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  • 1
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    MBNL proteins repress ES-cell-specific alternative splicing and reprogramming (2013)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2013-06-07
    Beschreibung: Previous investigations of the core gene regulatory circuitry that controls the pluripotency of embryonic stem (ES) cells have largely focused on the roles of transcription, chromatin and non-coding RNA regulators. Alternative splicing represents a widely acting mode of gene regulation, yet its role in regulating ES-cell pluripotency and differentiation is poorly understood. Here we identify the muscleblind-like RNA binding proteins, MBNL1 and MBNL2, as conserved and direct negative regulators of a large program of cassette exon alternative splicing events that are differentially regulated between ES cells and other cell types. Knockdown of MBNL proteins in differentiated cells causes switching to an ES-cell-like alternative splicing pattern for approximately half of these events, whereas overexpression of MBNL proteins in ES cells promotes differentiated-cell-like alternative splicing patterns. Among the MBNL-regulated events is an ES-cell-specific alternative splicing switch in the forkhead family transcription factor FOXP1 that controls pluripotency. Consistent with a central and negative regulatory role for MBNL proteins in pluripotency, their knockdown significantly enhances the expression of key pluripotency genes and the formation of induced pluripotent stem cells during somatic cell reprogramming.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3933998/" 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/PMC3933998/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Hong -- Irimia, Manuel -- Ross, P Joel -- Sung, Hoon-Ki -- Alipanahi, Babak -- David, Laurent -- Golipour, Azadeh -- Gabut, Mathieu -- Michael, Iacovos P -- Nachman, Emil N -- Wang, Eric -- Trcka, Dan -- Thompson, Tadeo -- O'Hanlon, Dave -- Slobodeniuc, Valentina -- Barbosa-Morais, Nuno L -- Burge, Christopher B -- Moffat, Jason -- Frey, Brendan J -- Nagy, Andras -- Ellis, James -- Wrana, Jeffrey L -- Blencowe, Benjamin J -- R01 HG002439/HG/NHGRI NIH HHS/ -- R33 MH087908/MH/NIMH NIH HHS/ -- R33MH087908/MH/NIMH NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2013 Jun 13;498(7453):241-5. doi: 10.1038/nature12270. Epub 2013 Jun 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Banting and Best Department of Medical Research and Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23739326" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Alternative Splicing/genetics ; Amino Acid Motifs ; Animals ; Cell Differentiation/genetics ; Cell Line ; *Cellular Reprogramming ; DNA-Binding Proteins/chemistry/deficiency/genetics/*metabolism ; Embryonic Stem Cells/*cytology/*metabolism ; Fibroblasts/cytology/metabolism ; Forkhead Transcription Factors/metabolism ; Gene Knockdown Techniques ; HEK293 Cells ; HeLa Cells ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; Kinetics ; Mice ; RNA-Binding Proteins/chemistry/genetics/*metabolism ; Repressor Proteins/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
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    Malignant Superior Vena Cava Syndrome: A Comparative Cohort Study of Treatment with Covered Stents versus Uncovered Stents [Vascular and Interventional Radiology] (2013)
    The Radiological Society of North America (RSNA)
    In: Radiology
    Details
    Publikationsdatum: 2013-02-22
    Beschreibung: Purpose: To evaluate outcomes of expanded polytetrafluoroethylene (ePTFE)-covered stents and compare them with outcomes of uncovered stents in patients with malignant superior vena cava (SVC) syndrome. Materials and Methods: This study was approved by the institutional review board and written informed consent was obtained. Thirty-seven consecutive patients (33 men, four women; mean age, 60.3 years; range, 35–81 years) who underwent ePTFE-covered stent placement for SVC syndrome were enrolled in a prospective study between January 2009 and September 2011. Their data were compared with retrospective data of 36 consecutive patients (31 men, five women; mean age, 62.3 years; range, 41–81 years) who underwent uncovered stent placement for SVC syndrome between January 2005 and December 2008. The causes of malignant SVC syndrome were squamous cell carcinoma ( n = 27), adenocarcinoma ( n = 25), small cell carcinoma ( n = 15), thymic carcinoma ( n = 3), invasive thymoma ( n = 2), and breast cancer ( n = 1). Stent patency and patient survival rates were calculated by using the Kaplan-Meier method, and groups were compared with the log-rank test. Results: Stent placement was technically successful in all patients. Complications did not occur in either group. Kaplan-Meier analysis revealed that covered stents had higher cumulative patency (97%, 94%, 94%, and 94% at 1, 3, 6, and 12 months, respectively) than uncovered stents (97%, 79%, 67%, and 48% at 1, 3, 6, and 12 months, respectively; P = .038). Clinical success rates did not significantly differ ( P = .674), nor did patient survival ( P = .549). Median survival in the covered stent group was 141 days (95% confidence interval: 81, 201 days) and 100 days in the uncovered stent group (95% confidence interval: 60, 140 days). Conclusion: Endovascular placement of ePTFE-covered stents appeared to be a safe and effective method to treat patients with malignant SVC syndrome and seemed to be superior to uncovered stents in terms of stent patency. © RSNA, 2012
    Schlagwort(e): Interventional Radiology, Vascular Imaging, Gastrointestinal Radiology
    Print ISSN: 0033-8419
    Digitale ISSN: 1527-1315
    Thema: Medizin
    Publiziert von The Radiological Society of North America (RSNA)
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
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    Gastric Varices and Hepatic Encephalopathy: Treatment with Vascular Plug and Gelatin Sponge-assisted Retrograde Transvenous Obliteration--A Primary Report [Vascular and Interventional Radiology] (2013)
    The Radiological Society of North America (RSNA)
    In: Radiology
    Details
    Publikationsdatum: 2013-06-22
    Beschreibung: Purpose: To evaluate technical safety, clinical safety, and effectiveness of vascular plug–assisted retrograde transvenous obliteration (RTO) for treatment of gastric varices (GV) and hepatic encephalopathy (HE). Materials and Methods: This retrospective study was approved by the institutional review board; written informed consent was waived. From April 2009 to December 2011, 20 patients (13, GV; seven, HE) who had undergone vascular plug–assisted RTO were retrospectively evaluated. After retrograde transvenous placement of a vascular plug in the left adrenal vein or gastrorenal shunt, subsequent gelatin-sponge embolization of both gastrorenal shunt and GV was performed. Follow-up computed tomography (CT) and upper gastrointestinal tract endoscopy were performed; clinical and laboratory data were collected to evaluate primary (technical success, complications, clinical success) and secondary (change of liver function by using the Child-Pugh score, worsening of esophageal varices) end points. Laboratory data before and after vascular plug–assisted RTO were compared (paired-sample t test). Results: Placement of the vascular plug and subsequent gelatin-sponge embolization were technically successful in all 20 patients, with no procedure-related complications. Follow-up CT within 1 week after vascular plug–assisted RTO showed complete thrombosis of GV and gastrorenal shunts in all patients. Clinical symptoms of HE completely resolved in all seven patients with HE; mean serum NH 3 level of 127.4 μmol/L ± 58 (standard deviation) before vascular plug–assisted RTO decreased significantly to 28.1 μmol/L ± 9.8 within 1 week after vascular plug–assisted RTO ( P = .002). Eighteen patients who underwent follow-up longer than 2 months showed complete obliteration of GV and gastrorenal shunts at CT and endoscopy. There were no cases of variceal bleeding or HE during mean follow-up of 422 days. Improvement in Child-Pugh score was observed in 12 of 18 (67%) patients 1 month after vascular plug–assisted RTO. Worsening of esophageal varices was observed in four (22%) patients at mean follow-up of 9.4 months. Conclusion: Vascular plug–assisted RTO is technically simple and safe and seems to be clinically effective for treatment of GV and HE. © RSNA, 2013
    Schlagwort(e): Interventional Radiology, Gastrointestinal Radiology
    Print ISSN: 0033-8419
    Digitale ISSN: 1527-1315
    Thema: Medizin
    Publiziert von The Radiological Society of North America (RSNA)
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    Obesity-associated variants within FTO form long-range functional connections with IRX3 (2014)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2014-03-22
    Beschreibung: Genome-wide association studies (GWAS) have reproducibly associated variants within introns of FTO with increased risk for obesity and type 2 diabetes (T2D). Although the molecular mechanisms linking these noncoding variants with obesity are not immediately obvious, subsequent studies in mice demonstrated that FTO expression levels influence body mass and composition phenotypes. However, no direct connection between the obesity-associated variants and FTO expression or function has been made. Here we show that the obesity-associated noncoding sequences within FTO are functionally connected, at megabase distances, with the homeobox gene IRX3. The obesity-associated FTO region directly interacts with the promoters of IRX3 as well as FTO in the human, mouse and zebrafish genomes. Furthermore, long-range enhancers within this region recapitulate aspects of IRX3 expression, suggesting that the obesity-associated interval belongs to the regulatory landscape of IRX3. Consistent with this, obesity-associated single nucleotide polymorphisms are associated with expression of IRX3, but not FTO, in human brains. A direct link between IRX3 expression and regulation of body mass and composition is demonstrated by a reduction in body weight of 25 to 30% in Irx3-deficient mice, primarily through the loss of fat mass and increase in basal metabolic rate with browning of white adipose tissue. Finally, hypothalamic expression of a dominant-negative form of Irx3 reproduces the metabolic phenotypes of Irx3-deficient mice. Our data suggest that IRX3 is a functional long-range target of obesity-associated variants within FTO and represents a novel determinant of body mass and composition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113484/" 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/PMC4113484/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smemo, Scott -- Tena, Juan J -- Kim, Kyoung-Han -- Gamazon, Eric R -- Sakabe, Noboru J -- Gomez-Marin, Carlos -- Aneas, Ivy -- Credidio, Flavia L -- Sobreira, Debora R -- Wasserman, Nora F -- Lee, Ju Hee -- Puviindran, Vijitha -- Tam, Davis -- Shen, Michael -- Son, Joe Eun -- Vakili, Niki Alizadeh -- Sung, Hoon-Ki -- Naranjo, Silvia -- Acemel, Rafael D -- Manzanares, Miguel -- Nagy, Andras -- Cox, Nancy J -- Hui, Chi-Chung -- Gomez-Skarmeta, Jose Luis -- Nobrega, Marcelo A -- DK020595/DK/NIDDK NIH HHS/ -- DK093972/DK/NIDDK NIH HHS/ -- DK20595/DK/NIDDK NIH HHS/ -- HL114010/HL/NHLBI NIH HHS/ -- HL119967/HL/NHLBI NIH HHS/ -- MH090937/MH/NIMH NIH HHS/ -- MH101820/MH/NIMH NIH HHS/ -- P30 DK020595/DK/NIDDK NIH HHS/ -- P60 DK020595/DK/NIDDK NIH HHS/ -- R01 DK093972/DK/NIDDK NIH HHS/ -- R01 HL114010/HL/NHLBI NIH HHS/ -- R01 HL119967/HL/NHLBI NIH HHS/ -- R01 MH090937/MH/NIMH NIH HHS/ -- R01 MH101820/MH/NIMH NIH HHS/ -- T32 HL007381/HL/NHLBI NIH HHS/ -- T32HL007381/HL/NHLBI NIH HHS/ -- U54 AR052646/AR/NIAMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2014 Mar 20;507(7492):371-5. doi: 10.1038/nature13138. Epub 2014 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Human Genetics, University of Chicago, Chicago, Illinois 60637, USA [2]. ; 1] Centro Andaluz de Biologia del Desarrollo (CABD), Consejo Superior de Investigaciones Cientificas/Universidad Pablo de Olavide, Carretera de Utrera Km1, Sevilla 41013, Spain [2]. ; 1] Program in Developmental & Stem Cell Biology, The Hospital for Sick Children, and Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S 1A8, Canada [2]. ; Section of Genetic Medicine, Department of Medicine, University of Chicago, Chicago, Illinois 60637, USA. ; Department of Human Genetics, University of Chicago, Chicago, Illinois 60637, USA. ; Centro Andaluz de Biologia del Desarrollo (CABD), Consejo Superior de Investigaciones Cientificas/Universidad Pablo de Olavide, Carretera de Utrera Km1, Sevilla 41013, Spain. ; Program in Developmental & Stem Cell Biology, The Hospital for Sick Children, and Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S 1A8, Canada. ; Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario M5T 3H7, Canada. ; Cardiovascular Development and Repair Department, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid 28029, Spain. ; 1] Department of Human Genetics, University of Chicago, Chicago, Illinois 60637, USA [2] Section of Genetic Medicine, Department of Medicine, University of Chicago, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24646999" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adipose Tissue/metabolism ; Animals ; Basal Metabolism/genetics ; Body Mass Index ; Body Weight/genetics ; Brain/metabolism ; Diabetes Mellitus, Type 2/genetics ; Diet ; Genes, Dominant/genetics ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Hypothalamus/metabolism ; Introns/*genetics ; Male ; Mice ; Mixed Function Oxygenases/*genetics ; Obesity/*genetics ; Oxo-Acid-Lyases/*genetics ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Promoter Regions, Genetic/genetics ; Proteins/*genetics ; Thinness/genetics ; Transcription Factors/deficiency/*genetics/metabolism ; Zebrafish/embryology/genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
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    Antisenescence effect of mouse embryonic stem cell conditioned medium through a PDGF/FGF pathway [Research Communication] (2016)
    The Federation of American Societies for Experimental Biology (FASEB)
    Details
    Publikationsdatum: 2016-03-02
    Beschreibung: Cellular senescence, an irreversible state of growth arrest, underlies organismal aging and age-related diseases. Recent evidence suggests that aging intervention based on inhibition of cellular senescence might be a promising strategy for treatment of aging and age-related diseases. Embryonic stem cells (ESCs) and ESC conditioned medium (CM) have been suggested as a desirable source for regenerative medicine. However, effects of ESC-CM on cellular senescence remain to be determined. We found that treatment of senescent human dermal fibroblasts with CM from mouse ESCs (mESCs) decreases senescence phenotypes. We found that platelet-derived growth factor BB in mESC-CM plays a critical role in antisenescence effect of mESC-CM through up-regulation of fibroblast growth factor 2. We confirmed that mESC-CM treatment accelerates the wound-healing process by down-regulating senescence-associated p53 expression in in vivo models. Taken together, our results suggest that mESC-CM has the ability to suppress cellular senescence and maintain proliferative capacity. Therefore, this strategy might emerge as a novel therapeutic strategy for aging and age-related diseases.—Bae, Y.-U., Choi, J.-H., Nagy, A., Sung, H.-K., Kim, J.-R. Antisenescence effect of mouse embryonic stem cell conditioned medium through a PDGF/FGF pathway.
    Print ISSN: 0892-6638
    Digitale ISSN: 1530-6860
    Thema: Biologie
    Publiziert von The Federation of American Societies for Experimental Biology (FASEB)
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    Sinus of Valsalva Aneurysm From Left Sinus: Value of Angioscopic View of a 3-Dimensional Computed Tomographic Angiography [Cardiovascular Images] (2013)
    American Heart Association (AHA)
    Details
    Publikationsdatum: 2013-01-16
    Schlagwort(e): Ablation/ICD/surgery, Acute coronary syndromes, CT and MRI, CV surgery: aortic and vascular disease, CV surgery: coronary artery disease
    Print ISSN: 1941-9651
    Digitale ISSN: 1942-0080
    Thema: Medizin
    Publiziert von American Heart Association (AHA)
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
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    iPS Cell-Derived Cardiogenicity is Hindered by Sustained Integration of Reprogramming Transgenes [Original Articles] (2014)
    American Heart Association (AHA)
    Details
    Publikationsdatum: 2014-10-22
    Beschreibung: Background— Nuclear reprogramming inculcates pluripotent capacity by which de novo tissue differentiation is enabled. Yet, introduction of ectopic reprogramming factors may desynchronize natural developmental schedules. This study aims to evaluate the effect of imposed transgene load on the cardiogenic competency of induced pluripotent stem (iPS) cells. Methods and Results— Targeted inclusion and exclusion of reprogramming transgenes ( c-MYC , KLF4 , OCT4 , and SOX2 ) was achieved using a drug-inducible and removable cassette according to the piggyBac transposon/transposase system. Pulsed transgene overexpression, before iPS cell differentiation, hindered cardiogenic outcomes. Delayed in counterparts with maintained integrated transgenes, transgene removal enabled proficient differentiation of iPS cells into functional cardiac tissue. Transgene-free iPS cells generated reproducible beating activity with robust expression of cardiac α-actinin, connexin 43, myosin light chain 2a, α/β-myosin heavy chain, and troponin I. Although operational excitation–contraction coupling was demonstrable in the presence or absence of transgenes, factor-free derivatives exhibited an expedited maturing phenotype with canonical responsiveness to adrenergic stimulation. Conclusions— A disproportionate stemness load, caused by integrated transgenes, affects the cardiogenic competency of iPS cells. Offload of transgenes in engineered iPS cells ensures integrity of cardiac developmental programs, underscoring the value of nonintegrative nuclear reprogramming for derivation of competent cardiogenic regenerative biologics.
    Schlagwort(e): Other myocardial biology, Cell biology/structural biology, Myogenesis
    Print ISSN: 1942-325X
    Digitale ISSN: 1942-3268
    Thema: Medizin
    Publiziert von American Heart Association (AHA)
    Standort Signatur Einschränkungen Verfügbarkeit
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