Down's syndrome suppression of tumour growth and the role of the calcineurin inhibitor DSCR1 - sprookjes - yvandenbroek - TriplyDB

Down's syndrome suppression of tumour growth and the role of the calcineurin inhibitor DSCR1

Down's syndrome suppression of tumour growth and the role of the calcineurin inhibitor DSCR1

http://www.wikidata.org/entity/Q24654657

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VEGF stimulates RCAN1.4 expression in endothelial cells via a pathway requiring Ca2+/calcineurin and protein kinase C-delta Concise review: new paradigms for Down syndrome research using induced pluripotent stem cells: tackling complex human genetic disease Down syndrome: searching for the genetic culprits NFAT promotes carcinoma invasive migration through glypican-6 The Robyn Barst Memorial Lecture: Differences between the fetal, newborn, and adult pulmonary circulations: relevance for age-specific therapies (2013 Grover Conference series)Metastatic mechanisms in follicular cell-derived thyroid cancer Neurological phenotypes for Down syndrome across the life span Synaptic Vesicle Recycling Is Unaffected in the Ts65Dn Mouse Model of Down Syndrome Germinal and Somatic Trisomy 21 Mosaicism: How Common is it, What are the Implications for Individual Carriers and How Does it Come About?Herpesviral G protein-coupled receptors activate NFAT to induce tumor formation via inhibiting the SERCA calcium ATPase Increased Skin Tumor Incidence and Keratinocyte Hyper-Proliferation in a Mouse Model of Down Syndrome The vertebrate RCAN gene family: novel insights into evolution, structure and regulation RCAN1 Overexpression Exacerbates Calcium Overloading-Induced Neuronal Apoptosis Integrative genomics identifies DSCR1 (RCAN1) as a novel NFAT-dependent mediator of phenotypic modulation in vascular smooth muscle cells.A mouse model of Down syndrome trisomic for all human chromosome 21 syntenic regions.Dosage of Dyrk1a shifts cells within a p21-cyclin D1 signaling map to control the decision to enter the cell cycle Yolk sac tumor of the bilateral basal ganglia in a patient with Down syndrome.A mouse embryonic stem cell bank for inducible overexpression of human chromosome 21 genes.Determining frequent patterns of copy number alterations in cancer.The biology, pathogenesis and clinical aspects of acute lymphoblastic leukemia in children with Down syndrome.Behavioral characterization of a mouse model overexpressing DSCR1/ RCAN1.NFAT proteins: emerging roles in cancer progression.Pluripotent stem cells in neurodegenerative and neurodevelopmental diseases.The CCAAT/enhancer binding protein beta (C/EBPbeta) cooperates with NFAT to control expression of the calcineurin regulatory protein RCAN1-4.Massive-scale RNA-Seq analysis of non ribosomal transcriptome in human trisomy 21.Riquiqui and minibrain are regulators of the hippo pathway downstream of Dachsous.Abnormal microRNA expression in Ts65Dn hippocampus and whole blood: contributions to Down syndrome phenotypes.Over-expression of RCAN1 causes Down syndrome-like hippocampal deficits that alter learning and memory.Kaposi's sarcoma herpesvirus K15 protein contributes to virus-induced angiogenesis by recruiting PLCγ1 and activating NFAT1-dependent RCAN1 expression.Transcriptome analysis of the spalax hypoxia survival response includes suppression of apoptosis and tight control of angiogenesis.Cyclosporin A promotes tumor angiogenesis in a calcineurin-independent manner by increasing mitochondrial reactive oxygen species.CXM: a new tool for mapping breast cancer risk in the tumor microenvironment.Evolving toward a human-cell based and multiscale approach to drug discovery for CNS disorders.Opposing roles for calcineurin and ATF3 in squamous skin cancer.Genetic variants within obesity-related genes are associated with tumor recurrence in patients with stages II/III colon cancer.Regulator of calcineurin 1 (RCAN1) facilitates neuronal apoptosis through caspase-3 activation.Survival and morbidity outcomes for very low birth weight infants with Down syndrome NGF upregulates the plasminogen activation inhibitor-1 in neurons via the calcineurin/NFAT pathway and the Down syndrome-related proteins DYRK1A and RCAN1 attenuate this effect DYRK1A protein kinase promotes quiescence and senescence through DREAM complex assembly.Metastatic dormancy and progression in thyroid cancer: targeting cells in the metastatic frontier.

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Down's syndrome suppression of tumour growth and the role of the calcineurin inhibitor DSCR1

http://www.wikidata.org/entity/Q24654657

description

2009 nî lūn-bûn

@nan

2009 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի հունիսին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

Down's syndrome suppression of ...... he calcineurin inhibitor DSCR1

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Down's syndrome suppression of ...... he calcineurin inhibitor DSCR1

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Down's syndrome suppression of ...... he calcineurin inhibitor DSCR1

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Down's syndrome suppression of ...... he calcineurin inhibitor DSCR1

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Down's syndrome suppression of ...... he calcineurin inhibitor DSCR1

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Down's syndrome suppression of ...... he calcineurin inhibitor DSCR1

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Alexander Zaslavsky

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Carmella Britt

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In-Hyun Park

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Judah Folkman

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Julie R Korenberg

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Kwan-Hyuck Baek

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M William Lensch

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Richard J Siarey

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Ryan C Lynch

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Sam S Yoon

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P2860

A genome-wide Drosophila RNAi screen identifies DYRK-family kinases as regulators of NFAT

Disease-specific induced pluripotent stem cells

Down syndrome critical region protein 1 (DSCR1), a novel VEGF target gene that regulates expression of inflammatory markers on activated endothelial cells

Genomic organization, alternative splicing, and expression patterns of the DSCR1 (Down syndrome candidate region 1) gene

Down syndrome candidate region 1,a downstream target of VEGF, participates in endothelial cell migration and angiogenesis

Calcineurin is a common target of cyclophilin-cyclosporin A and FKBP-FK506 complexes

VEGF selectively induces Down syndrome critical region 1 gene expression in endothelial cells: a mechanism for feedback regulation of angiogenesis?

Vascular endothelial growth factor- and thrombin-induced termination factor, Down syndrome critical region-1, attenuates endothelial cell proliferation and angiogenesis

A chromosome 21 critical region does not cause specific Down syndrome phenotypes.

Mortality associated with Down's syndrome in the USA from 1983 to 1997: a population-based study.

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1126-30

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10.1038/NATURE08062

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7250

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459

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George Q. Daley

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2009-06-25T00:00:00Z

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24442822

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1030270548

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19458618

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2724004

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