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  • 1
    Online Resource
    Online Resource
    Differentiation Pathways in Human Embryonic Stem Cell‐Derived Cardiomyocytes
    Wiley ; 2005
    In:  Annals of the New York Academy of Sciences Vol. 1047, No. 1 ( 2005-06), p. 50-65
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1047, No. 1 ( 2005-06), p. 50-65
    Abstract: A bstract : Human embryonic stem (hES) cells are pluripotent cell lines derived from the inner cell mass of the blastocyst‐stage embryo. These unique cell lines can be propagated in the undifferentiated state in culture, while retaining the capacity to differentiate into derivatives of all three germ layers, including cardiomyocytes. The derivation of the hES cell lines presents a powerful tool to explore the early events of cardiac progenitor cell specification and differentiation, and it also provides a novel cell source for the emerging field of cardiovascular regenerative medicine. A spontaneous differentiation system of these stem cells to cardiomyocytes was established and the generated myocytes displayed molecular, structural, and functional properties of early‐stage heart cells. In order to follow the in vitro differentiation process, the temporal expression of signaling molecules and transcription factors governing early cardiac differentiation was examined throughout the process. A characteristic pattern was noted recapitulating the normal in vivo cardiac differentiation scheme observed in other model systems. This review discusses the known pathways involved in cardiac specification and the possible factors that may be used to enhance cardiac differentiation of hES cells, as well as the steps required to fully harness the enormous potential of these unique cells.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1341.005
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2005
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    SSG: 11
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    Extracellular signal‐regulated kinase 1/2 (ERK1/2) signaling in cardiac hypertrophy
    Wiley ; 2010
    In:  Annals of the New York Academy of Sciences Vol. 1188, No. 1 ( 2010-02), p. 96-102
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1188, No. 1 ( 2010-02), p. 96-102
    Abstract: Cardiac hypertrophy results from increased mechanical load on the heart and through the action of neurohumoral mediators. ERK1/2 are known to be activated in response to almost every stress‐ and agonist‐induced hypertrophic stimulus examined to date, suggesting the straightforward hypothesis that these kinases are required for promoting the cardiac growth response. However, recent data from genetically modified mouse models suggest a more complicated picture. For example, inducible expression of dual‐specificity phosphatase 6, an ERK1/2‐inactivating phosphatase, eliminated ERK1/2 phosphorylation in transgenic mice, but it did not diminish the hypertrophic response to pressure overload. Similarly, Erk1 −/− and Erk2 +/− mice showed no reduction in stimulus‐induced cardiac growth in vivo . However, blockade or deletion of cardiac ERK1/2 did predispose the heart to decompensation and failure after long‐term pressure overload. Thus, ERK1/2 signaling is not to be absolutely necessary for mediating cardiac hypertrophy, although it does appear to provide critical protective effects/signals during stress‐stimulation.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.2010.1188.issue-1
    DOI: 10.1111/j.1749-6632.2009.05088.x
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2010
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    SSG: 11
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  • 3
    Online Resource
    Online Resource
    Numerous proteins with unique characteristics are degraded by the 26S proteasome following monoubiquitination
    Proceedings of the National Academy of Sciences ; 2016
    In:  Proceedings of the National Academy of Sciences Vol. 113, No. 32 ( 2016-08-09)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 113, No. 32 ( 2016-08-09)
    Abstract: The “canonical” proteasomal degradation signal is a substrate-anchored polyubiquitin chain. However, a handful of proteins were shown to be targeted following monoubiquitination. In this study, we established—in both human and yeast cells—a systematic approach for the identification of monoubiquitination-dependent proteasomal substrates. The cellular wild-type polymerizable ubiquitin was replaced with ubiquitin that cannot form chains. Using proteomic analysis, we screened for substrates that are nevertheless degraded under these conditions compared with those that are stabilized, and therefore require polyubiquitination for their degradation. For randomly sampled representative substrates, we confirmed that their cellular stability is in agreement with our screening prediction. Importantly, the two groups display unique features: monoubiquitinated substrates are smaller than the polyubiquitinated ones, are enriched in specific pathways, and, in humans, are structurally less disordered. We suggest that monoubiquitination-dependent degradation is more widespread than assumed previously, and plays key roles in various cellular processes.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1608644113
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2016
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  • 4
    Online Resource
    Online Resource
    The Role of Basic Leucine Zipper Protein‐Mediated Transcription in Physiological and Pathological Myocardial Hypertrophy
    Wiley ; 2006
    In:  Annals of the New York Academy of Sciences Vol. 1080, No. 1 ( 2006-10), p. 97-109
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1080, No. 1 ( 2006-10), p. 97-109
    Abstract: Abstract:  Accumulating evidence suggests that nuclear transcription factors from the basic leucine zipper (bZIP) family play an important role in cardiac development and function. This class includes the CREB/ATF family of transcription factors, namely CREB, cAMP response element modulator (CREM), ATF, and the related AP‐1 and C/EBP families. An effort has been made to elucidate the role of specific bZIP members in the heart. Unfortunately, little insight could be gained from knockout experiments, either due to embryonic lethal phenotypes or functional compensation by other bZIP family members. Surprisingly, cardiac overexpression of several inhibitory transcription factors from the bZIP family, such as a nonphosphorylatable form of CREB (CREB ser133 ), a nonfunctional isoform of CREM, or ATF3 resulted in massive atrial dilatation. In order to try and characterize this pathway we have expressed the potent bZIP inhibitory protein, Jun dimerization protein 2 (JDP2), specifically in the mouse heart in a temporally controlled manner. Expression of JDP2 resulted in massive biatrial dilatation; loss of connexin 40 (Cx40), connexin43 (C×43), and myosin light chain 2 (MLC2a) expression; atrioventricular defects in conduction; and a lethal phenotype. All these effects were independent of any developmental events acquired during adulthood, and were totally reversible upon abolishing the bZIP inhibition. The results of this article suggest that bZIP inhibition is sufficient to cause atrial dilation, that this dilatation is acquired postnatally, and that it is reversible upon the relief of inhibition. Thus, bZIP repressors may serve as novel drug targets for the prevention of atrial dilatation a major risk of atrial fibrillation (AF).
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1380.009
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2006
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    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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