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  • 1
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    A Drosophila LexA Enhancer-Trap Resource for Developmental Biology and Neuroendocrine Research (2016)
    Genetics Society of America (GSA)
    Details
    Publication Date: 2016-10-14
    Description: Novel binary gene expression tools like the LexA-LexAop system could powerfully enhance studies of metabolism, development, and neurobiology in Drosophila . However, specific LexA drivers for neuroendocrine cells and many other developmentally relevant systems remain limited. In a unique high school biology course, we generated a LexA-based enhancer trap collection by transposon mobilization. The initial collection provides a source of novel LexA-based elements that permit targeted gene expression in the corpora cardiaca, cells central for metabolic homeostasis, and other neuroendocrine cell types. The collection further contains specific LexA drivers for stem cells and other enteric cells in the gut, and other developmentally relevant tissue types. We provide detailed analysis of nearly 100 new LexA lines, including molecular mapping of insertions, description of enhancer-driven reporter expression in larval tissues, and adult neuroendocrine cells, comparison with established enhancer trap collections and tissue specific RNAseq. Generation of this open-resource LexA collection facilitates neuroendocrine and developmental biology investigations, and shows how empowering secondary school science can achieve research and educational goals.
    Electronic ISSN: 2160-1836
    Topics: Biology
    Published by Genetics Society of America (GSA)
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  • 2
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    CD95 promotes tumour growth (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-05-28
    Description: CD95 (also called Fas and APO-1) is a prototypical death receptor that regulates tissue homeostasis mainly in the immune system through the induction of apoptosis. During cancer progression CD95 is frequently downregulated or cells are rendered apoptosis resistant, raising the possibility that loss of CD95 is part of a mechanism for tumour evasion. However, complete loss of CD95 is rarely seen in human cancers and many cancer cells express large quantities of CD95 and are highly sensitive to CD95-mediated apoptosis in vitro. Furthermore, cancer patients frequently have elevated levels of the physiological ligand for CD95, CD95L. These data raise the possibility that CD95 could actually promote the growth of tumours through its non-apoptotic activities. Here we show that cancer cells in general, regardless of their CD95 apoptosis sensitivity, depend on constitutive activity of CD95, stimulated by cancer-produced CD95L, for optimal growth. Consistently, loss of CD95 in mouse models of ovarian cancer and liver cancer reduces cancer incidence as well as the size of the tumours. The tumorigenic activity of CD95 is mediated by a pathway involving JNK and Jun. These results demonstrate that CD95 has a growth-promoting role during tumorigenesis and indicate that efforts to inhibit its activity rather than to enhance it should be considered during cancer therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879093/" 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/PMC2879093/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Lina -- Park, Sun-Mi -- Tumanov, Alexei V -- Hau, Annika -- Sawada, Kenjiro -- Feig, Christine -- Turner, Jerrold R -- Fu, Yang-Xin -- Romero, Iris L -- Lengyel, Ernst -- Peter, Marcus E -- CA112240/CA/NCI NIH HHS/ -- K12 HD000849/HD/NICHD NIH HHS/ -- L30 CA153336/CA/NCI NIH HHS/ -- R01 CA095319/CA/NCI NIH HHS/ -- R01 CA11182/CA/NCI NIH HHS/ -- R01 CA112240/CA/NCI NIH HHS/ -- R01 CA112240-01A1/CA/NCI NIH HHS/ -- R01 CA112240-02/CA/NCI NIH HHS/ -- R01 CA112240-03/CA/NCI NIH HHS/ -- R01 CA112240-04/CA/NCI NIH HHS/ -- R01 CA112240-05/CA/NCI NIH HHS/ -- England -- Nature. 2010 May 27;465(7297):492-6. doi: 10.1038/nature09075.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Ben May Department for Cancer Research, The University of Chicago, 924 E 57th Street, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20505730" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/deficiency/genetics/*metabolism ; Apoptosis ; Carcinoma, Endometrioid/metabolism/pathology ; Cell Line, Tumor ; Cell Proliferation ; Fas Ligand Protein/antagonists & inhibitors/immunology/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Hepatocytes/enzymology/metabolism/pathology ; Humans ; Liver Neoplasms/enzymology/metabolism/pathology ; Male ; Mice ; Mitogen-Activated Protein Kinase 8/deficiency/genetics/metabolism ; Neoplasms/*metabolism/*pathology ; Ovarian Neoplasms/metabolism/pathology
    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)
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  • 3
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    The novel gene twenty-four defines a critical translational step in the Drosophila clock (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-02-19
    Description: Daily oscillations of gene expression underlie circadian behaviours in multicellular organisms. While attention has been focused on transcriptional and post-translational mechanisms, other post-transcriptional modes have been less clearly delineated. Here we report mutants of a novel Drosophila gene twenty-four (tyf) that show weak behavioural rhythms. Weak rhythms are accompanied by marked reductions in the levels of the clock protein Period (PER) as well as more modest effects on Timeless (TIM). Nonetheless, PER induction in pacemaker neurons can rescue tyf mutant rhythms. TYF associates with a 5'-cap-binding complex, poly(A)-binding protein (PABP), as well as per and tim transcripts. Furthermore, TYF activates reporter expression when tethered to reporter messenger RNA even in vitro. Taken together, these data indicate that TYF potently activates PER translation in pacemaker neurons to sustain robust rhythms, revealing a new and important role for translational control in the Drosophila circadian clock.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073513/" 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/PMC3073513/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, Chunghun -- Lee, Jongbin -- Choi, Changtaek -- Kilman, Valerie L -- Kim, Juwon -- Park, Sung Mi -- Jang, Sung Key -- Allada, Ravi -- Choe, Joonho -- R01 MH067870/MH/NIMH NIH HHS/ -- R01 MH067870-05/MH/NIMH NIH HHS/ -- R01 NS052903/NS/NINDS NIH HHS/ -- R01 NS052903-04/NS/NINDS NIH HHS/ -- R01 NS059042/NS/NINDS NIH HHS/ -- R01 NS059042-04/NS/NINDS NIH HHS/ -- R01MH067870/MH/NIMH NIH HHS/ -- R01NS052903/NS/NINDS NIH HHS/ -- R01NS059042/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Feb 17;470(7334):399-403. doi: 10.1038/nature09728.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21331043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Circadian Clocks/*genetics/physiology ; Circadian Rhythm/genetics/physiology ; Drosophila Proteins/biosynthesis/genetics/*metabolism ; Drosophila melanogaster/*genetics/*physiology ; Genes, Insect/*genetics ; Genes, Reporter/genetics ; Mutation/genetics ; Neurons/metabolism/physiology ; Period Circadian Proteins/*biosynthesis/genetics/metabolism ; Poly(A)-Binding Proteins/metabolism ; Protein Binding ; Protein Biosynthesis/genetics/*physiology ; RNA, Messenger/genetics/metabolism ; Up-Regulation
    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)
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