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  • 1
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    Fzd2 controls branch-point formation in the lung [Developmental Biology] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-08-27
    Description: Changing the morphology of a simple epithelial tube to form a highly ramified branching network requires changes in cell behavior that lead to tissue-wide changes in organ shape. How epithelial cells in branched organs modulate their shape and behavior to promote bending and sculpting of the epithelial sheet is not...
    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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  • 2
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    Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-08-27
    Description: The causes of amyotrophic lateral sclerosis (ALS), a devastating human neurodegenerative disease, are poorly understood, although the protein TDP-43 has been suggested to have a critical role in disease pathogenesis. Here we show that ataxin 2 (ATXN2), a polyglutamine (polyQ) protein mutated in spinocerebellar ataxia type 2, is a potent modifier of TDP-43 toxicity in animal and cellular models. ATXN2 and TDP-43 associate in a complex that depends on RNA. In spinal cord neurons of ALS patients, ATXN2 is abnormally localized; likewise, TDP-43 shows mislocalization in spinocerebellar ataxia type 2. To assess the involvement of ATXN2 in ALS, we analysed the length of the polyQ repeat in the ATXN2 gene in 915 ALS patients. We found that intermediate-length polyQ expansions (27-33 glutamines) in ATXN2 were significantly associated with ALS. These data establish ATXN2 as a relatively common ALS susceptibility gene. Furthermore, these findings indicate that the TDP-43-ATXN2 interaction may be a promising target for therapeutic intervention in ALS and other TDP-43 proteinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2965417/" 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/PMC2965417/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elden, Andrew C -- Kim, Hyung-Jun -- Hart, Michael P -- Chen-Plotkin, Alice S -- Johnson, Brian S -- Fang, Xiaodong -- Armakola, Maria -- Geser, Felix -- Greene, Robert -- Lu, Min Min -- Padmanabhan, Arun -- Clay-Falcone, Dana -- McCluskey, Leo -- Elman, Lauren -- Juhr, Denise -- Gruber, Peter J -- Rub, Udo -- Auburger, Georg -- Trojanowski, John Q -- Lee, Virginia M-Y -- Van Deerlin, Vivianna M -- Bonini, Nancy M -- Gitler, Aaron D -- 1DP2OD004417-01/OD/NIH HHS/ -- 1R01NS065317-01/NS/NINDS NIH HHS/ -- AG-10124/AG/NIA NIH HHS/ -- AG-17586/AG/NIA NIH HHS/ -- DP2 OD004417/OD/NIH HHS/ -- DP2 OD004417-01/OD/NIH HHS/ -- K08 AG-033101-01/AG/NIA NIH HHS/ -- P01 AG-09215/AG/NIA NIH HHS/ -- R01 NS065317/NS/NINDS NIH HHS/ -- R01 NS065317-01/NS/NINDS NIH HHS/ -- R01 NS065317-02/NS/NINDS NIH HHS/ -- R01 NS065317-03/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Aug 26;466(7310):1069-75. doi: 10.1038/nature09320.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20740007" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Amyotrophic Lateral Sclerosis/*genetics ; Animals ; Ataxins ; Cell Line ; DNA-Binding Proteins/metabolism/toxicity ; Drosophila/drug effects/genetics ; Female ; *Genetic Predisposition to Disease ; Humans ; Male ; Middle Aged ; Nerve Tissue Proteins/*genetics/*metabolism ; Neurons/pathology ; Peptides/chemistry/*genetics ; Repetitive Sequences, Amino Acid/*genetics ; Risk Factors ; Saccharomyces cerevisiae/drug effects/genetics/metabolism ; Young Adult
    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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  • 3
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    Hedgehog actively maintains adult lung quiescence and regulates repair and regeneration (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-10-06
    Description: Postnatal tissue quiescence is thought to be a default state in the absence of a proliferative stimulus such as injury. Although previous studies have demonstrated that certain embryonic developmental programs are reactivated aberrantly in adult organs to drive repair and regeneration, it is not well understood how quiescence is maintained in organs such as the lung, which displays a remarkably low level of cellular turnover. Here we demonstrate that quiescence in the adult lung is an actively maintained state and is regulated by hedgehog signalling. Epithelial-specific deletion of sonic hedgehog (Shh) during postnatal homeostasis in the murine lung results in a proliferative expansion of the adjacent lung mesenchyme. Hedgehog signalling is initially downregulated during the acute phase of epithelial injury as the mesenchyme proliferates in response, but returns to baseline during injury resolution as quiescence is restored. Activation of hedgehog during acute epithelial injury attenuates the proliferative expansion of the lung mesenchyme, whereas inactivation of hedgehog signalling prevents the restoration of quiescence during injury resolution. Finally, we show that hedgehog also regulates epithelial quiescence and regeneration in response to injury via a mesenchymal feedback mechanism. These results demonstrate that epithelial-mesenchymal interactions coordinated by hedgehog actively maintain postnatal tissue homeostasis, and deregulation of hedgehog during injury leads to aberrant repair and regeneration in the lung.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4713039/" 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/PMC4713039/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peng, Tien -- Frank, David B -- Kadzik, Rachel S -- Morley, Michael P -- Rathi, Komal S -- Wang, Tao -- Zhou, Su -- Cheng, Lan -- Lu, Min Min -- Morrisey, Edward E -- HL087825/HL/NHLBI NIH HHS/ -- HL100405/HL/NHLBI NIH HHS/ -- HL110942/HL/NHLBI NIH HHS/ -- K08-HL121146/HL/NHLBI NIH HHS/ -- R01 HL087825/HL/NHLBI NIH HHS/ -- T32 HL007915/HL/NHLBI NIH HHS/ -- U01 HL100405/HL/NHLBI NIH HHS/ -- U01 HL110942/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Oct 22;526(7574):578-82. doi: 10.1038/nature14984. Epub 2015 Oct 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Pediatrics, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Penn Center for Pulmonary Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Penn Cardiovascular Institute, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Penn Institute for Regenerative Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26436454" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Down-Regulation ; Epithelial Cells/cytology/metabolism/pathology ; Feedback, Physiological ; Hedgehog Proteins/deficiency/genetics/*metabolism ; Homeostasis ; Lung/*cytology/*metabolism/pathology ; Lung Injury/*metabolism/*pathology ; Male ; Mesoderm/cytology/metabolism ; Mice ; Paracrine Communication ; *Regeneration ; *Wound Healing
    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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  • 4
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    Interconversion between intestinal stem cell populations in distinct niches (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-15
    Description: Intestinal epithelial stem cell identity and location have been the subject of substantial research. Cells in the +4 niche are slow-cycling and label-retaining, whereas a different stem cell niche located at the crypt base is occupied by crypt base columnar (CBC) cells. CBCs are distinct from +4 cells, and the relationship between them is unknown, though both give rise to all intestinal epithelial lineages. We demonstrate that Hopx, an atypical homeobox protein, is a specific marker of +4 cells. Hopx-expressing cells give rise to CBCs and all mature intestinal epithelial lineages. Conversely, CBCs can give rise to +4 Hopx-positive cells. These findings demonstrate a bidirectional lineage relationship between active and quiescent stem cells in their niches.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705713/" 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/PMC3705713/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, Norifumi -- Jain, Rajan -- LeBoeuf, Matthew R -- Wang, Qiaohong -- Lu, Min Min -- Epstein, Jonathan A -- R01 HL071546/HL/NHLBI NIH HHS/ -- U01 HL100405/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 9;334(6061):1420-4. doi: 10.1126/science.1213214. Epub 2011 Nov 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22075725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Epithelial Cells/*cytology ; Homeodomain Proteins/analysis/genetics ; Intestinal Mucosa/*cytology/drug effects ; Intestine, Small/*cytology/drug effects ; Mice ; Models, Biological ; Multipotent Stem Cells/*cytology/physiology ; Paneth Cells/cytology ; *Stem Cell Niche ; Tamoxifen/pharmacology
    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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    Advanced cardiac morphogenesis does not require heart tube fusion (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-14
    Description: The bilateral cardiac mesoderm migrates from the lateral region of the embryo to the ventral midline, where it fuses to form the primitive heart tube. It is generally accepted that migration and fusion are essential for subsequent stages of cardiac morphogenesis. We present evidence that, in Foxp4 mutant embryonic mice, each bilateral heart-forming region is capable of developing into a highly differentiated four-chambered mammalian heart in the absence of midline fusion. These data demonstrate that left-right chamber specification, cardiac looping, septation, cardiac myocyte differentiation, and endocardial cushion formation are preprogrammed in the precardiac mesoderm and do not require midline positional identity or heart tube fusion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Shanru -- Zhou, Deying -- Lu, Min Min -- Morrisey, Edward E -- HL71589/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Sep 10;305(5690):1619-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15361625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Atrial Natriuretic Factor/metabolism ; Basic Helix-Loop-Helix Transcription Factors ; Body Patterning ; Cell Differentiation ; DNA-Binding Proteins/genetics/metabolism ; Endocardium/embryology ; Endoderm/cytology/metabolism ; Forkhead Transcription Factors ; Gene Targeting ; Heart/*embryology ; Heart Atria/embryology ; Heart Ventricles/embryology ; In Situ Hybridization ; Mesoderm/physiology ; Mice ; Morphogenesis ; Mutation ; Myocytes, Cardiac/*cytology ; Proto-Oncogene Proteins c-myc/metabolism ; Transcription Factors/metabolism ; 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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  • 6
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    Regulation of blood and lymphatic vascular separation by signaling proteins SLP-76 and Syk (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-11
    Description: Lymphatic vessels develop from specialized endothelial cells in preexisting blood vessels, but the molecular signals that regulate this separation are unknown. Here we identify a failure to separate emerging lymphatic vessels from blood vessels in mice lacking the hematopoietic signaling protein SLP-76 or Syk. Blood-lymphatic connections lead to embryonic hemorrhage and arteriovenous shunting. Expression of slp-76 could not be detected in endothelial cells, and blood-filled lymphatics also arose in wild-type mice reconstituted with SLP-76-deficient bone marrow. These studies reveal a hematopoietic signaling pathway required for separation of the two major vascular networks in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2982679/" 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/PMC2982679/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abtahian, Farhad -- Guerriero, Anastasia -- Sebzda, Eric -- Lu, Min-Min -- Zhou, Rong -- Mocsai, Attila -- Myers, Erin E -- Huang, Bin -- Jackson, David G -- Ferrari, Victor A -- Tybulewicz, Victor -- Lowell, Clifford A -- Lepore, John J -- Koretzky, Gary A -- Kahn, Mark L -- R21 EB002473/EB/NIBIB NIH HHS/ -- R21 EB002473-02/EB/NIBIB NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 10;299(5604):247-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signal Transduction Program, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12522250" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Animals ; Animals, Newborn ; Antigens, CD34/metabolism ; Blood Vessels/abnormalities/cytology/*embryology/metabolism ; Bone Marrow Cells/cytology/physiology ; Bone Marrow Transplantation ; Dextrans ; Endothelium, Lymphatic/cytology/metabolism ; Endothelium, Vascular/cytology/metabolism ; Enzyme Precursors/genetics/*metabolism ; Fluorescein-5-isothiocyanate/*analogs & derivatives ; Glycoproteins/metabolism ; Hemorrhage ; Homeodomain Proteins/genetics/metabolism ; Intestines/blood supply ; Intracellular Signaling Peptides and Proteins ; Lymphatic System/abnormalities/cytology/*embryology/metabolism ; Mesenteric Arteries/abnormalities ; Mesenteric Veins/abnormalities ; Mice ; Phosphoproteins/genetics/*metabolism ; Protein-Tyrosine Kinases/genetics/*metabolism ; *Signal Transduction ; Stem Cells/physiology ; Tumor Suppressor Proteins ; Vascular Endothelial Growth Factor Receptor-3/metabolism ; Veins/cytology/embryology/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Coordination of heart and lung co-development by a multipotent cardiopulmonary progenitor (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-07-23
    Description: Co-development of the cardiovascular and pulmonary systems is a recent evolutionary adaption to terrestrial life that couples cardiac output with the gas exchange function of the lung. Here we show that the murine pulmonary vasculature develops even in the absence of lung development. We have identified a population of multipotent cardiopulmonary mesoderm progenitors (CPPs) within the posterior pole of the heart that are marked by the expression of Wnt2, Gli1 and Isl1. We show that CPPs arise from cardiac progenitors before lung development. Lineage tracing and clonal analysis demonstrates that CPPs generate the mesoderm lineages within the cardiac inflow tract and lung including cardiomyocytes, pulmonary vascular and airway smooth muscle, proximal vascular endothelium, and pericyte-like cells. CPPs are regulated by hedgehog expression from the foregut endoderm, which is required for connection of the pulmonary vasculature to the heart. Together, these studies identify a novel population of multipotent cardiopulmonary progenitors that coordinates heart and lung co-development that is required for adaptation to terrestrial existence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3758448/" 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/PMC3758448/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peng, Tien -- Tian, Ying -- Boogerd, Cornelis J -- Lu, Min Min -- Kadzik, Rachel S -- Stewart, Kathleen M -- Evans, Sylvia M -- Morrisey, Edward E -- HL087825/HL/NHLBI NIH HHS/ -- HL100405/HL/NHLBI NIH HHS/ -- HL110942/HL/NHLBI NIH HHS/ -- HL117649/HL/NHLBI NIH HHS/ -- P30 NS047101/NS/NINDS NIH HHS/ -- R01 HL074066/HL/NHLBI NIH HHS/ -- R01 HL087825/HL/NHLBI NIH HHS/ -- T32 HL07586-23/HL/NHLBI NIH HHS/ -- U01 HL107442/HL/NHLBI NIH HHS/ -- England -- Nature. 2013 Aug 29;500(7464):589-92. doi: 10.1038/nature12358. Epub 2013 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23873040" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiac Output ; Cell Lineage ; Endoderm/metabolism ; Heart/anatomy & histology/*embryology ; Hedgehog Proteins/metabolism ; Kruppel-Like Transcription Factors/metabolism ; LIM-Homeodomain Proteins/metabolism ; Lung/blood supply/*cytology/*embryology ; Mesoderm/cytology ; Mice ; Models, Animal ; Multipotent Stem Cells/*cytology ; Myoblasts, Cardiac/*cytology ; *Organogenesis ; Pericytes/cytology ; Pulmonary Gas Exchange ; Transcription Factors/metabolism ; Wnt Proteins/metabolism
    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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  • 8
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    HEART DEVELOPMENT. Integration of Bmp and Wnt signaling by Hopx specifies commitment of cardiomyoblasts (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-06-27
    Description: Cardiac progenitor cells are multipotent and give rise to cardiac endothelium, smooth muscle, and cardiomyocytes. Here, we define and characterize the cardiomyoblast intermediate that is committed to the cardiomyocyte fate, and we characterize the niche signals that regulate commitment. Cardiomyoblasts express Hopx, which functions to coordinate local Bmp signals to inhibit the Wnt pathway, thus promoting cardiomyogenesis. Hopx integrates Bmp and Wnt signaling by physically interacting with activated Smads and repressing Wnt genes. The identification of the committed cardiomyoblast that retains proliferative potential will inform cardiac regenerative therapeutics. In addition, Bmp signals characterize adult stem cell niches in other tissues where Hopx-mediated inhibition of Wnt is likely to contribute to stem cell quiescence and to explain the role of Hopx as a tumor suppressor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jain, Rajan -- Li, Deqiang -- Gupta, Mudit -- Manderfield, Lauren J -- Ifkovits, Jamie L -- Wang, Qiaohong -- Liu, Feiyan -- Liu, Ying -- Poleshko, Andrey -- Padmanabhan, Arun -- Raum, Jeffrey C -- Li, Li -- Morrisey, Edward E -- Lu, Min Min -- Won, Kyoung-Jae -- Epstein, Jonathan A -- 5-T32-GM-007170/GM/NIGMS NIH HHS/ -- K08 HL119553/HL/NHLBI NIH HHS/ -- K08 HL119553-02/HL/NHLBI NIH HHS/ -- R01 HL071546/HL/NHLBI NIH HHS/ -- U01 HL100405/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2015 Jun 26;348(6242):aaa6071. doi: 10.1126/science.aaa6071.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Penn Cardiovascular Institute, Institute of Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Genetics, Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Cell and Developmental Biology, Penn Cardiovascular Institute, Institute of Regenerative Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. epsteinj@upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26113728" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bone Morphogenetic Proteins/genetics/*metabolism ; Cell Lineage/genetics ; Gene Expression ; *Gene Expression Regulation, Developmental ; Heart/*embryology ; Homeodomain Proteins/genetics/*metabolism ; Mice ; Mice, Mutant Strains ; Molecular Sequence Data ; Muscle, Smooth/cytology/metabolism ; Myoblasts, Cardiac/cytology/*metabolism ; Organogenesis/*genetics ; Stem Cell Niche/genetics/physiology ; Tumor Suppressor Proteins/genetics/*metabolism ; Wnt Signaling Pathway/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Electronic Resource
    Electronic Resource
    Cloning and expression analysis of murine lupin, a member of a novel gene family that is conserved through evolution and associated with Lupus inclusions (2000)
    Springer
    Development genes and evolution 210 (2000), S. 512-517 
    Details
    ISSN: 1432-041X
    Keywords: Key words Systemic lupus erythematosis ; AIDS ; HIV ; p36 ; Cytoplasmic inclusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  We describe here the first full-length sequence of a member of a novel gene family encoding a protein in the mouse that we call Lupin. Lupin is homologous to a human protein previously called p36, which was purified from α-interferon-treated cells that formed lupus inclusions. Lupus inclusions are dense intracellular deposits found in endothelial cells and lymphocytes of patients with systemic lupus erythematosis and AIDS. Proteins closely related to Lupin exist in evolutionarily divergent species including Caenorhabditis elegans, Drosophila and zebrafish. At least one other lupin-related gene is expressed in the mouse and in man. Lupin is expressed in mouse embryos and adults, notably in liver, spleen, central nervous system, multiple epithelia and all types of muscle. In skeletal muscle, expression analysis suggests that Lupin associates with the contractile apparatus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004270000093
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  • 10
    Electronic Resource
    Electronic Resource
    Postnatal isl1 + cardioblasts enter fully differentiated cardiomyocyte lineages (2007)
    [s.l.] : Nature Publishing Group
    Nature 446 (2007), S. 934-934 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Nature 433, 647–653 (2005) It has been drawn to Nature’s attention that K.R.C., S.E., C.-L.C., A.M. and K.-L.L. filed a patent application relevant to this work (patent number WO 2004/070013) in 2004, which should therefore have ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature05790
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