ArticleCirculation research2018
Down Syndrome Critical Region 1 Gene,
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Article in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model.eLife · 2026Article
- Dysregulated calcium signaling underlies hyposalivation and microbial dysbiosis in Down syndrome.Cell reports · 2026Article
- Article
- Mitochondrial dynamics in neurodevelopment and neurodevelopmental disorders.Nature reviews. Neuroscience · 2026Review
- Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model.bioRxiv : the preprint server for biology · 2026Article
- mTOR inhibition triggers mitochondrial fragmentation in cardiomyocytes through proteosome-dependent prohibitin degradation and OPA-1 cleavage.Cell communication and signaling : CCS · 2025Article
- 17-beta estradiol prevents cardiac myocyte hypertrophy by regulating mitochondrial E3 ubiquitin ligase 1.Cell death & disease · 2025Article
- A dynamic in vitro model of Down syndrome neurogenesis with trisomy 21 gene dosage correction.Science advances · 2024Article
- lncRNA Oip5-as1 inhibits excessive mitochondrial fission in myocardial ischemia/reperfusion injury by modulating DRP1 phosphorylation.Cellular & molecular biology letters · 2024Article
- Gene Expression Studies in Down Syndrome: What Do They Tell Us about Disease Phenotypes?International journal of molecular sciences · 2024Review
- Dysregulated systemic metabolism in a Down syndrome mouse model.Molecular metabolism · 2023Article
- Identification and validation of key genes associated with atrial fibrillation in the elderly.Frontiers in cardiovascular medicine · 2023Article
- Overexpression ofCells · 2022Article
- Article
- Upregulation of RCAN1.4 by HIF1α alleviates OGD-induced inflammatory response in astrocytes.Annals of clinical and translational neurology · 2022Article
- Neuronal Rubicon Represses Extracellular APP/Amyloid β Deposition in Alzheimer's Disease.Cells · 2022Article
- Altered Mitochondrial Opa1-Related Fusion in Mouse Promotes Endothelial Cell Dysfunction and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2022Article
- Evidence of Energy Metabolism Alterations in Cultured Neonatal Astrocytes Derived from the Ts65Dn Mouse Model of Down Syndrome.Brain sciences · 2022Article
- Building the Future Therapies for Down Syndrome: The Third International Conference of the T21 Research Society.Molecular syndromology · 2021Article
- NADCirculation research · 2021Article
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Authors and funding
12 authors at 1 institution in 1 country.
Valentina ParraFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.). beverly.rothermel@utsouthwestern.edu vparra@ciq.uchile.cl.
Francisco AltamiranoFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
Carolina P Hernández-FuentesFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
Dan TongFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
Victoriia KyrychenkoFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
David RotterFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
Zully PedrozoFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
Joseph A HillFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
Verónica EisnerFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
Sergio LavanderoFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
Jay W SchneiderFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.).
Beverly A RothermelFrom the Advanced Center for Chronic Diseases and Center for Molecular Studies of the Cell, Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine (V.P., C.P.H.-F., Z.P., S.L.) and Institute of Biomedical Sciences, School of Medicine (Z.P.), University of Chile, Santiago; Department of Internal Medicine/Cardiology (V.P., F.A., D.T., V.K., D.R., Z.P., J.A.H., S.L., J.W.S., B.A.R.) and Department of Molecular Biology (V.K., J.A.H., B.A.R.), University of Texas Southwestern Medical Center, Dallas; and Department of Molecular and Cellular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago (V.E.). beverly.rothermel@utsouthwestern.edu vparra@ciq.uchile.cl.
The University of Texas Southwestern Medical Center · US
Funding
Modulating Calcineurin Signaling Pathways in MuscleR01HL072016 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI ROTHERMEL, BEVERLY A · 2003 to 2012
$3.7MMechanisms of obesity-dependent alterations in cardiomyocyte metabolismR01HL128215 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2017 to 2020
$1.6MFoxO-dependent Control of Cardiovascular RemodelingR01HL126012 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2016 to 2019
$1.6MCalcineurin's role in circadian regulation of cardiac function and remodelingR01HL097768 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI ROTHERMEL, BEVERLY A · 2009 to 2012
$1.6MSTIM1: Master Regulator of Calcium Homeostasis in CardiomyocytesR01HL120732 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 2013 to 2016
$1.6MUT Southwestern-Progenitor Cell Biology Consortium GroupR03HL096261 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SCHNEIDER, JAY W · 2009 to 2009
$39kNHLBI NIH HHS R01 HL072016NHLBI NIH HHS R01 HL097768NHLBI NIH HHS R01 HL120732NHLBI NIH HHS R01 HL126012NHLBI NIH HHS R01 HL128215NHLBI NIH HHS R03 HL096261
Abstract
rationaleThe regulator of calcineurin 1 (RCAN1) inhibits CN (calcineurin), a Ca
objectiveMitochondria are key mediators of I/R damage. The goal of these studies was to determine the impact of RCAN1 on mitochondrial dynamics and function. METHODS AND
resultsUsing both neonatal and isolated adult cardiomyocytes, we show that, when RCAN1 is depleted, the mitochondrial network is more fragmented because of increased CN-dependent activation of the fission protein, DRP1 (dynamin-1-like). Mitochondria in RCAN1-depleted cardiomyocytes have reduced membrane potential, O
conclusionsRCAN1 helps maintain a more interconnected mitochondrial network, and maintaining appropriate RCAN1 levels is important to human health and disease.
Indexed as
Mitochondrial DynamicsAnimalsCalcium-Binding ProteinsCalpainCell LineCells, CulturedDynaminsHumansIntracellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMitochondria, HeartMuscle ProteinsMyocardial Reperfusion InjuryOxygenCalcium-Binding ProteinsCalpainDnm1l protein, mouseDSCR1 protein, mouseDynaminsIntracellular Signaling Peptides and ProteinsMuscle ProteinsOxygencalcineurincalpainDown syndromeischemia reperfusion injurymitochondriamitochondrial dynamics
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