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  • 1
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    Actin mutations in dilated cardiomyopathy, a heritable form of heart failure (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: To test the hypothesis that actin dysfunction leads to heart failure, patients with hereditary idiopathic dilated cardiomyopathy (IDC) were examined for mutations in the cardiac actin gene (ACTC). Missense mutations in ACTC that cosegregate with IDC were identified in two unrelated families. Both mutations affect universally conserved amino acids in domains of actin that attach to Z bands and intercalated discs. Coupled with previous data showing that dystrophin mutations also cause dilated cardiomyopathy, these results raise the possibility that defective transmission of force in cardiac myocytes is a mechanism underlying heart failure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, T M -- Michels, V V -- Thibodeau, S N -- Tai, Y S -- Keating, M T -- 5-P50-HL-53773/HL/NHLBI NIH HHS/ -- M01-RR00064/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1998 May 1;280(5364):750-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Division of Cardiology, University of Utah Health Sciences Center, Salt Lake City, UT 84112, USA. timo@howard.genetics.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9563954" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/chemistry/*genetics/physiology ; Adolescent ; Adult ; Cardiomyopathy, Dilated/*genetics/metabolism/pathology ; Child ; Child, Preschool ; Chromosomes, Human, Pair 15 ; Exons ; Female ; Heart/physiopathology ; Humans ; Male ; *Mutation ; Myocardium/chemistry/pathology ; Pedigree ; Phenotype ; Polymorphism, Single-Stranded Conformational ; Protein Conformation ; Sarcomeres/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Heart regeneration in zebrafish (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-12-14
    Description: Cardiac injury in mammals and amphibians typically leads to scarring, with minimal regeneration of heart muscle. Here, we demonstrate histologically that zebrafish fully regenerate hearts within 2 months of 20% ventricular resection. Regeneration occurs through robust proliferation of cardiomyocytes localized at the leading epicardial edge of the new myocardium. The hearts of zebrafish with mutations in the Mps1 mitotic checkpoint kinase, a critical cell cycle regulator, failed to regenerate and formed scars. Thus, injury-induced cardiomyocyte proliferation in zebrafish can overcome scar formation, allowing cardiac muscle regeneration. These findings indicate that zebrafish will be useful for genetically dissecting the molecular mechanisms of cardiac regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poss, Kenneth D -- Wilson, Lindsay G -- Keating, Mark T -- New York, N.Y. -- Science. 2002 Dec 13;298(5601):2188-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Howard Hughes Medical Institute, Harvard Medical School, Children's Hospital, 320 Longwood Avenue, Boston, MA 02115, USA. kposs@enders.tch.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12481136" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Coagulation ; Bromodeoxyuridine/metabolism ; *Cell Division ; Collagen/analysis ; Fibrin ; Fibrosis ; Gene Expression Regulation ; Heart/*physiology ; Heart Injuries/pathology/physiopathology ; Heart Ventricles/pathology/surgery ; Mitosis ; Models, Biological ; Mutation ; Myocardial Contraction ; Myocardium/metabolism/pathology ; Myocytes, Cardiac/*physiology ; Protein-Serine-Threonine Kinases/genetics/physiology ; Protein-Tyrosine Kinases/genetics/physiology ; *Regeneration/genetics/physiology ; Time Factors ; Ventricular Function ; Zebrafish/genetics/*physiology ; *Zebrafish Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Variant of SCN5A sodium channel implicated in risk of cardiac arrhythmia (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-24
    Description: Every year, approximately 450,000 individuals in the United States die suddenly of cardiac arrhythmia. We identified a variant of the cardiac sodium channel gene SCN5A that is associated with arrhythmia in African Americans (P = 0.000028) and linked with arrhythmia risk in an African-American family (P = 0.005). In transfected cells, the variant allele (Y1102) accelerated channel activation, increasing the likelihood of abnormal cardiac repolarization and arrhythmia. About 13.2% of African Americans carry the Y1102 allele. Because Y1102 has a subtle effect on risk, most carriers will never have an arrhythmia. However, Y1102 may be a useful molecular marker for the prediction of arrhythmia susceptibility in the context of additional acquired risk factors such as the use of certain medications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Splawski, Igor -- Timothy, Katherine W -- Tateyama, Michihiro -- Clancy, Colleen E -- Malhotra, Alka -- Beggs, Alan H -- Cappuccio, Francesco P -- Sagnella, Giuseppe A -- Kass, Robert S -- Keating, Mark T -- HL53773/HL/NHLBI NIH HHS/ -- P01 HL 67849/HL/NHLBI NIH HHS/ -- R01 HL 56810/HL/NHLBI NIH HHS/ -- R01 HL48074/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2002 Aug 23;297(5585):1333-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Children's Hospital, Harvard Medical School and Howard Hughes Medical Institute, Boston, MA 02115, USA. igor@enders.tch.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12193783" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; African Continental Ancestry Group/*genetics ; Aged ; Alleles ; Amino Acid Sequence ; Arrhythmias, Cardiac/etiology/*genetics ; Case-Control Studies ; Cell Line ; Child ; Electrocardiography ; Female ; *Genetic Predisposition to Disease ; *Genetic Variation ; Humans ; Ion Channel Gating ; Long QT Syndrome/genetics ; Male ; Middle Aged ; Molecular Sequence Data ; NAV1.5 Voltage-Gated Sodium Channel ; Patch-Clamp Techniques ; Pedigree ; *Point Mutation ; Polymorphism, Single-Stranded Conformational ; Probability ; Risk Factors ; Sodium Channels/chemistry/*genetics/metabolism ; Syncope ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    fgf20 is essential for initiating zebrafish fin regeneration (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-24
    Description: Epimorphic regeneration requires the presence or creation of pluripotent cells capable of reproducing lost organs. Zebrafish fin regeneration is mediated by the creation of blastema cells. Here, we characterize the devoid of blastema (dob) mutant that fails fin regeneration during initial steps, forms abnormal regeneration epithelium, and does not form blastema. This mutation has no impact on embryonic survival. Dob results from an fgf20a null mutation, Y148S. Fgf20a is expressed during initiation of fin regeneration at the epithelial-mesenchymal boundary and later overlaps with the blastema marker msxb. Thus, fgf20a has a regeneration-specific requirement, initiating fin regeneration, and controlling blastema formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitehead, Geoffrey G -- Makino, Shinji -- Lien, Ching-Ling -- Keating, Mark T -- New York, N.Y. -- Science. 2005 Dec 23;310(5756):1957-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Cell Biology, Harvard Medical School, Department of Cardiology, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16373575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Extremities ; Fibroblast Growth Factors/*physiology ; Homeodomain Proteins/biosynthesis ; Male ; Mesoderm ; Mutation ; Regeneration/genetics/*physiology ; Temperature ; Wound Healing ; Zebrafish ; Zebrafish Proteins/biosynthesis/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Molecular genetic insights into cardiovascular disease (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-03
    Description: The recent application of molecular genetic tools to inherited forms of cardiovascular disease has provided important insight into the molecular mechanisms underlying cardiac arrhythmias, cardiomyopathies, and vascular diseases. These studies point to defects in ion channels, contractile proteins, structural proteins, and signaling molecules as key players in disease pathogenesis. Genetic testing is now available for a subset of inherited cardiovascular diseases, and new mechanism-based therapies may be available in the near future. This remarkable progress and the implications it may have for more common forms of cardiovascular disease are reviewed here.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keating, M T -- Sanguinetti, M C -- New York, N.Y. -- Science. 1996 May 3;272(5262):681-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Utah, Salt Lake City, 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614827" target="_blank"〉PubMed〈/a〉
    Keywords: Arrhythmias, Cardiac/diagnosis/*genetics ; Cardiomyopathies/diagnosis/*genetics ; Contractile Proteins/genetics ; Genetic Predisposition to Disease ; Genetic Testing ; Humans ; Ion Channels/genetics ; Mutation ; Myocardium/metabolism ; Prognosis ; Risk Factors ; Vascular Diseases/diagnosis/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Autocrine stimulation of intracellular PDGF receptors in v-sis-transformed cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-02-19
    Description: Autocrine activation of platelet-derived growth factor (PDGF) receptors is the mechanism of transformation by the v-sis oncogene. Since the addition of PDGF does not transform normal cells, autocrine mechanisms may involve unique pathways of receptor activation. In this study autocrine stimulation of the PDGF receptor was observed in v-sis-transformed normal rat kidney (NRK) cells. In contrast to receptor activation in normal cells, autocrine activation of PDGF receptors in v-sis-transformed cells occurred in intracellular compartments, disrupting receptor processing and diverting receptors and their precursors to a chloroquine-sensitive degradation pathway. These findings show that intracellular activation of receptors by autocrine mechanisms may play a role in cell transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keating, M T -- Williams, L T -- 5 K11 HL01556-02/HL/NHLBI NIH HHS/ -- R01 HL32898-04/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Feb 19;239(4842):914-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, San Francisco, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2829358" target="_blank"〉PubMed〈/a〉
    Keywords: Ammonium Chloride/pharmacology ; Animals ; Cell Line, Transformed ; Cell Membrane/metabolism ; Chloroquine/pharmacology ; Half-Life ; Hexosaminidases/pharmacology ; Immunosorbent Techniques ; Molecular Weight ; *Oncogenes ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; Protein Precursors/metabolism ; Rats ; Receptors, Cell Surface/drug effects/*metabolism ; Receptors, Platelet-Derived Growth Factor ; Trypsin/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
    Electronic Resource
    Electronic Resource
    Coassembly of K V LQT1 and minK (IsK) proteins to form cardiac I KS potassium channel (1996)
    [s.l.] : Nature Publishing Group
    Nature 384 (1996), S. 80-83 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The previously described KVLQT1 complementary DNA pre-dicted a protein with six hydrophobia membrane-spanning a-helices (S1-S6), and a typical K+ channel pore-signature sequence11. However, this cDNA seemed to be lacking the amino-terminal domain and was not able to undergo functional expres-sion. ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/384080a0
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    Paper (German National Licenses)
    Fulltext
  • 8
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    Heat-shock protein 60 is required for blastema formation and maintenance during regeneration (2005)
    National Academy of Sciences
    Details
    Publication Date: 2005-10-04
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 9
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    Mammalian myotube dedifferentiation induced by newt regeneration extract (2001)
    National Academy of Sciences
    Details
    Publication Date: 2001-11-20
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Severe arrhythmia disorder caused by cardiac L-type calcium channel mutations (2005)
    National Academy of Sciences
    Details
    Publication Date: 2005-04-29
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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