sorted by citations
Ramonet, D., Daerr, A., & Hallbeck, M. (2025) · Acta Neuropathologica Communications · doi:10.1186/s40478-025-02096-8 · Cited by 7
Metadata
- Authors
- Takeshima, H., Hoshijima, M., & Song, L.-S.
- Venue
- Cell Calcium
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 58
- Issue
- 4
- Pages
- 349-356
- ISSN
- 0143-4160
- PMC
- PMC5159448
- Cited by
- 85
- References
- 0
- Language
- en
- Licence
- Funders
- JSPS Core-to-Core Program
- Human Frontier Science Program (RGP0027/2013)
- MEXT Platform for Drug Discovery, Informatics and Structural Life Science
- US NIH (R01 HL090905)
- American Heart Association (0635056N, 0840013N)
- Takeda Science Foundation
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review