Literature DB >> 18601931

Genetic approaches for changing the heart and dissecting complex syndromes.

Michael-Alice Moga1, Tomoki Nakamura, Jeffrey Robbins.   

Abstract

The genetic, biochemical and molecular bases of human cardiac disease have been the focus of extensive research efforts for many years. Early animal models of cardiovascular disease used pharmacologic or surgical interventions, or took advantage of naturally occurring genetic abnormalities and the data obtained were largely correlative. The inability to directly alter an organism's genetic makeup and cellular protein content and accurately measure the results of that manipulation precluded rigorous examination of true cause-effect and structure-function relationships. Directed genetic manipulation in the mouse gave researchers the ability to modify and control the mammalian heart's protein content, resulting in the rational design of models that could provide critical links between the mutated or absent protein and disease. Two techniques that have proven particularly useful are transgenesis, which involves the random insertion of ectopic genetic material of interest into a "host" genome, and gene targeting, which utilizes homologous recombination at a pre-selected locus. Initially, transgenesis and gene targeting were used to examine systemic loss-of-function and gain-of-function, respectively, but further refinements in both techniques have allowed for investigations of organ-specific, cell type-specific, developmental stage-sensitive and dose-dependent effects. Genetically engineered animal models of pediatric and adult cardiac disease have proven that, when used appropriately, these tools have the power to extend mere observation to the establishment of true causative proof. We illustrate the power of the general approach by showing how genetically engineered mouse models can define the precise signaling pathways that are affected by the gain-of-function mutation that underlies Noonan syndrome. Increasingly precise and modifiable animal models of human cardiac disease will allow researchers to determine not only pathogenesis, but also guide treatment and the development of novel therapies.

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Year:  2008        PMID: 18601931      PMCID: PMC2562559          DOI: 10.1016/j.yjmcc.2008.06.002

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN: 0022-2828            Impact factor:   5.000


  104 in total

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Authors:  M Golam Mohi; Benjamin G Neel
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Review 3.  How do Shp2 mutations that oppositely influence its biochemical activity result in syndromes with overlapping symptoms?

Authors:  T Edouard; A Montagner; M Dance; F Conte; A Yart; B Parfait; M Tauber; J P Salles; P Raynal
Journal:  Cell Mol Life Sci       Date:  2007-07       Impact factor: 9.261

4.  Gene silencing by double-stranded RNA.

Authors:  Andrew Z Fire
Journal:  Cell Death Differ       Date:  2007-12       Impact factor: 15.828

5.  PTPN11 is the first identified proto-oncogene that encodes a tyrosine phosphatase.

Authors:  Rebecca J Chan; Gen-Sheng Feng
Journal:  Blood       Date:  2006-10-19       Impact factor: 22.113

6.  Germline gain-of-function mutations in SOS1 cause Noonan syndrome.

Authors:  Amy E Roberts; Toshiyuki Araki; Kenneth D Swanson; Kate T Montgomery; Taryn A Schiripo; Victoria A Joshi; Li Li; Yosuf Yassin; Alex M Tamburino; Benjamin G Neel; Raju S Kucherlapati
Journal:  Nat Genet       Date:  2006-12-03       Impact factor: 38.330

7.  Dysregulation of cardiogenesis, cardiac conduction, and cell cycle in mice lacking miRNA-1-2.

Authors:  Yong Zhao; Joshua F Ransom; Ankang Li; Vasanth Vedantham; Morgan von Drehle; Alecia N Muth; Takatoshi Tsuchihashi; Michael T McManus; Robert J Schwartz; Deepak Srivastava
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8.  Mediating ERK 1/2 signaling rescues congenital heart defects in a mouse model of Noonan syndrome.

Authors:  Tomoki Nakamura; Melissa Colbert; Maike Krenz; Jeffery D Molkentin; Harvey S Hahn; Gerald W Dorn; Jeffrey Robbins
Journal:  J Clin Invest       Date:  2007-08       Impact factor: 14.808

9.  Gain-of-function SOS1 mutations cause a distinctive form of Noonan syndrome.

Authors:  Marco Tartaglia; Len A Pennacchio; Chen Zhao; Kamlesh K Yadav; Valentina Fodale; Anna Sarkozy; Bhaswati Pandit; Kimihiko Oishi; Simone Martinelli; Wendy Schackwitz; Anna Ustaszewska; Joel Martin; James Bristow; Claudio Carta; Francesca Lepri; Cinzia Neri; Isabella Vasta; Kate Gibson; Cynthia J Curry; Juan Pedro López Siguero; Maria Cristina Digilio; Giuseppe Zampino; Bruno Dallapiccola; Dafna Bar-Sagi; Bruce D Gelb
Journal:  Nat Genet       Date:  2006-12-13       Impact factor: 38.330

Review 10.  Cardiovascular development and the colonizing cardiac neural crest lineage.

Authors:  Paige Snider; Michael Olaopa; Anthony B Firulli; Simon J Conway
Journal:  ScientificWorldJournal       Date:  2007-07-03
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  7 in total

Review 1.  Cardiac-specific inducible and conditional gene targeting in mice.

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Review 2.  Vascular smooth muscle phenotypic diversity and function.

Authors:  Steven A Fisher
Journal:  Physiol Genomics       Date:  2010-08-24       Impact factor: 3.107

Review 3.  Cardiotoxicity of kinase inhibitors: the prediction and translation of preclinical models to clinical outcomes.

Authors:  Thomas Force; Kyle L Kolaja
Journal:  Nat Rev Drug Discov       Date:  2011-02       Impact factor: 84.694

Review 4.  Probing human cardiovascular congenital disease using transgenic mouse models.

Authors:  Paige Snider; Simon J Conway
Journal:  Prog Mol Biol Transl Sci       Date:  2011       Impact factor: 3.622

Review 5.  Matrix-dependent perturbation of TGFβ signaling and disease.

Authors:  Jefferson J Doyle; Elizabeth E Gerber; Harry C Dietz
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6.  Cardiac-specific, inducible ClC-3 gene deletion eliminates native volume-sensitive chloride channels and produces myocardial hypertrophy in adult mice.

Authors:  Dazhi Xiong; Nathanael S Heyman; Judith Airey; Mi Zhang; Cherie A Singer; Shanti Rawat; Linda Ye; Rebecca Evans; Dean J Burkin; Honglin Tian; Diana T McCloskey; Maria Valencik; Fiona C Britton; Dayue Duan; Joseph R Hume
Journal:  J Mol Cell Cardiol       Date:  2009-07-15       Impact factor: 5.000

Review 7.  With great power comes great responsibility: using mouse genetics to study cardiac hypertrophy and failure.

Authors:  Jeffery D Molkentin; Jeffrey Robbins
Journal:  J Mol Cell Cardiol       Date:  2008-09-19       Impact factor: 5.000

  7 in total

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