Affinage

CAMTA1

Calmodulin-binding transcription activator 1 · UniProt Q9Y6Y1

Length
1673 aa
Mass
183.7 kDa
Annotated
2026-06-09
55 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge faithfulness: 6/7 claims corpus-supported (86%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CAMTA1 is a calcium-responsive transcriptional regulator with dual roles as a developmental/neuronal transcription factor and, when disrupted by chromosomal rearrangement, as the substrate for a potent oncogenic fusion (PMID:25049392, PMID:21584898). In the nervous system, loss of CAMTA1 in mice causes Purkinje cell degeneration, cerebellar atrophy, and dysregulation of large neuronal gene sets, and a consensus CAMTA-binding DNA motif links it directly to these targets, establishing CAMTA1 as a transcriptional regulator required for Purkinje cell survival (PMID:25049392); acute hippocampal knockdown selectively impairs long-term memory and alters genes controlling synaptic transmission and neuronal excitability (PMID:27194798). Across multiple tumor contexts CAMTA1 acts as a tumor suppressor: it slows proliferation, drives neuronal/neurosphere differentiation, and suppresses xenograft growth in neuroblastoma and glioblastoma stem cells (PMID:21385898, PMID:21857646). Its activity intersects calcium signaling through participation in a complex with the calcineurin subunit PPP3CA and NFATc4, where CAMTA1 competes with PPP3CA for NFATc4 binding to restrain NFAT activation (PMID:35332122). The recurrent t(1;3) translocation fuses WWTR1 (TAZ) to CAMTA1, generating a fusion oncoprotein that escapes LATS1/2-imposed cytoplasmic retention and is constitutively nuclear, activating a TAZ-like, TEAD-dependent transcriptional program and transforming cells (PMID:25961935, PMID:33766984); this fusion is sufficient to initiate epithelioid hemangioendothelioma specifically in endothelial cells in vivo (PMID:33766982). Mechanistically the fusion recruits the ATAC histone acetyltransferase complex via YEATS2 and ZZZ3 to remodel chromatin alongside TEAD activation (PMID:33913810), induces the tumorigenic target CTGF, which signals through integrin αIIbβ3 and upstream of Ras-MAPK (PMID:35443056), and drives a hypertranscription state producing DNA damage and senescence that CDKN2A loss bypasses to accelerate tumorigenesis (PMID:37980390, PMID:36598859). CAMTA1 domain architecture (CG-1, TIG, ankyrin repeats, calmodulin-binding IQ motifs) defines it as a calmodulin-binding transcription activator family member (PMID:12964007).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 2003 Low

    Before functional studies, the question was what kind of protein CAMTA1 is; domain analysis defined it as a calmodulin-binding transcription activator, framing a calcium-sensitive transcription factor.

    Evidence in silico domain analysis and cDNA assembly identifying CG-1, TIG, ankyrin, and IQ domains

    PMID:12964007

    Open questions at the time
    • Computational prediction only; no experimental validation of domain activities
    • Calmodulin binding to IQ motifs not functionally tested
    • No demonstration of transcriptional activity
  2. 2011 High

    It was unknown whether CAMTA1 has a physiological growth-control role; ectopic expression showed it suppresses proliferation and drives neuronal differentiation, establishing a tumor-suppressor function.

    Evidence inducible CAMTA1 expression in neuroblastoma cells with cell cycle, soft-agar, xenograft, and transcriptome readouts; miRNA targeting and NPPA induction in glioblastoma stem cells

    PMID:21385898 PMID:21857646

    Open questions at the time
    • Direct transcriptional targets driving the phenotype not fully defined
    • Calcium-dependence of this activity not addressed
  3. 2011 High

    The molecular lesion behind epithelioid hemangioendothelioma was unknown; identification of the recurrent t(1;3) WWTR1-CAMTA1 fusion established a tumor-specific molecular abnormality.

    Evidence FISH positional cloning and RT-PCR across multiple anatomic sites in an EHE cohort

    PMID:21584898

    Open questions at the time
    • Did not establish whether the fusion is causal or how it transforms cells
    • Functional contribution of the CAMTA1 moiety unresolved
  4. 2014 High

    The in vivo role of CAMTA1 in the nervous system was unclear; conditional knockout revealed it is required for Purkinje cell survival and directly regulates neuronal genes via a defined DNA motif.

    Evidence global and nervous-system-specific knockout mice with gene-expression analysis and consensus binding-motif determination

    PMID:25049392

    Open questions at the time
    • Direct genomic occupancy at endogenous targets not mapped by ChIP
    • Role of calmodulin/calcium in this regulation not tested
  5. 2015 High

    Whether the WWTR1-CAMTA1 fusion is oncogenic and by what mechanism was open; the fusion was shown to be constitutively nuclear, escaping LATS-regulated degradation, and to transform cells via a TAZ-like program.

    Evidence fusion expression in cell lines with subcellular fractionation, anoikis assays, and transcriptional reporters

    PMID:25961935

    Open questions at the time
    • Required transcriptional cofactors not yet identified
    • In vivo sufficiency not demonstrated in this study
  6. 2021 High

    It was unknown whether the fusion alone causes EHE and which effectors it requires; endogenous-locus knock-in showed endothelial-specific tumor formation, and dominant-negative TEAD established TEAD as a required effector, while proteomics identified ATAC complex recruitment.

    Evidence conditional knock-in and endothelial transgenic mouse models with dominant-negative TEAD rescue; Co-IP/MS and ChIP-seq/RNA-seq identifying YEATS2/ZZZ3 (ATAC complex)

    PMID:33766982 PMID:33766984 PMID:33913810

    Open questions at the time
    • Mechanism by which the fusion recruits ATAC not structurally defined
    • Cell-of-origin specificity for endothelium not fully explained
  7. 2022 High

    The downstream effectors linking fusion-driven transcription to tumor growth were unclear; CTGF was identified as a tumorigenic target acting via integrin αIIbβ3 and upstream of Ras-MAPK, defining a druggable axis.

    Evidence NIH3T3 transformation, CTGF knockdown, xenografts, and pharmacologic MAPK inhibition (trametinib)

    PMID:35443056

    Open questions at the time
    • Direct binding of fusion to the CTGF promoter not shown
    • Relevance of integrin αIIbβ3 in patient tumors not established
  8. 2023 High

    Why CDKN2A loss is the most common secondary mutation in EHE was unknown; the fusion was shown to induce hypertranscription, DNA damage, impaired homologous recombination, and senescence, which CDKN2A loss bypasses to accelerate tumorigenesis.

    Evidence inducible fusion in primary endothelial cells with DNA-damage foci, cell-cycle and senescence assays; conditional fusion + Cdkn2a knockout mouse and scRNA-seq

    PMID:36598859 PMID:37980390

    Open questions at the time
    • Source of the hypertranscription-induced DNA damage not mechanistically resolved
    • Other cooperating events beyond CDKN2A not surveyed
  9. 2022 Medium

    Whether wild-type CAMTA1 intersects calcium signaling at the protein level was unaddressed; it was shown to form a complex with calcineurin (PPP3CA) and NFATc4, competing with PPP3CA to restrain NFAT activation.

    Evidence Co-IP of the CAMTA1-PPP3CA-NFATc4 complex with knockdown, NFATc4 phosphorylation assays, and xenografts in colorectal cancer cells

    PMID:35332122

    Open questions at the time
    • Single Co-IP-based complex without reciprocal/structural validation
    • Not independently replicated
    • Relationship to CAMTA1 transcriptional activity unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CAMTA1's calmodulin-binding/calcium-sensing architecture mechanistically couples to its transcriptional output, and whether the wild-type protein's tumor-suppressor and the fusion's oncogenic programs share regulatory logic, remains unresolved.
  • Calcium/calmodulin dependence of CAMTA1 transcription not experimentally demonstrated
  • Genome-wide direct targets of wild-type CAMTA1 not mapped
  • Structural basis of the fusion-ATAC-TEAD assembly unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 3 GO:0003677 DNA binding 1
Localization
GO:0005634 nucleus 1
Pathway
R-HSA-1643685 Disease 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-112316 Neuronal System 2 R-HSA-162582 Signal Transduction 2
Partners
NFATC4NKX2-2PPP3CATEADWWTR1YEATS2ZZZ3
Complex memberships
ATAC histone acetyltransferase complexCAMTA1-PPP3CA-NFATc4 complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 The WWTR1-CAMTA1 (TAZ-CAMTA1) fusion gene is generated by a recurrent t(1;3)(p36.3;q25) chromosomal translocation in epithelioid hemangioendothelioma (EHE). RT-PCR confirmed the fusion transcript in EHE from bone, soft tissue, and visceral locations, establishing it as a consistent molecular abnormality specific to this tumor type. FISH positional cloning, RT-PCR Genes, chromosomes & cancer High 21584898
2015 The TAZ-CAMTA1 (TC) fusion protein localizes constitutively to the nucleus (escaping the cytoplasmic retention and degradation normally imposed by LATS1/2 phosphorylation of TAZ), activates a TAZ-like transcriptional program, confers resistance to anoikis, and causes oncogenic transformation of cells. The oncogenic activity depends on nuclear localization driven by loss of the LATS-regulated phosphodegron in the TAZ moiety. Expression of fusion construct in cell lines, anoikis resistance assay, transcriptional reporter assays, subcellular fractionation/localization Oncogene High 25961935
2021 TAZ-CAMTA1 and YAP-TFE3 fusion oncoproteins both interact with YEATS2 and ZZZ3, components of the ATAC histone acetyltransferase complex, as identified by a proteomic/genetic screen. The fusions drive a unique transcriptome by simultaneously hyperactivating a TEAD-based transcriptional program and modulating chromatin via the ATAC complex. Proteomic/genetic screen (Co-IP/MS), integrative next-generation sequencing (ChIP-seq, RNA-seq) in human and murine cell lines eLife High 33913810
2021 Conditional knock-in of Wwtr1-Camta1 to the endogenous Wwtr1 locus in mice is sufficient to drive EHE tumor formation exclusively in endothelial cells, demonstrating that TAZ-CAMTA1 is the key oncogenic driver. Expression in endothelial cells recapitulates the human disease histologically, immunohistochemically, and genetically. Conditional knock-in mouse model (Cre-activated Wwtr1-Camta1 allele targeted to Wwtr1 locus), histological and molecular characterization Genes & development High 33766982
2021 TAZ-CAMTA1 expression in endothelial cells initiates an angiogenic and regenerative-like transcriptional program. Disruption of the TAZ-CAMTA1–TEAD interaction (by dominant-negative TEAD expression in vivo) inhibits TAZ-CAMTA1-mediated vascular tumor formation, establishing TEAD as a required transcriptional effector of the fusion oncoprotein. Endothelial-specific transgenic mouse model, dominant-negative TEAD in vivo rescue experiment, transcriptome profiling Genes & development High 33766984
2022 CTGF is a tumorigenic transcriptional target of the TAZ-CAMTA1 fusion. CTGF binds integrin αIIbβ3 to sustain anchorage-independent proliferation of TC-transformed cells, and acts upstream of Ras-MAPK signaling. Pharmacologic MAPK inhibition (trametinib) or CTGF knockdown abrogates TC-driven growth in vitro and in xenograft models. NIH3T3 cell transformation model, soft-agar/suspension growth assays, CTGF knockdown, xenograft model, pharmacologic MAPK inhibition (trametinib, PD0325901) Clinical cancer research High 35443056
2023 Upon TAZ-CAMTA1 expression in primary endothelial cells, cells rapidly enter a hypertranscription state, triggering DNA damage, S-phase arrest, and impaired homologous recombination (reduced BRCA1 and RAD51 foci), leading to senescence. Loss of CDKN2A bypasses this senescence to allow uncontrolled growth, providing a mechanistic basis for CDKN2A as the most common secondary mutation in EHE. Doxycycline-inducible TAZ-CAMTA1 in primary endothelial cells, DNA damage foci (γH2AX, BRCA1, RAD51) immunofluorescence, cell cycle analysis, senescence assays, Cdkn2a knockout mouse model Communications biology High 37980390
2023 Loss of CDKN2A in the context of the TAZ-CAMTA1 (TC) fusion in endothelial cells produces more aggressive EHE with earlier morbidity/mortality and enhanced tumor cell proliferation in a conditional mouse model, establishing CDKN2A loss as a cooperating oncogenic event with TC. EHE cell lines derived from these tumors are addicted to the TC oncoprotein. Conditional mouse model (TC allele + Cdkn2a knockout + endothelial Cre), single-cell RNA-seq, ex vivo cell line derivation and xenograft Clinical cancer research High 36598859
2011 CAMTA1 functions as a tumor suppressor in neuroblastoma: ectopic CAMTA1 expression slowed cell proliferation (increased G1/G0), inhibited anchorage-independent colony formation, suppressed xenograft growth, and induced neurite-like processes and neuronal differentiation markers. Transcriptome analysis identified 683 CAMTA1-regulated genes enriched for neuronal function and differentiation. Retinoic acid and other differentiation stimuli upregulated CAMTA1 expression. Inducible ectopic CAMTA1 expression in neuroblastoma cell lines, cell cycle analysis, soft-agar colony assay, xenograft model, transcriptome analysis Cancer research High 21385898
2011 CAMTA1 is a direct target of miR-9/9* and miR-17 in glioblastoma stem cells. CAMTA1 induces expression of the anti-proliferative cardiac hormone NPPA, reduces neurosphere formation, and suppresses tumor growth in nude mice, supporting a tumor suppressor function. miR-9/9* inhibition reduced neurosphere formation and stimulated differentiation. miRNA target validation (miR-9/9*, miR-17 → CAMTA1), CAMTA1 overexpression in glioblastoma stem cells, neurosphere formation assay, nude mouse tumor growth assay The EMBO journal High 21857646
2014 Global or nervous-system-specific deletion of CAMTA1 in mice causes severe ataxia with Purkinje cell degeneration and cerebellar atrophy. Gene-expression analysis identified a large set of neuronal genes dysregulated in CAMTA1-mutant brains, and a consensus CAMTA-binding DNA sequence was determined and associated with many of these genes, establishing CAMTA1 as a direct transcriptional regulator required for Purkinje cell function and survival. Conditional knockout mouse (global and nervous-system-specific), gene-expression analysis, consensus DNA binding motif determination Proceedings of the National Academy of Sciences of the United States of America High 25049392
2016 Acute hippocampal knockdown of CAMTA1 (but not CAMTA2) in adult mice impairs contextual fear conditioning and object-place recognition (long-term memory), without affecting short-term memory or neuronal morphology. Gene expression profiling revealed CAMTA1-dependent regulation of genes related to synaptic transmission and neuronal excitability, and patch-clamp recordings confirmed CAMTA1-dependent electrophysiological changes. shRNA knockdown in adult mouse hippocampus, behavioral memory tests (fear conditioning, object-place recognition), transcriptome profiling, patch-clamp electrophysiology Learning & memory (Cold Spring Harbor, N.Y.) High 27194798
2016 CAMTA1 knockdown in pancreatic beta cells (INS-1 832/13 and Wistar rat islets) reduced miR-212/miR-132 promoter activity and expression, decreased insulin secretion and voltage-dependent Ca2+ currents, and altered insulin content. CAMTA1 protein physically interacts with the homeodomain transcription factor Nkx2-2. These results place CAMTA1 as a regulator of the miR-212/miR-132 cluster and of multiple steps in beta-cell insulin secretion. Camta1 siRNA knockdown in INS-1 cells and rat islets, miR-212/miR-132 promoter-reporter assay, insulin secretion/content assays, patch-clamp (Ca2+ currents), Co-IP (CAMTA1–Nkx2-2 interaction) The Journal of biological chemistry Medium 27402838
2012 Ca2+-dependent upregulation of CAMTA1 in mesenchymal stem cells co-cultured with cardiomyocytes precedes activation of a myocardial gene program. CAMTA1 loss-of-function minimized cardiac gene program activation in stem cells, establishing CAMTA1 as an early Ca2+-dependent intermediate required for cardiomyocyte-lineage commitment. Co-culture of mesenchymal stem cells with neonatal cardiomyocytes, Ca2+ imaging, CAMTA1 loss-of-function (knockdown), cardiac gene expression profiling PloS one Medium 22715383
2020 CAMTA1 overexpression in glioma cells inhibited cell growth, migration, invasion, and cell cycle progression, and enhanced temozolomide-induced apoptosis. Overexpression decreased ITGA5, ITGB1, p-AKT, p-FAK, and Myc protein levels, placing CAMTA1 as a suppressor upstream of integrin/AKT/FAK/Myc signaling in glioma. CAMTA1 overexpression in glioma cell lines, cell viability/migration/invasion assays, flow cytometry cell cycle/apoptosis analysis, Western blot for signaling proteins, xenograft model Cellular signalling Medium 33316386
2022 CAMTA1 forms a multi-protein complex with PPP3CA (calcineurin A) and NFATc4. CAMTA1 and PPP3CA competitively bind to NFATc4; CAMTA1 knockdown promotes PPP3CA-mediated dephosphorylation and activation of NFATc4, leading to upregulation of NFATc4 target genes, increased proliferation/invasion, and oxaliplatin resistance in colorectal cancer cells. Co-IP (CAMTA1–PPP3CA–NFATc4 complex), CAMTA1 and PPP3CA knockdown, NFATc4 phosphorylation/expression assays, cell proliferation/invasion/apoptosis assays, xenograft model Cell death discovery Medium 35332122
2013 lncCAMTA1 physically associates with the CAMTA1 promoter, induces a repressive chromatin structure, and thereby inhibits CAMTA1 transcription in hepatocellular carcinoma. CAMTA1 is required for the effects of lncCAMTA1 on HCC cell proliferation and cancer stem cell-like properties. ChIP (chromatin association of lncCAMTA1 at CAMTA1 promoter), lncCAMTA1 overexpression/knockdown, CAMTA1 rescue experiments, in vitro and in vivo functional assays International journal of molecular sciences Medium 27669232
2022 CAMTA1 knockout in SH-SY5Y cells increased cyclin D1 (CCND1) expression under oxygen-glucose deprivation/reoxygenation (OGD/R) conditions, and RNA-seq revealed pathways involved in cellular proliferation and cell cycle enriched in CAMTA1 KO cells, establishing CAMTA1 as a regulator of cyclin D1 and cell-cycle progression in the context of ischemia-reperfusion injury. CAMTA1 CRISPR knockout in SH-SY5Y cells, RNA-seq, CCND1 protein/mRNA quantification under OGD/R model, methylation analysis (850K BeadChip) Frontiers in cellular neuroscience Medium 36159397
2003 Bioinformatic characterization of the CAMTA1 protein domain structure identified: a CG-1 domain, TIG domain, ankyrin repeats, and IQ motifs (calmodulin-binding), defining CAMTA1 as a member of the calmodulin-binding transcription activator (CAMTA) family. KIAA0833 was identified as the representative human CAMTA1 cDNA. Mouse Camta1 was determined to share 94.1% amino acid identity with human CAMTA1. Bioinformatics/in silico domain analysis, cDNA sequence assembly International journal of oncology Low 12964007

Source papers

Stage 0 corpus · 55 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 A novel WWTR1-CAMTA1 gene fusion is a consistent abnormality in epithelioid hemangioendothelioma of different anatomic sites. Genes, chromosomes & cancer 397 21584898
2016 Nuclear Expression of CAMTA1 Distinguishes Epithelioid Hemangioendothelioma From Histologic Mimics. The American journal of surgical pathology 194 26414223
2005 Allelic losses at 1p36 and 19q13 in gliomas: correlation with histologic classification, definition of a 150-kb minimal deleted region on 1p36, and evaluation of CAMTA1 as a candidate tumor suppressor gene. Clinical cancer research : an official journal of the American Association for Cancer Research 143 15709179
2011 CAMTA1 is a novel tumour suppressor regulated by miR-9/9* in glioblastoma stem cells. The EMBO journal 129 21857646
2015 Mechanism of action of a WWTR1(TAZ)-CAMTA1 fusion oncoprotein. Oncogene 92 25961935
2015 CAMTA1 is a useful immunohistochemical marker for diagnosing epithelioid haemangioendothelioma. Histopathology 89 25879300
2015 Thoracic epithelioid malignant vascular tumors: a clinicopathologic study of 52 cases with emphasis on pathologic grading and molecular studies of WWTR1-CAMTA1 fusions. The American journal of surgical pathology 85 25353289
2011 CAMTA1, a 1p36 tumor suppressor candidate, inhibits growth and activates differentiation programs in neuroblastoma cells. Cancer research 76 21385898
2007 Calmodulin-binding transcription activator 1 (CAMTA1) alleles predispose human episodic memory performance. Human molecular genetics 67 17470457
2016 Association of a Locus in the CAMTA1 Gene With Survival in Patients With Sporadic Amyotrophic Lateral Sclerosis. JAMA neurology 62 27244217
2003 Identification and characterization of FLJ10737 and CAMTA1 genes on the commonly deleted region of neuroblastoma at human chromosome 1p36.31-p36.23. International journal of oncology 62 12964007
2021 WWTR1(TAZ)-CAMTA1 gene fusion is sufficient to dysregulate YAP/TAZ signaling and drive epithelioid hemangioendothelioma tumorigenesis. Genes & development 59 33766982
2016 Long Noncoding RNA lncCAMTA1 Promotes Proliferation and Cancer Stem Cell-Like Properties of Liver Cancer by Inhibiting CAMTA1. International journal of molecular sciences 58 27669232
2015 Molecular characterization of epithelioid haemangioendotheliomas identifies novel WWTR1-CAMTA1 fusion variants. Histopathology 58 25817592
2021 TAZ-CAMTA1 and YAP-TFE3 alter the TAZ/YAP transcriptome by recruiting the ATAC histone acetyltransferase complex. eLife 57 33913810
2006 Reduced expression of CAMTA1 correlates with adverse outcome in neuroblastoma patients. Clinical cancer research : an official journal of the American Association for Cancer Research 53 16397034
2021 WWTR1(TAZ)-CAMTA1 reprograms endothelial cells to drive epithelioid hemangioendothelioma. Genes & development 46 33766984
2014 Ataxia and Purkinje cell degeneration in mice lacking the CAMTA1 transcription factor. Proceedings of the National Academy of Sciences of the United States of America 36 25049392
2012 Intragenic CAMTA1 rearrangements cause non-progressive congenital ataxia with or without intellectual disability. Journal of medical genetics 36 22693284
2016 Epithelioid hemangioendotheliomas with TFE3 gene translocations are compossible with CAMTA1 gene rearrangements. Oncotarget 33 26840265
2016 The calmodulin-binding transcription activator CAMTA1 is required for long-term memory formation in mice. Learning & memory (Cold Spring Harbor, N.Y.) 29 27194798
2022 The TAZ-CAMTA1 Fusion Protein Promotes Tumorigenesis via Connective Tissue Growth Factor and Ras-MAPK Signaling in Epithelioid Hemangioendothelioma. Clinical cancer research : an official journal of the American Association for Cancer Research 28 35443056
2016 Integrator of Stress Responses Calmodulin Binding Transcription Activator 1 (Camta1) Regulates miR-212/miR-132 Expression and Insulin Secretion. The Journal of biological chemistry 26 27402838
2023 Loss of CDKN2A Cooperates with WWTR1(TAZ)-CAMTA1 Gene Fusion to Promote Tumor Progression in Epithelioid Hemangioendothelioma. Clinical cancer research : an official journal of the American Association for Cancer Research 24 36598859
2014 Intragenic CAMTA1 deletions are associated with a spectrum of neurobehavioral phenotypes. Clinical genetics 20 24738973
2017 Long Noncoding RNA CAMTA1 Promotes Proliferation and Mobility of the Human Breast Cancer Cell Line MDA-MB-231 via Targeting miR-20b. Oncology research 18 28550685
2022 Unraveling the Biology of Epithelioid Hemangioendothelioma, a TAZ-CAMTA1 Fusion Driven Sarcoma. Cancers 16 35740643
2021 LncRNA RBPMS-AS1 promotes NRGN transcription to enhance the radiosensitivity of glioblastoma through the microRNA-301a-3p/CAMTA1 axis. Translational oncology 15 34800915
2019 CAMTA-1 Expression in 24 Cases of Hepatic Epithelioid Hemangioendothelioma in a Single Institute: Diagnostic Utility for Differential Diagnosis from Hepatic Angiosarcoma. In vivo (Athens, Greece) 15 31662570
2020 CAMTA1, a novel antitumor gene, regulates proliferation and the cell cycle in glioma by inhibiting AKT phosphorylation. Cellular signalling 12 33316386
2012 Calcium dependent CAMTA1 in adult stem cell commitment to a myocardial lineage. PloS one 12 22715383
2011 CAMTA1 T polymorphism is associated with neuropsychological test performance in older adults with cardiovascular disease. Psychogeriatrics : the official journal of the Japanese Psychogeriatric Society 11 21951953
2007 Allelic variants of CAMTA1 and FLJ10737 within a commonly deleted region at 1p36 in neuroblastoma. European journal of cancer (Oxford, England : 1990) 11 17222547
2020 Expanding the molecular spectrum and the neurological phenotype related to CAMTA1 variants. Clinical genetics 10 33131045
2014 CAMTA1 immunostaining is not useful in differentiating epithelioid hemangioendothelioma from its potential mimickers. Turk patoloji dergisi 10 25110239
2023 The oncogenic fusion protein TAZ::CAMTA1 promotes genomic instability and senescence through hypertranscription. Communications biology 9 37980390
2016 CANPMR syndrome and chromosome 1p32-p31 deletion syndrome coexist in two related individuals affected by simultaneous haplo-insufficiency of CAMTA1 and NIFA genes. Molecular cytogenetics 9 26848311
2022 CAMTA1 gene affects the ischemia-reperfusion injury by regulating CCND1. Frontiers in cellular neuroscience 8 36159397
2022 CAMTA1-PPP3CA-NFATc4 multi-protein complex mediates the resistance of colorectal cancer to oxaliplatin. Cell death discovery 6 35332122
2022 The role of Calmodulin Binding Transcription Activator 1 (CAMTA1) gene and its putative genetic partners in the human nervous system. Psychogeriatrics : the official journal of the Japanese Psychogeriatric Society 5 35949142
2020 Fluorescence in situ hybridization for WWTR1-CAMTA1 has higher sensitivity and specificity for epithelioid hemangioendothelioma diagnosis. American journal of translational research 5 32913529
2018 A Case of Large Meningeal Epithelioid Hemangioendothelioma With WWTR1-CAMTA1 Gene Rearrangement and Slow Growth Over 15 Years. Journal of neuropathology and experimental neurology 5 30085199
2013 Neuropsychological and neuroimaging phenotype induced by a CAMTA1 mutation. Brain & development 5 24145135
2023 MBNL1-AS1 Promotes Hypoxia-Induced Myocardial Infarction via the miR-132-3p/RAB14/CAMTA1 Axis. Oxidative medicine and cellular longevity 4 36785792
2023 Codonopsis pilosula polysaccharide alleviates rotenone-induced murine brain organoids death through downregulation of gene body DNA methylation modification in the ZIC4/PGM5/CAMTA1 axis. Biochemistry and biophysics reports 4 38074999
2013 Epithelioid hemangioendothelioma with extensive cystic change and CAMTA1 rearrangement. Pathology international 4 24134632
2025 CAMTA1-immunonegative epithelioid hemangioendotheliomas of the liver: a clinicopathological and molecular analysis of seven cases. Frontiers in oncology 3 40040722
2024 Clinical and genetic features of dominant Essential Tremor in Tuscany, Italy: FUS, CAMTA1, ATXN1 and beyond. Journal of the neurological sciences 3 38626532
2023 CAMTA1-related disorder: Phenotypic and molecular characterization of 26 new individuals and literature review. Clinical genetics 3 38044714
2024 Primary pulmonary epithelioid hemangioendothelioma metastatic to the pleura and mediastinal lymph node with a prominent rhabdoid cytomorphology showing CAMTA1::WWTR1 fusion and novel PRDM1 and TNFRSF14 mutations. Cytopathology : official journal of the British Society for Clinical Cytology 2 38943251
2024 Circ-CAMTA1 regulated by Ca2+ influx inhibited pyruvate carboxylase activity and modulate T cell function in patients with systemic lupus erythematosus. Arthritis research & therapy 2 39473004
2024 [MiR-132-3p negatively regulates CAMTA1 to promote Schwann cell proliferation and migration and alleviates I-125 seeds-induced exacerbation of facial nerve injury in rats]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 1 38597449
2026 Hypoxia‑induced exosomal CAMTA1 promotes radio‑resistance in MDA‑MB‑231 cells by regulating NRG1 to mediate M2 macrophage polarization. International journal of oncology 0 41891984
2024 Retraction: Long noncoding RNA CAMTA1 promotes proliferation and mobility of the human breast cancer cell line MDA-MB-231 via targeting miR-20b. Oncology research 0 39308521
2021 Novel detection of the CAMTA1-WWTR1 fusion gene in extra-adrenal myelolipoma-like lesion: a case report. Virchows Archiv : an international journal of pathology 0 34231054

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