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  • 1
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    Control of mouse cardiac morphogenesis and myogenesis by transcription factor MEF2C (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-30
    Description: Members of the myocyte enhancer factor-2 (MEF2) family of MADS (MCM1, agamous, deficiens, serum response factor)-box transcription factors bind an A-T-rich DNA sequence associated with muscle-specific genes. The murine MEF2C gene is expressed in heart precursor cells before formation of the linear heart tube. In mice homozygous for a null mutation of MEF2C, the heart tube did not undergo looping morphogenesis, the future right ventricle did not form, and a subset of cardiac muscle genes was not expressed. The absence of the right ventricular region of the mutant heart correlated with down-regulation of the dHAND gene, which encodes a basic helix-loop-helix transcription factor required for cardiac morphogenesis. Thus, MEF2C is an essential regulator of cardiac myogenesis and right ventricular development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4437729/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4437729/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Q -- Schwarz, J -- Bucana, C -- Olson, E N -- R01 HL053351/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 May 30;276(5317):1404-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Oncology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9148, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9162005" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/metabolism ; Animals ; Gene Expression Regulation, Developmental ; Gene Targeting ; Heart/*embryology ; Heart Ventricles/cytology/embryology ; In Situ Hybridization ; MEF2 Transcription Factors ; Mice ; Mice, Inbred C57BL ; *Morphogenesis/genetics/physiology ; Mutagenesis ; Myocardium/cytology ; Myogenic Regulatory Factors/genetics/*physiology ; Stem Cells
    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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    Type VII collagen is required for Ras-driven human epidermal tumorigenesis (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-19
    Description: Type VII collagen defects cause recessive dystrophic epidermolysis bullosa (RDEB), a blistering skin disorder often accompanied by epidermal cancers. To study the role of collagen VII in these cancers, we examined Ras-driven tumorigenesis in RDEB keratinocytes. Cells devoid of collagen VII did not form tumors in mice, whereas those retaining a specific collagen VII fragment (the amino-terminal noncollagenous domain NC1) were tumorigenic. Forced NC1 expression restored tumorigenicity to collagen VII-null epidermis in a non-cell-autonomous fashion. Fibronectin-like sequences within NC1 (FNC1) promoted tumor cell invasion in a laminin 5-dependent manner and were required for tumorigenesis. Tumor-stroma interactions mediated by collagen VII thus promote neoplasia, and retention of NC1 sequences in a subset of RDEB patients may contribute to their increased susceptibility to squamous cell carcinoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ortiz-Urda, Susana -- Garcia, John -- Green, Cheryl L -- Chen, Lei -- Lin, Qun -- Veitch, Dallas P -- Sakai, Lynn Y -- Lee, Hyangkyu -- Marinkovich, M Peter -- Khavari, Paul A -- AR43799/AR/NIAMS NIH HHS/ -- AR44012/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1773-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉VA Palo Alto Healthcare System, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774758" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Antibodies/immunology ; Apoptosis ; Carcinoma, Squamous Cell/etiology/*physiopathology ; Cell Adhesion Molecules/immunology/metabolism ; Cell Proliferation ; Cell Transformation, Neoplastic ; Child ; Collagen Type VII/chemistry/*genetics/immunology/*physiology ; Disease Susceptibility ; Epidermolysis Bullosa Dystrophica/complications/*genetics/metabolism/pathology ; Female ; *Genes, ras ; Humans ; I-kappa B Proteins/genetics/metabolism ; Keratinocytes/*metabolism/pathology ; Male ; Mice ; Mice, SCID ; Middle Aged ; Mutation ; Neoplasm Invasiveness ; Protein Structure, Tertiary ; Skin Neoplasms/etiology/pathology/*physiopathology
    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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    Human adult germline stem cells in question (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-06-26
    Description: Conrad et al. have generated human adult germline stem cells (haGSCs) from human testicular tissue, which they claim have similar pluripotent properties to human embryonic stem cells (hESCs). Here we investigate the pluripotency of haGSCs by using global gene-expression analysis based on their gene array data and comparing the expression of pluripotency marker genes in haGSCs and hESCs, and in haGSCs and human fibroblast samples derived from different laboratories, including our own. We find that haGSCs and fibroblasts have a similar gene-expression profile, but that haGSCs and hESCs do not. The pluripotency of Conrad and colleagues' haGSCs is therefore called into question.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ko, Kinarm -- Arauzo-Bravo, Marcos J -- Tapia, Natalia -- Kim, Julee -- Lin, Qiong -- Bernemann, Christof -- Han, Dong Wook -- Gentile, Luca -- Reinhardt, Peter -- Greber, Boris -- Schneider, Rebekka K -- Kliesch, Sabine -- Zenke, Martin -- Scholer, Hans R -- England -- Nature. 2010 Jun 24;465(7301):E1; discussion E3. doi: 10.1038/nature09089.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Munster 48149, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20577160" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Biomarkers/analysis ; Biopsy ; Cells, Cultured ; Embryonic Stem Cells/cytology/metabolism ; Fibroblasts/cytology/metabolism ; Gene Expression Profiling ; Germ Cells/*cytology ; Humans ; Induced Pluripotent Stem Cells/*cytology/*metabolism ; Male ; Mice ; RNA, Messenger/analysis/genetics ; Reproducibility of Results ; Testis/cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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