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    Retinal tumor induced in the baboon by human adenovirus 12 (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-11-28
    Description: Three of 21 newborn baboons injected intraocularly with human adenovirus type 12 developed an intravitreal mass 12 to 36 months later. Two of the masses were indistinguishable from human retinoblastoma, a retinal tumor that afflicts children. To our knowledge this is the first time a retinoblastoma-like tumor has been induced experimentally by adenovirus type 12 in a nonhuman primate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mukai, N -- Kalter, S S -- Cummins, L B -- Matthews, V A -- Nishida, T -- Nakajima, T -- EY-03170/EY/NEI NIH HHS/ -- RR-00036/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1980 Nov 28;210(4473):1023-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7434012" target="_blank"〉PubMed〈/a〉
    Keywords: *Adenoviruses, Human ; Animals ; Cell Transformation, Neoplastic/pathology ; Cell Transformation, Viral ; *Disease Models, Animal ; Eye Neoplasms/*microbiology ; Neoplasms, Experimental/microbiology ; Papio ; Retinoblastoma/*microbiology/pathology
    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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  • 2
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    Adult-onset obesity is triggered by impaired mitochondrial gene expression (2017)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2017-08-17
    Description: Mitochondrial gene expression is essential for energy production; however, an understanding of how it can influence physiology and metabolism is lacking. Several proteins from the pentatricopeptide repeat (PPR) family are essential for the regulation of mitochondrial gene expression, but the functions of the remaining members of this family are poorly understood. We created knockout mice to investigate the role of the PPR domain 1 (PTCD1) protein and show that loss of PTCD1 is embryonic lethal, whereas haploinsufficient, heterozygous mice develop age-induced obesity. The molecular defects and metabolic consequences of mitochondrial protein haploinsufficiency in vivo have not been investigated previously. We show that PTCD1 haploinsufficiency results in increased RNA metabolism, in response to decreased protein synthesis and impaired RNA processing that affect the biogenesis of the respiratory chain, causing mild uncoupling and changes in mitochondrial morphology. We demonstrate that with age, these effects lead to adult-onset obesity that results in liver steatosis and cardiac hypertrophy in response to tissue-specific differential regulation of the mammalian target of rapamycin pathways. Our findings indicate that changes in mitochondrial gene expression have long-term consequences on energy metabolism, providing evidence that haploinsufficiency of PTCD1 can be a major predisposing factor for the development of metabolic syndrome.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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