ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    APJ acts as a dual receptor in cardiac hypertrophy (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-20
    Description: Cardiac hypertrophy is initiated as an adaptive response to sustained overload but progresses pathologically as heart failure ensues. Here we report that genetic loss of APJ, a G-protein-coupled receptor, confers resistance to chronic pressure overload by markedly reducing myocardial hypertrophy and heart failure. In contrast, mice lacking apelin (the endogenous APJ ligand) remain sensitive, suggesting an apelin-independent function of APJ. Freshly isolated APJ-null cardiomyocytes exhibit an attenuated response to stretch, indicating that APJ is a mechanosensor. Activation of APJ by stretch increases cardiomyocyte cell size and induces molecular markers of hypertrophy. Whereas apelin stimulates APJ to activate Galphai and elicits a protective response, stretch signals in an APJ-dependent, G-protein-independent fashion to induce hypertrophy. Stretch-mediated hypertrophy is prevented by knockdown of beta-arrestins or by pharmacological doses of apelin acting through Galphai. Taken together, our data indicate that APJ is a bifunctional receptor for both mechanical stretch and the endogenous peptide apelin. By sensing the balance between these stimuli, APJ occupies a pivotal point linking sustained overload to cardiomyocyte hypertrophy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422434/" 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/PMC3422434/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scimia, Maria Cecilia -- Hurtado, Cecilia -- Ray, Saugata -- Metzler, Scott -- Wei, Ke -- Wang, Jianming -- Woods, Chris E -- Purcell, Nicole H -- Catalucci, Daniele -- Akasaka, Takeshi -- Bueno, Orlando F -- Vlasuk, George P -- Kaliman, Perla -- Bodmer, Rolf -- Smith, Layton H -- Ashley, Euan -- Mercola, Mark -- Brown, Joan Heller -- Ruiz-Lozano, Pilar -- NS05422/NS/NINDS NIH HHS/ -- P01 HL085577/HL/NHLBI NIH HHS/ -- R01 HL054732/HL/NHLBI NIH HHS/ -- R01 HL086879/HL/NHLBI NIH HHS/ -- R01HL054732/HL/NHLBI NIH HHS/ -- R01HL083463/HL/NHLBI NIH HHS/ -- R01HL086879/HL/NHLBI NIH HHS/ -- R01HL28143/HL/NHLBI NIH HHS/ -- R37 HL028143/HL/NHLBI NIH HHS/ -- R37HL059502/HL/NHLBI NIH HHS/ -- England -- Nature. 2012 Aug 16;488(7411):394-8. doi: 10.1038/nature11263.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanford-Burnham Medical Research Institute, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22810587" target="_blank"〉PubMed〈/a〉
    Keywords: Adipokines ; Animals ; Aorta/pathology ; Arrestins/deficiency/genetics/metabolism ; Blood Pressure ; Cardiomegaly/*metabolism/pathology/physiopathology/prevention & control ; Female ; GTP-Binding Protein alpha Subunits, Gi-Go/metabolism ; Intercellular Signaling Peptides and ; Proteins/deficiency/genetics/metabolism/pharmacology ; Male ; Mechanoreceptors/metabolism ; Mechanotransduction, Cellular/drug effects/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Cardiac/drug effects/pathology ; Receptors, G-Protein-Coupled/agonists/deficiency/genetics/*metabolism ; Signal Transduction/drug effects
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Diversity of endogenous epitopes bound to MHC class II molecules limited by invariant chain (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-04
    Description: The invariant chain (Ii) binds nascent major histocompatibility complex (MHC) class II molecules, blocking peptide binding until the complex dissociates in the endosomes. This may serve to differentiate the MHC class I and II antigen presentation pathways and enable class II molecules to efficiently bind peptides in the endosomes. This hypothesis was addressed by probing spleen cells from a combination of knock-out and transgenic mice with a large panel of T cell hybridomas. The Ii molecule blocked the presentation of a range of endogenously synthesized epitopes, but some epitopes actually required Ii. Thus, the influence of Ii on presentation does not follow simple rules. In addition, mice expressing Ii were not tolerant to epitopes unmasked in its absence, a finding with possible implications for autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bodmer, H -- Viville, S -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1284-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7510069" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigen-Presenting Cells/*immunology ; *Antigens, Differentiation, B-Lymphocyte ; Epitopes/*immunology ; Histocompatibility Antigens Class II/genetics/*immunology ; Hybridomas ; Mice ; Mice, Knockout ; Mice, Transgenic ; Molecular Sequence Data ; Myelin Basic Protein/immunology ; Recombinant Fusion Proteins/immunology ; T-Lymphocytes/*immunology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Sestrin as a feedback inhibitor of TOR that prevents age-related pathologies (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-06
    Description: Sestrins are conserved proteins that accumulate in cells exposed to stress, potentiate adenosine monophosphate-activated protein kinase (AMPK), and inhibit activation of target of rapamycin (TOR). We show that the abundance of Drosophila sestrin (dSesn) is increased upon chronic TOR activation through accumulation of reactive oxygen species that cause activation of c-Jun amino-terminal kinase and transcription factor Forkhead box O (FoxO). Loss of dSesn resulted in age-associated pathologies including triglyceride accumulation, mitochondrial dysfunction, muscle degeneration, and cardiac malfunction, which were prevented by pharmacological activation of AMPK or inhibition of TOR. Hence, dSesn appears to be a negative feedback regulator of TOR that integrates metabolic and stress inputs and prevents pathologies caused by chronic TOR activation that may result from diminished autophagic clearance of damaged mitochondria, protein aggregates, or lipids.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866632/" 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/PMC2866632/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jun Hee -- Budanov, Andrei V -- Park, Eek Joong -- Birse, Ryan -- Kim, Teddy E -- Perkins, Guy A -- Ocorr, Karen -- Ellisman, Mark H -- Bodmer, Rolf -- Bier, Ethan -- Karin, Michael -- AI070654/AI/NIAID NIH HHS/ -- CA118165/CA/NCI NIH HHS/ -- DK082080/DK/NIDDK NIH HHS/ -- ES006376/ES/NIEHS NIH HHS/ -- NS29870/NS/NINDS NIH HHS/ -- P30 CA023100/CA/NCI NIH HHS/ -- P30-CA23100/CA/NCI NIH HHS/ -- P41-RR004050/RR/NCRR NIH HHS/ -- P42 ES010337/ES/NIEHS NIH HHS/ -- P42 ES010337-10S20010/ES/NIEHS NIH HHS/ -- P42-ES010337/ES/NIEHS NIH HHS/ -- R01 CA118165/CA/NCI NIH HHS/ -- R01 CA118165-04/CA/NCI NIH HHS/ -- R01 ES006376/ES/NIEHS NIH HHS/ -- R01 ES006376-17/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 5;327(5970):1223-8. doi: 10.1126/science.1182228.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California San Diego (UCSD), La Jolla, CA 92093-0723, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203043" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; *Aging ; Amino Acid Sequence ; Animals ; Autophagy ; Cell Size ; Drosophila Proteins/antagonists & ; inhibitors/chemistry/genetics/metabolism/*physiology ; Drosophila melanogaster/cytology/growth & development/metabolism/*physiology ; Fat Body/metabolism ; Feedback, Physiological ; Forkhead Transcription Factors/metabolism ; Gene Expression Regulation ; Heart/physiology ; Heat-Shock Proteins/chemistry/genetics/*physiology ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mitochondria, Muscle/physiology/ultrastructure ; Models, Animal ; Molecular Sequence Data ; Muscles/physiology ; Oxidative Stress ; Protein Kinases/*metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases ; Transcription, Genetic ; Triglycerides/metabolism ; Wings, Animal/cytology/growth & development/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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...