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  • 1
    Publication Date: 2011-08-13
    Description: Atlantic cod (Gadus morhua) is a large, cold-adapted teleost that sustains long-standing commercial fisheries and incipient aquaculture. Here we present the genome sequence of Atlantic cod, showing evidence for complex thermal adaptations in its haemoglobin gene cluster and an unusual immune architecture compared to other sequenced vertebrates. The genome assembly was obtained exclusively by 454 sequencing of shotgun and paired-end libraries, and automated annotation identified 22,154 genes. The major histocompatibility complex (MHC) II is a conserved feature of the adaptive immune system of jawed vertebrates, but we show that Atlantic cod has lost the genes for MHC II, CD4 and invariant chain (Ii) that are essential for the function of this pathway. Nevertheless, Atlantic cod is not exceptionally susceptible to disease under natural conditions. We find a highly expanded number of MHC I genes and a unique composition of its Toll-like receptor (TLR) families. This indicates how the Atlantic cod immune system has evolved compensatory mechanisms in both adaptive and innate immunity in the absence of MHC II. These observations affect fundamental assumptions about the evolution of the adaptive immune system and its components in vertebrates.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3537168/" 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/PMC3537168/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Star, Bastiaan -- Nederbragt, Alexander J -- Jentoft, Sissel -- Grimholt, Unni -- Malmstrom, Martin -- Gregers, Tone F -- Rounge, Trine B -- Paulsen, Jonas -- Solbakken, Monica H -- Sharma, Animesh -- Wetten, Ola F -- Lanzen, Anders -- Winer, Roger -- Knight, James -- Vogel, Jan-Hinnerk -- Aken, Bronwen -- Andersen, Oivind -- Lagesen, Karin -- Tooming-Klunderud, Ave -- Edvardsen, Rolf B -- Tina, Kirubakaran G -- Espelund, Mari -- Nepal, Chirag -- Previti, Christopher -- Karlsen, Bard Ove -- Moum, Truls -- Skage, Morten -- Berg, Paul R -- Gjoen, Tor -- Kuhl, Heiner -- Thorsen, Jim -- Malde, Ketil -- Reinhardt, Richard -- Du, Lei -- Johansen, Steinar D -- Searle, Steve -- Lien, Sigbjorn -- Nilsen, Frank -- Jonassen, Inge -- Omholt, Stig W -- Stenseth, Nils Chr -- Jakobsen, Kjetill S -- 098051/Wellcome Trust/United Kingdom -- England -- Nature. 2011 Aug 10;477(7363):207-10. doi: 10.1038/nature10342.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Ecological and Evolutionary Synthesis, Department of Biology, University of Oslo, PO Box 1066, Blindern, N-0316 Oslo, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21832995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Evolution, Molecular ; Gadus morhua/*genetics/*immunology ; Genome/*genetics ; Genomics ; Hemoglobins/genetics ; Immune System/*immunology ; Immunity/*genetics/immunology ; Major Histocompatibility Complex/genetics/immunology ; Male ; Polymorphism, Genetic/genetics ; Synteny/genetics ; Toll-Like Receptors/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    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
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-02-15
    Description: There is a daily rhythm in the production of the pineal hormone melatonin in all mammalian species. Production is stimulated by darkness and inhibited by light. This provides a signal reflecting the changing environmental lighting cycle. In seasonally breeding mammals that use changes in the photoperiod to time their reproductive cycles, temporal signals to the reproductive system are controlled by the daily rhythm in melatonin production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tamarkin, L -- Baird, C J -- Almeida, O F -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):714-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3881822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Circadian Rhythm ; Estrus ; Female ; Gonads/physiology ; Hypothalamo-Hypophyseal System/physiology ; Light ; Male ; Mammals/physiology ; Melatonin/*physiology ; Pineal Gland/*physiology ; Pregnancy ; *Reproduction ; Seasons ; Sexual Maturation
    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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  • 4
    Publication Date: 1981-08-14
    Description: Two maternally derived chromosome sets and both maternal histocompatibility antigen haplotypes were identified in the tissues of a malformed triploid acardiac twin that developed within the same chorion as its normal twin. These findings indicate that the twins arose as a result of independent fertilizations, by two different spermatozoa, of a normal haploid ovum and its diploid first-meiotic-division polar body.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bieber, F R -- Nance, W E -- Morton, C C -- Brown, J A -- Redwine, F O -- Jordan, R L -- Mohanakumar, T -- New York, N.Y. -- Science. 1981 Aug 14;213(4509):775-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7196086" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Severe Teratoid/*genetics ; Female ; Fertilization ; HLA Antigens/genetics ; Heart Defects, Congenital/*genetics ; Humans ; Infant, Newborn ; Karyotyping ; Male ; Meiosis ; Polyploidy ; Pregnancy ; *Twins
    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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