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Srivastava, Deepak
| Result Number | Material Type | Add to My Shelf Action | Record Details and Options |
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| 1 |
Material Type: Article
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Congenital heart disease-causing Gata4 mutation displays functional deficits in vivoPLoS genetics, 2012-05, Vol.8 (5), p.e1002690 [Peer Reviewed Journal]COPYRIGHT 2012 Public Library of Science ;COPYRIGHT 2012 Public Library of Science ;2012 Misra et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Misra C, Sachan N, McNally CR, Koenig SN, Nichols HA, et al. (2012) Congenital Heart Disease-Causing Gata4 Mutation Displays Functional Deficits In Vivo. PLoS Genet 8(5): e1002690. doi:10.1371/journal.pgen.1002690 ;Misra et al. 2012 ;ISSN: 1553-7404 ;ISSN: 1553-7390 ;EISSN: 1553-7404 ;DOI: 10.1371/journal.pgen.1002690 ;PMID: 22589735Full text available |
| 2 |
Material Type: Book
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Etiology and Morphogenesis of Congenital Heart DiseaseISBN4-431-54627-8;ISBN4-431-54628-6Digital Resources/Online E-Resources |
| 3 |
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Congenital Heart Disease: Entering a New Era of Human GeneticsCirculation research, 2014-02, Vol.114 (4), p.598-599 [Peer Reviewed Journal]2014 American Heart Association, Inc. ;ISSN: 0009-7330 ;EISSN: 1524-4571 ;DOI: 10.1161/CIRCRESAHA.113.303060 ;PMID: 24526674Full text available |
| 4 |
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A transcriptional switch governs fibroblast activation in heart diseaseNature (London), 2021-07, Vol.595 (7867), p.438-443 [Peer Reviewed Journal]2021. The Author(s), under exclusive licence to Springer Nature Limited. ;COPYRIGHT 2021 Nature Publishing Group ;Copyright Nature Publishing Group Jul 15, 2021 ;ISSN: 0028-0836 ;EISSN: 1476-4687 ;DOI: 10.1038/s41586-021-03674-1 ;PMID: 34163071Full text available |
| 5 |
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Contribution of rare inherited and de novo variants in 2,871 congenital heart disease probandsNature genetics, 2017-11, Vol.49 (11), p.1593-1601 [Peer Reviewed Journal]COPYRIGHT 2017 Nature Publishing Group ;COPYRIGHT 2017 Nature Publishing Group ;Copyright Nature Publishing Group Nov 2017 ;ISSN: 1061-4036 ;EISSN: 1546-1718 ;DOI: 10.1038/ng.3970 ;PMID: 28991257Full text available |
| 6 |
Material Type: Book
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Etiology and Morphogenesis of Congenital Heart Disease : From Gene Function and Cellular interaction To Morphologyhttps://creativecommons.org/licenses/by-nc/4.0/legalcode ;ISBN: 9783662488454 ;ISBN: 3662488450 ;ISBN: 9784431546276 ;ISBN: 4431546278 ;EISBN: 9784431546283 ;EISBN: 4431546286 ;DOI: 10.1007/978-4-431-54628-3 ;OCLC: OCN: 953026830 ;OCLC: 953026830 ;OCLC: 1048185765Full text available |
| 7 |
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Genomic analyses implicate noncoding de novo variants in congenital heart diseaseNature genetics, 2020-08, Vol.52 (8), p.769-777 [Peer Reviewed Journal]COPYRIGHT 2020 Nature Publishing Group ;Copyright Nature Publishing Group Aug 2020 ;ISSN: 1061-4036 ;EISSN: 1546-1718 ;DOI: 10.1038/s41588-020-0652-z ;PMID: 32601476Full text available |
| 8 |
Material Type: Article
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Making or Breaking the Heart: From Lineage Determination to MorphogenesisCell, 2006-09, Vol.126 (6), p.1037-1048 [Peer Reviewed Journal]2006 Elsevier Inc. ;ISSN: 0092-8674 ;EISSN: 1097-4172 ;DOI: 10.1016/j.cell.2006.09.003 ;PMID: 16990131Full text available |
| 9 |
Material Type: Article
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Long telomeres protect against age-dependent cardiac disease caused by NOTCH1 haploinsufficiencyThe Journal of clinical investigation, 2017-05, Vol.127 (5), p.1683-1688 [Peer Reviewed Journal]COPYRIGHT 2017 American Society for Clinical Investigation ;Copyright American Society for Clinical Investigation May 2017 ;Copyright © 2017, American Society for Clinical Investigation 2017 American Society for Clinical Investigation ;ISSN: 0021-9738 ;EISSN: 1558-8238 ;DOI: 10.1172/JCI90338 ;PMID: 28346225Full text available |
| 10 |
Material Type: Article
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Mutations in NOTCH1 cause aortic valve diseaseNature, 2005-09, Vol.437 (7056), p.270-274 [Peer Reviewed Journal]2005 INIST-CNRS ;COPYRIGHT 2005 Nature Publishing Group ;Copyright Nature Publishing Group Sep 8, 2005 ;ISSN: 0028-0836 ;EISSN: 1476-4687 ;DOI: 10.1038/nature03940 ;PMID: 16025100 ;CODEN: NATUASFull text available |
| 11 |
Material Type: Article
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Transcription factor protein interactomes reveal genetic determinants in heart diseaseCell, 2022-03, Vol.185 (5), p.794-814.e30 [Peer Reviewed Journal]2022 Elsevier Inc. ;Copyright © 2022 Elsevier Inc. All rights reserved. ;ISSN: 0092-8674 ;EISSN: 1097-4172 ;DOI: 10.1016/j.cell.2022.01.021 ;PMID: 35182466Full text available |
| 12 |
Material Type: Article
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Potential of stem-cell-based therapies for heart diseaseNature, 2006-06, Vol.441 (7097), p.1097-1099 [Peer Reviewed Journal]2006 INIST-CNRS ;COPYRIGHT 2006 Nature Publishing Group ;COPYRIGHT 2006 Nature Publishing Group ;Copyright Nature Publishing Group Jun 29, 2006 ;ISSN: 0028-0836 ;EISSN: 1476-4687 ;EISSN: 1476-4679 ;DOI: 10.1038/nature04961 ;PMID: 16810246 ;CODEN: NATUASFull text available |
| 13 |
Material Type: Article
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Hepatic venous blood and the development of pulmonary arteriovenous malformations in congenital heart diseaseCirculation (New York, N.Y.), 1995-09, Vol.92 (5), p.1217-1222 [Peer Reviewed Journal]1995 INIST-CNRS ;Copyright American Heart Association, Inc. Sep 1, 1995 ;ISSN: 0009-7322 ;EISSN: 1524-4539 ;DOI: 10.1161/01.cir.92.5.1217 ;PMID: 7648668 ;CODEN: CIRCAZFull text available |
| 14 |
Material Type: Article
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Neither cardiac mitochondrial DNA variation nor copy number contribute to congenital heart disease riskAmerican journal of human genetics, 2022-05, Vol.109 (5), p.961-966 [Peer Reviewed Journal]Copyright © 2022. Published by Elsevier Inc. ;2022. 2022 ;ISSN: 0002-9297 ;EISSN: 1537-6605 ;DOI: 10.1016/j.ajhg.2022.03.011 ;PMID: 35397206Full text available |
| 15 |
Material Type: Article
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EM-mosaic detects mosaic point mutations that contribute to congenital heart diseaseGenome medicine, 2020-04, Vol.12 (1), p.42-42, Article 42 [Peer Reviewed Journal]COPYRIGHT 2020 BioMed Central Ltd. ;COPYRIGHT 2020 BioMed Central Ltd. ;2020. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2020 ;ISSN: 1756-994X ;EISSN: 1756-994X ;DOI: 10.1186/s13073-020-00738-1 ;PMID: 32349777Full text available |
| 16 |
Material Type: Article
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Abstract 11332: Integration of Protein Interactome Networks with Congenital Heart Disease Variants Reveals Candidate Disease GenesCirculation (New York, N.Y.), 2021-11, Vol.144 (Suppl_1) [Peer Reviewed Journal]ISSN: 0009-7322 ;EISSN: 1524-4539 ;DOI: 10.1161/circ.144.suppl_1.11332Full text available |
| 17 |
Material Type: Article
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Direct Cardiac Reprogramming: From Developmental Biology to Cardiac RegenerationCirculation research, 2013-09, Vol.113 (7), p.915-921 [Peer Reviewed Journal]2013 American Heart Association, Inc. ;ISSN: 0009-7330 ;EISSN: 1524-4571 ;DOI: 10.1161/CIRCRESAHA.112.300625 ;PMID: 24030021Full text available |
| 18 |
Material Type: Article
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Heart disease An ongoing genetic battle?Nature, 2004-06, Vol.429 (6994), p.819-822 [Peer Reviewed Journal]COPYRIGHT 2004 Nature Publishing Group ;ISSN: 0028-0836 ;EISSN: 1476-4687 ;DOI: 10.1038/429819a ;PMID: 15215849Full text available |
| 19 |
Material Type: Article
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Screening and biochemical analysis of GATA4 sequence variations identified in patients with congenital heart diseaseAmerican journal of medical genetics. Part A, 2007-04, Vol.143A (8), p.817-823 [Peer Reviewed Journal]Copyright © 2007 Wiley‐Liss, Inc. ;2007 INIST-CNRS ;Copyright 2007 Wiley-Liss, Inc. ;ISSN: 1552-4825 ;EISSN: 1552-4833 ;DOI: 10.1002/ajmg.a.31652 ;PMID: 17352393Full text available |
| 20 |
Material Type: Article
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De Novo Damaging Variants, Clinical Phenotypes, and Post-Operative Outcomes in Congenital Heart DiseaseCirculation. Genomic and precision medicine, 2020-08, Vol.13 (4), p.e002836-e002836 [Peer Reviewed Journal]2020 The Authors. 2020 ;ISSN: 2574-8300 ;EISSN: 2574-8300 ;DOI: 10.1161/circgen.119.002836 ;PMID: 32812804Full text available |
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