Affinage

CALM2

Calmodulin-2 · UniProt P0DP24

Round 2 corrected
Length
149 aa
Mass
16.8 kDa
Annotated
2026-04-28
52 papers in source corpus 13 papers cited in narrative 13 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CALM2 is one of three human genes (CALM1, CALM2, CALM3) encoding the identical calmodulin protein, a ubiquitous Ca²⁺ sensor that undergoes a conformational change upon Ca²⁺ binding to regulate diverse downstream targets including ion channels and kinases (PMID:9278050). In the human heart, CALM2 contributes approximately 44% of total calmodulin mRNA and translated protein, making it a dominant source of cardiac calmodulin (PMID:41846582). Heterozygous missense variants in CALM2 reduce Ca²⁺ binding affinity and impair Ca²⁺-dependent inactivation of the L-type Ca²⁺ channel (CaV1.2) in a dominant-negative manner, prolonging action potential duration and causing long-QT syndrome and catecholaminergic polymorphic ventricular tachycardia, with allele-specific CRISPR knockout rescuing the electrophysiological phenotype in patient-derived cardiomyocytes (PMID:23388215, PMID:26969752, PMID:28335032). In cancer cell contexts, CALM2 knockdown inhibits Akt signaling to derepress the FoxO3a–Puma apoptotic axis and downregulates E2F5-mediated cell cycle progression (PMID:36460225, PMID:33788723).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1997 High

    The demonstration that calmodulin undergoes a large Ca²⁺-dependent conformational change around target peptides — sufficient to drive FRET between flanking fluorophores — established calmodulin as a bona fide intramolecular Ca²⁺ switch and enabled genetically encoded Ca²⁺ indicators for live-cell imaging.

    Evidence Recombinant calmodulin-M13 fusion protein with GFP variants; FRET measurements in HeLa cells

    PMID:9278050

    Open questions at the time
    • This study used calmodulin generically without distinguishing contributions of CALM1, CALM2, or CALM3
    • Conformational dynamics on full-length channel targets were not assessed
  2. 1998 Medium

    Genomic characterization of CALM2 defined its gene structure, promoter elements, and relative transcriptional activity compared with CALM1 and CALM3, showing CALM2 was moderately transcribed in proliferating cells.

    Evidence Genomic library screening, nuclear run-on assays, and luciferase reporter assays in human teratoma cells

    PMID:9681195

    Open questions at the time
    • Transcriptional analysis limited to a single teratoma cell line; tissue-specific regulation uncharacterized
    • Post-transcriptional control of CALM2 mRNA not addressed
  3. 2012 High

    Genetic linkage of calmodulin missense mutations to catecholaminergic polymorphic ventricular tachycardia, combined with biochemical evidence of reduced Ca²⁺ binding and aberrant RyR2 interaction, established calmodulin genes as direct genetic determinants of lethal cardiac arrhythmia.

    Evidence Genome-wide linkage in affected families; recombinant calmodulin Ca²⁺ binding and RYR2 peptide interaction assays

    PMID:23040497

    Open questions at the time
    • Initial study focused on CALM1; CALM2 variants were identified shortly after but not in this cohort
    • Full-length RyR2 channel interaction not tested
  4. 2013 High

    De novo CALM2 missense mutations were directly shown to reduce Ca²⁺ binding affinity of recombinant calmodulin and alter RyR2 calmodulin-binding-domain interaction at low Ca²⁺, establishing CALM2-specific pathogenicity in infant arrhythmias.

    Evidence Exome sequencing of parent–child trios; recombinant protein Ca²⁺ affinity assays and RYR2 peptide binding

    PMID:23388215

    Open questions at the time
    • Effects on L-type Ca²⁺ channel inactivation not yet tested for these specific CALM2 variants
    • Dominant-negative mechanism versus haploinsufficiency not resolved
  5. 2016 High

    The CALM2-E141G variant was shown to cause an 11-fold reduction in Ca²⁺ affinity and channel-specific consequences — dominant loss of CaV1.2 inactivation and mild NaV1.5 late current enhancement without RyR2 effects — revealing that individual CALM2 mutations differentially affect distinct ion channel targets.

    Evidence Recombinant protein Ca²⁺ binding assays; patch-clamp electrophysiology on CaV1.2, NaV1.5, and RyR2 in heterologous expression systems

    PMID:26969752

    Open questions at the time
    • Mechanism by which the same Ca²⁺-binding deficit selectively affects CaV1.2 but not RyR2 is unknown
    • No structural data explaining variant-specific channel selectivity
  6. 2017 High

    CRISPR-Cas9 allele-specific knockout of the CALM2-N98S mutant allele in patient iPSC-derived cardiomyocytes rescued prolonged action potential duration and impaired L-type Ca²⁺ channel inactivation, definitively proving a dominant-negative mechanism for CALM2-linked long-QT syndrome.

    Evidence hiPSC-derived cardiomyocytes; patch-clamp action potential and LTCC current recordings; allele-specific CRISPR-Cas9 knockout

    PMID:28335032

    Open questions at the time
    • Whether the dominant-negative mechanism generalizes to all CALM2 arrhythmia variants is untested
    • Stoichiometric threshold of mutant versus wild-type calmodulin required to produce pathology is unknown
  7. 2021 Medium

    CALM2 knockdown in hepatocellular carcinoma cells suppressed proliferation, migration, and in vivo tumor growth through downregulation of E2F5, positioning CALM2 as an upstream regulator of E2F5-dependent cell cycle progression in a cancer context.

    Evidence siRNA knockdown; transcriptomic profiling; proliferation and invasion assays; xenograft tumor formation

    PMID:33788723

    Open questions at the time
    • Mechanistic link between calmodulin and E2F5 transcription not characterized
    • Whether calmodulin's Ca²⁺-sensing activity is required for E2F5 regulation is unknown
  8. 2022 Medium

    In HER2-amplified gastric cancer cells, CALM2 knockdown inhibited Akt phosphorylation, derepressing the FoxO3a–Puma apoptotic axis in a caspase-dependent manner, establishing CALM2 as an upstream activator of Akt-mediated survival signaling.

    Evidence siRNA knockdown; Western blot for phospho-Akt, FoxO3a, Puma; caspase assays; pharmacological epistasis experiments

    PMID:36460225

    Open questions at the time
    • Whether calmodulin directly activates Akt or acts through CaMKK/CaMKII intermediaries is not resolved
    • Findings limited to a single cancer cell type
  9. 2024 Medium

    A suppression-and-replacement gene therapy strategy simultaneously knocking down all three CALM genes and replacing with shRNA-immune wild-type calmodulin partially rescued prolonged action potential duration in CALM2-D130G patient cardiomyocytes, providing proof-of-principle for therapeutic intervention in calmodulinopathy.

    Evidence shRNA knockdown with RT-qPCR validation; voltage-sensing dye APD measurements in CALM2-D130G hiPSC-derived cardiomyocytes

    PMID:39069900

    Open questions at the time
    • Rescue was partial (66% attenuation); full APD normalization not achieved
    • In vivo efficacy and delivery to cardiomyocytes not tested
    • Long-term effects on total calmodulin protein levels not assessed
  10. 2025 Medium

    Ribosome profiling confirmed that CALM2 contributes ~44% of cardiac calmodulin protein translation, explaining why CALM2 variants cause more severe arrhythmia phenotypes than CALM3 variants and providing a quantitative basis for the genotype–phenotype relationship.

    Evidence GTEx RNA-seq; ribosome profiling of human left ventricle; gnomAD variant constraint analysis; International Calmodulinopathy Registry outcomes

    PMID:41846582

    Open questions at the time
    • Whether translational contribution varies across cardiac chambers or developmental stages is unknown
    • Protein-level quantification of CALM2-derived calmodulin (indistinguishable from other CALM gene products) relies on ribosome profiling as a proxy

Open questions

Synthesis pass · forward-looking unresolved questions
  • Structural and biophysical understanding of how individual CALM2 missense variants differentially disrupt specific ion channel targets (CaV1.2 versus RyR2 versus NaV1.5) remains incomplete, and the stoichiometric threshold of mutant calmodulin required for dominant-negative pathology has not been determined.
  • No high-resolution structure of mutant calmodulin bound to full-length CaV1.2 or RyR2
  • Quantitative dose-response for mutant-to-wild-type calmodulin ratio and electrophysiological phenotype not established
  • In vivo gene therapy efficacy for CALM2-linked arrhythmias untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0140299 molecular sensor activity 3
Localization
GO:0005829 cytosol 1
Pathway
R-HSA-1643685 Disease 4 R-HSA-162582 Signal Transduction 3 R-HSA-5357801 Programmed Cell Death 2
Partners
AKT1CACNA1CE2F5RYR2SCN5A

Evidence

Reading pass · 13 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 De novo heterozygous missense mutations in CALM1 and CALM2 (encoding calmodulin) reduce calcium binding affinity of the recombinant protein by several-fold. A CALM2 mutation (N97S in CALM2 context) also showed aberrant interaction with the RYR2 calmodulin-binding-domain peptide at low calcium concentrations, establishing that calmodulin mutations disrupt Ca2+ binding and alter RyR2 interactions, causing life-threatening ventricular arrhythmias in infants. Exome sequencing of parent-child trios; recombinant mutant calmodulin calcium binding affinity assays; calmodulin-binding-domain peptide interaction assays Circulation High 23388215
2012 Heterozygous missense mutations in CALM1 (encoding calmodulin) causing catecholaminergic polymorphic ventricular tachycardia demonstrate compromised calcium binding and aberrant interaction with the RYR2 calmodulin-binding-domain peptide at low calcium concentrations, establishing calmodulin genes (including CALM2 as a candidate) as genetic determinants of severe cardiac arrhythmia. Genome-wide linkage analysis; Sanger sequencing; recombinant calmodulin calcium binding assays; RYR2 calmodulin-binding-domain peptide interaction assays American journal of human genetics High 23040497
2016 A novel CALM2 variant E141G reduces Ca2+ binding affinity of calmodulin by 11-fold and causes a dominant loss of inactivation of the cardiac L-type calcium channel (CaV1.2), mild accentuation of NaV1.5 late current, but no effect on intracellular RyR2-mediated calcium release, establishing channel-specific functional consequences of this CALM2 variant. Whole-exome sequencing; recombinant protein Ca2+ binding affinity assays; patch-clamp electrophysiology of CaV1.2, NaV1.5, and RyR2 Circulation. Cardiovascular genetics High 26969752
2017 The CALM2-N98S mutation in hiPSC-derived cardiomyocytes causes significantly lower beating rates, prolonged action potential durations, and impaired inactivation of L-type Ca2+ channel (LTCC) currents compared with control cells. Allele-specific CRISPR-Cas9 knockout of the mutant allele rescued these electrophysiological abnormalities, demonstrating that the CALM2-N98S mutant allele acts in a dominant-negative manner to suppress LTCC inactivation and thereby prolong action potential duration. hiPSC differentiation into cardiomyocytes; patch-clamp electrophysiology (action potential recordings, LTCC current measurements); CRISPR-Cas9 allele-specific knockout Human molecular genetics High 28335032
1997 Calmodulin (encoded by CALM genes) wraps around the calmodulin-binding peptide M13 upon Ca2+ binding, increasing fluorescence resonance energy transfer (FRET) between flanking GFP variants. This conformational change was harnessed to create genetically encoded Ca2+ indicators ('cameleons') enabling real-time visualization of Ca2+ dynamics in specific subcellular compartments including cytosol, nucleus, and endoplasmic reticulum. Recombinant fusion protein construction; FRET measurements; transfection in HeLa cells; live-cell fluorescence microscopy; calmodulin mutagenesis to tune Ca2+ affinity Nature High 9278050
1998 The CALM2 gene spans approximately 16 kb with intron interruptions at identical positions to CALM1 and CALM3. Its 5' flanking region contains a TATA-like sequence 27 nucleotides upstream of the transcriptional start site. In proliferating human teratoma cells, CALM3 is at least 5-fold more actively transcribed than CALM1 or CALM2, and the 5' untranslated regions are required for full promoter activation in luciferase reporter assays. Genomic library screening; genomic PCR; nuclear run-on transcription assays; luciferase reporter transfection assays; mRNA quantification Cell calcium Medium 9681195
2024 A suppression-and-replacement (SupRep) gene therapy construct simultaneously knocks down endogenous CALM1, CALM2, and CALM3 using gene-specific shRNAs (71% knockdown for CALM2) while delivering a shRNA-immune CALM1 replacement. In CALM2-D130G hiPSC-derived cardiomyocytes with pathologically prolonged APD90 (647±9 ms vs. 359±12 ms in WT), CALM-SupRep transfection shortened APD90 to 457±19 ms (66% attenuation), demonstrating proof-of-principle for gene therapy targeting CALM2-mediated long-QT syndrome. shRNA knockdown efficiency testing by RT-qPCR; voltage-sensing dye action potential measurements in hiPSC-derived cardiomyocytes; CALM2-D130G patient-derived iPSC lines Circulation. Arrhythmia and electrophysiology Medium 39069900
2022 Knockdown of CALM2 in HER2-amplified gastric cancer cells inhibits Akt signaling, which derepresses the FoxO3a/Puma axis, promoting mitochondrial apoptosis in a caspase-dependent manner and sensitizing cells to afatinib. Inhibition of either FoxO3a or Puma abrogated the pro-apoptotic effects of CALM2 knockdown, placing CALM2 upstream of the Akt–FoxO3a–Puma signaling cascade. siRNA knockdown of CALM2; Western blot for Akt phosphorylation, FoxO3a, Puma; caspase activity assays; flow cytometry for apoptosis; pharmacological inhibition of FoxO3a and Puma Toxicology in vitro Medium 36460225
2021 Knockdown of CALM2 in hepatocellular carcinoma (HCC) cells inhibits proliferation, colony formation, migration, and invasion, and reduces tumor formation in vivo. At the molecular level, CALM2-specific knockdown leads to downregulation of E2F transcription factor 5 (E2F5), which is functionally associated with migration, invasion, and proliferation, placing CALM2 upstream of E2F5-mediated cell cycle progression in HCC. siRNA knockdown of CALM2; transcriptomic profiling of dysregulated genes; cell proliferation and colony formation assays; migration/invasion assays; in vivo tumor formation; HCC clinical sample validation Anticancer research Medium 33788723
2021 In cardiac myocytes subjected to oxygen-glucose deprivation (OGD), circ_0010729 acts as a sponge for miR-338-3p, which directly targets CALM2 mRNA. Knockdown of circ_0010729 increases miR-338-3p availability, reducing CALM2 expression and attenuating OGD-induced apoptosis and autophagy in AC16 cells, establishing CALM2 as a downstream effector in this non-coding RNA regulatory axis during cardiac ischemic injury. RT-qPCR and Western blot for CALM2 expression; dual-luciferase reporter assay validating miR-338-3p targeting of CALM2; siRNA knockdown; flow cytometry for apoptosis; cell viability assays Journal of cardiovascular pharmacology Low 33951696
2019 In post-myocardial infarction myocardial cells, GAS5 lncRNA acts as a sponge for miR-525-5p, which targets CALM2 mRNA. Overexpression of CALM2 promotes apoptosis and inhibits proliferation of myocardial cells, while miR-525-5p can reverse CALM2-induced MI effects. Dual luciferase reporter and RIP assays confirmed the targeting relationships among GAS5, miR-525-5p, and CALM2. RT-qPCR; Western blot; flow cytometry; MTT assay; dual luciferase reporter assay; RNA-binding protein immunoprecipitation (RIP); knockdown experiments Journal of cellular biochemistry Low 31429119
2026 RNA sequencing and ribosome profiling of left ventricular tissue show that CALM2 contributes approximately 44% of total calmodulin-coding mRNA (versus 37% for CALM1 and 21% for CALM3) and approximately 44% of calmodulin protein translation, making CALM1 and CALM2 the dominant sources of calmodulin in the human heart. This greater contribution of CALM2 relative to CALM3 explains why CALM3 missense variants are under less negative selection and cause less severe cardiac phenotypes. GTEx RNA sequencing data analysis; ribosome profiling of left ventricle; Genome Aggregation Database (gnomAD) observed-to-expected variant ratio analysis; International Calmodulinopathy Registry clinical outcomes Europace Medium 41846582
2025 LncRNA ABHD11-AS1 acts as a sponge for miR-876-5p, which targets CALM2 mRNA, in thyroid cancer cells. ABHD11-AS1 knockdown reduces CALM2 expression and inhibits migration, invasion, and EMT of thyroid cancer cells; these effects are counteracted by miR-876-5p inhibition or CALM2 overexpression, placing CALM2 downstream in the ABHD11-AS1/miR-876-5p/CALM2 regulatory axis promoting thyroid cancer metastasis. Scratch assay; transwell invasion assay; RT-qPCR; Western blot; dual-luciferase reporter assay; siRNA and overexpression approaches Biochemical genetics Low 40117023

Source papers

Stage 0 corpus · 52 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 Fluorescent indicators for Ca2+ based on green fluorescent proteins and calmodulin. Nature 2324 9278050
2005 Towards a proteome-scale map of the human protein-protein interaction network. Nature 2090 16189514
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2014 A proteome-scale map of the human interactome network. Cell 977 25416956
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2004 A physical and functional map of the human TNF-alpha/NF-kappa B signal transduction pathway. Nature cell biology 841 14743216
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2007 Large-scale mapping of human protein-protein interactions by mass spectrometry. Molecular systems biology 733 17353931
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2011 Mapping the NPHP-JBTS-MKS protein network reveals ciliopathy disease genes and pathways. Cell 507 21565611
2015 A Dynamic Protein Interaction Landscape of the Human Centrosome-Cilium Interface. Cell 433 26638075
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2002 DAP kinase and DRP-1 mediate membrane blebbing and the formation of autophagic vesicles during programmed cell death. The Journal of cell biology 408 11980920
2007 Cep97 and CP110 suppress a cilia assembly program. Cell 386 17719545
2007 Functional specialization of beta-arrestin interactions revealed by proteomic analysis. Proceedings of the National Academy of Sciences of the United States of America 360 17620599
2011 Acetylation regulates gluconeogenesis by promoting PEPCK1 degradation via recruiting the UBR5 ubiquitin ligase. Molecular cell 337 21726808
2007 The ankyrin repeats of TRPV1 bind multiple ligands and modulate channel sensitivity. Neuron 334 17582331
2002 Structural basis for the activation of anthrax adenylyl cyclase exotoxin by calmodulin. Nature 323 11807546
2010 Dynamics of cullin-RING ubiquitin ligase network revealed by systematic quantitative proteomics. Cell 318 21145461
2005 Nephrocystin-5, a ciliary IQ domain protein, is mutated in Senior-Loken syndrome and interacts with RPGR and calmodulin. Nature genetics 311 15723066
2013 Calmodulin mutations associated with recurrent cardiac arrest in infants. Circulation 308 23388215
2012 Mutations in calmodulin cause ventricular tachycardia and sudden cardiac death. American journal of human genetics 296 23040497
2009 Characterization of exosome-like vesicles released from human tracheobronchial ciliated epithelium: a possible role in innate defense. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 284 19190083
2007 AKAP79/150 anchoring of calcineurin controls neuronal L-type Ca2+ channel activity and nuclear signaling. Neuron 284 17640527
2018 Enhancer Activity Requires CBP/P300 Bromodomain-Dependent Histone H3K27 Acetylation. Cell reports 274 30110629
1996 Calcineurin binds the transcription factor NFAT1 and reversibly regulates its activity. The Journal of biological chemistry 253 8631904
2010 MHC class II-associated proteins in B-cell exosomes and potential functional implications for exosome biogenesis. Immunology and cell biology 221 20458337
2008 CP110 suppresses primary cilia formation through its interaction with CEP290, a protein deficient in human ciliary disease. Developmental cell 220 18694559
2016 Spectrum and Prevalence of CALM1-, CALM2-, and CALM3-Encoded Calmodulin Variants in Long QT Syndrome and Functional Characterization of a Novel Long QT Syndrome-Associated Calmodulin Missense Variant, E141G. Circulation. Cardiovascular genetics 109 26969752
1993 Localization of the human bona fide calmodulin genes CALM1, CALM2, and CALM3 to chromosomes 14q24-q31, 2p21.1-p21.3, and 19q13.2-q13.3. Genomics 80 8314583
2017 Allele-specific ablation rescues electrophysiological abnormalities in a human iPS cell model of long-QT syndrome with a CALM2 mutation. Human molecular genetics 72 28335032
1998 Characterization of the human CALM2 calmodulin gene and comparison of the transcriptional activity of CALM1, CALM2 and CALM3. Cell calcium 61 9681195
2019 lncRNA GAS5 regulates myocardial infarction by targeting the miR-525-5p/CALM2 axis. Journal of cellular biochemistry 37 31429119
2005 High expression of calcium-binding proteins, S100A10, S100A11 and CALM2 in anaplastic large cell lymphoma. British journal of haematology 36 16351635
2018 Identification of TAF1, HNF4A, and CALM2 as potential therapeutic target genes for liver fibrosis. Journal of cellular physiology 28 30317608
1991 Characterization of two novel human retropseudogenes related to the calmodulin-encoding gene, CaMII. Gene 23 1999288
2010 Identification of sequence polymorphisms in CALM2 and analysis of association with hip osteoarthritis in a Japanese population. Journal of bone and mineral metabolism 14 20198394
2019 Long QT syndrome with a de novo CALM2 mutation in a 4-year-old boy. Pediatrics international : official journal of the Japan Pediatric Society 13 31283864
2014 Investigation into the promoter DNA methylation of three genes (CAMK1D, CRY2 and CALM2) in the peripheral blood of patients with type 2 diabetes. Experimental and therapeutic medicine 13 25009623
2022 Knockdown of CALM2 increases the sensitivity to afatinib in HER2-amplified gastric cancer cells by regulating the Akt/FoxO3a/Puma axis. Toxicology in vitro : an international journal published in association with BIBRA 12 36460225
2024 Single Construct Suppression and Replacement Gene Therapy for the Treatment of All CALM1-, CALM2-, and CALM3-Mediated Arrhythmia Disorders. Circulation. Arrhythmia and electrophysiology 11 39069900
2021 Targeting CALM2 Inhibits Hepatocellular Carcinoma Growth and Metastasis by Suppressing E2F5-mediated Cell Cycle Progression. Anticancer research 10 33788723
2021 Circular RNA circ_0010729 Knockdown Attenuates Oxygen-Glucose Deprivation-Induced Human Cardiac Myocytes Injury by miR-338-3p/CALM2 Axis. Journal of cardiovascular pharmacology 6 33951696
2024 A rare case report of catecholaminergic polymorphic ventricular tachycardia with an uncommon CALM2 mutation. European heart journal. Case reports 2 39104518
2022 Case report: Prenatal diagnosis of fetal non-compaction cardiomyopathy with bradycardia accompanied by de novo CALM2 mutation. Frontiers in pediatrics 1 36507129
2026 The first case of a Caucasian child with calmodulinopathy related to CALM2 N98S mutation. Cardiology in the young 0 41665141
2026 CALM1, CALM2, and CALM3 expression and translation efficiency provide insight into the severity of calmodulinopathy. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology 0 41846582
2025 LncRNA ABHD11-AS1 Elevates CALM2 to Promote Metastasis of Thyroid Cancer Through Sponging miR-876-5p. Biochemical genetics 0 40117023
2025 Long-term follow-up of patients with catecholaminergic polymorphic ventricular tachycardia related to a novel CALM2 variant. Journal of cardiology cases 0 41550621
2024 Generation of a human induced pluripotent stem cell line ZZUNEUi030-A from a female patient carrying a heterozygous CALM2 (c.395 A > T) mutation. Stem cell research 0 39137556