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  • 1
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    Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1999-07-03
    Beschreibung: Epithelia permit selective and regulated flux from apical to basolateral surfaces by transcellular passage through cells or paracellular flux between cells. Tight junctions constitute the barrier to paracellular conductance; however, little is known about the specific molecules that mediate paracellular permeabilities. Renal magnesium ion (Mg2+) resorption occurs predominantly through a paracellular conductance in the thick ascending limb of Henle (TAL). Here, positional cloning has identified a human gene, paracellin-1 (PCLN-1), mutations in which cause renal Mg2+ wasting. PCLN-1 is located in tight junctions of the TAL and is related to the claudin family of tight junction proteins. These findings provide insight into Mg2+ homeostasis, demonstrate the role of a tight junction protein in human disease, and identify an essential component of a selective paracellular conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simon, D B -- Lu, Y -- Choate, K A -- Velazquez, H -- Al-Sabban, E -- Praga, M -- Casari, G -- Bettinelli, A -- Colussi, G -- Rodriguez-Soriano, J -- McCredie, D -- Milford, D -- Sanjad, S -- Lifton, R P -- F.1/Telethon/Italy -- R01DK51696/DK/NIDDK NIH HHS/ -- TGM06S01/Telethon/Italy -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390358" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Calcium/urine ; Chromosomes, Human, Pair 3/genetics ; Claudins ; Cloning, Molecular ; Female ; Genes, Recessive ; Homeostasis ; Humans ; Kidney Diseases/*genetics/metabolism ; Kidney Tubules/chemistry ; Loop of Henle/chemistry/*metabolism ; Magnesium/blood/*metabolism ; Magnesium Deficiency/*genetics/metabolism ; Male ; Membrane Proteins/analysis/chemistry/genetics/*physiology ; Molecular Sequence Data ; Mutation ; Pedigree ; Physical Chromosome Mapping ; Tight Junctions/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Mitotic recombination in patients with ichthyosis causes reversion of dominant mutations in KRT10 (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2010-08-28
    Beschreibung: Somatic loss of wild-type alleles can produce disease traits such as neoplasia. Conversely, somatic loss of disease-causing mutations can revert phenotypes; however, these events are infrequently observed. Here we show that ichthyosis with confetti, a severe, sporadic skin disease in humans, is associated with thousands of revertant clones of normal skin that arise from loss of heterozygosity on chromosome 17q via mitotic recombination. This allowed us to map and identify disease-causing mutations in the gene encoding keratin 10 (KRT10); all result in frameshifts into the same alternative reading frame, producing an arginine-rich C-terminal peptide that redirects keratin 10 from the cytokeratin filament network to the nucleolus. The high frequency of somatic reversion in ichthyosis with confetti suggests that revertant stem cell clones are under strong positive selection and/or that the rate of mitotic recombination is elevated in individuals with this disorder.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085938/" 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/PMC3085938/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choate, Keith A -- Lu, Yin -- Zhou, Jing -- Choi, Murim -- Elias, Peter M -- Farhi, Anita -- Nelson-Williams, Carol -- Crumrine, Debra -- Williams, Mary L -- Nopper, Amy J -- Bree, Alanna -- Milstone, Leonard M -- Lifton, Richard P -- K08 AR056305/AR/NIAMS NIH HHS/ -- K08 AR056305-01/AR/NIAMS NIH HHS/ -- K08 AR056305-02/AR/NIAMS NIH HHS/ -- K08 AR056305-03/AR/NIAMS NIH HHS/ -- K08 AR056305-04/AR/NIAMS NIH HHS/ -- T32 AR007016/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):94-7. doi: 10.1126/science.1192280. Epub 2010 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798280" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Cell Nucleolus/metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 17/*genetics ; Female ; *Frameshift Mutation ; Humans ; Ichthyosiform Erythroderma, Congenital/*genetics/pathology ; Intermediate Filaments/metabolism/ultrastructure ; Keratin-10/chemistry/*genetics/metabolism ; Keratins/metabolism ; Loss of Heterozygosity ; Male ; *Mitosis ; Molecular Sequence Data ; Mosaicism ; Mutant Proteins/chemistry/genetics/metabolism ; *Recombination, Genetic ; Selection, Genetic ; Skin/pathology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Spongiform degeneration in mahoganoid mutant mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2003-02-01
    Beschreibung: mahoganoid is a mouse coat-color mutation whose pigmentary phenotype and genetic interactions resemble those of Attractin (Atrn). Atrn mutations also cause spongiform neurodegeneration. Here, we show that a null mutation for mahoganoid causes a similar age-dependent neuropathology that includes many features of prion diseases but without accumulation of protease-resistant prion protein. The gene mutated in mahoganoid encodes a RING-containing protein with E3 ubiquitin ligase activity in vitro. Similarities in phenotype, expression, and genetic interactions suggest that mahoganoid and Atrn genes are part of a conserved pathway for regulated protein turnover whose function is essential for neuronal viability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Lin -- Lu, Xin-Yun -- Jolly, Aaron F -- Eldridge, Adam G -- Watson, Stanley J -- Jackson, Peter K -- Barsh, Gregory S -- Gunn, Teresa M -- New York, N.Y. -- Science. 2003 Jan 31;299(5607):710-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Department of Genetics, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12560552" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Amino Acid Sequence ; Animals ; Blotting, Northern ; Brain/metabolism/*pathology ; Carrier Proteins/chemistry/*genetics/*metabolism ; Crosses, Genetic ; Female ; Gene Expression ; Ligases/metabolism ; Male ; Membrane Proteins/genetics ; Mice ; Mice, Inbred C3H ; Mice, Mutant Strains ; Mice, Transgenic ; Models, Biological ; Molecular Sequence Data ; *Mutation ; Neurodegenerative Diseases/*genetics/metabolism/*pathology ; Neurons/metabolism/pathology ; Pigmentation ; Prions/metabolism ; RNA, Messenger/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Transgenes ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases ; Vacuoles/ultrastructure
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    In situ stable isotope probing of methanogenic archaea in the rice rhizosphere (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2005-08-16
    Beschreibung: Microorganisms living in anoxic rice soils contribute 10 to 25% of global methane emissions. The most important carbon source for CH4 production is plant-derived carbon that enters soil as root exudates and debris. Pulse labeling of rice plants with 13CO2 resulted in incorporation of 13C into the ribosomal RNA of Rice Cluster I Archaea in the soil, indicating that this archaeal group plays a key role in CH4 production from plant-derived carbon. This group of microorganisms has not yet been isolated but appears to be of global environmental importance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Yahai -- Conrad, Ralf -- New York, N.Y. -- Science. 2005 Aug 12;309(5737):1088-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Resources and Environmental Sciences, China Agricultural University, Beijing 100094, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16099988" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Archaea/classification/genetics/growth & development/*metabolism ; Carbon Dioxide/metabolism ; Carbon Isotopes/*metabolism ; Cloning, Molecular ; *Ecosystem ; Hydrogen/metabolism ; Methane/*metabolism ; Molecular Sequence Data ; Oryza/metabolism/*microbiology ; Photosynthesis ; Phylogeny ; Plant Roots/metabolism/microbiology ; Polymorphism, Restriction Fragment Length ; RNA, Archaeal/metabolism ; RNA, Ribosomal, 16S/genetics/metabolism ; *Soil Microbiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Analyses of pig genomes provide insight into porcine demography and evolution (2012)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2012-11-16
    Beschreibung: For 10,000 years pigs and humans have shared a close and complex relationship. From domestication to modern breeding practices, humans have shaped the genomes of domestic pigs. Here we present the assembly and analysis of the genome sequence of a female domestic Duroc pig (Sus scrofa) and a comparison with the genomes of wild and domestic pigs from Europe and Asia. Wild pigs emerged in South East Asia and subsequently spread across Eurasia. Our results reveal a deep phylogenetic split between European and Asian wild boars approximately 1 million years ago, and a selective sweep analysis indicates selection on genes involved in RNA processing and regulation. Genes associated with immune response and olfaction exhibit fast evolution. Pigs have the largest repertoire of functional olfactory receptor genes, reflecting the importance of smell in this scavenging animal. The pig genome sequence provides an important resource for further improvements of this important livestock species, and our identification of many putative disease-causing variants extends the potential of the pig as a biomedical model.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3566564/" 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/PMC3566564/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Groenen, Martien A M -- Archibald, Alan L -- Uenishi, Hirohide -- Tuggle, Christopher K -- Takeuchi, Yasuhiro -- Rothschild, Max F -- Rogel-Gaillard, Claire -- Park, Chankyu -- Milan, Denis -- Megens, Hendrik-Jan -- Li, Shengting -- Larkin, Denis M -- Kim, Heebal -- Frantz, Laurent A F -- Caccamo, Mario -- Ahn, Hyeonju -- Aken, Bronwen L -- Anselmo, Anna -- Anthon, Christian -- Auvil, Loretta -- Badaoui, Bouabid -- Beattie, Craig W -- Bendixen, Christian -- Berman, Daniel -- Blecha, Frank -- Blomberg, Jonas -- Bolund, Lars -- Bosse, Mirte -- Botti, Sara -- Bujie, Zhan -- Bystrom, Megan -- Capitanu, Boris -- Carvalho-Silva, Denise -- Chardon, Patrick -- Chen, Celine -- Cheng, Ryan -- Choi, Sang-Haeng -- Chow, William -- Clark, Richard C -- Clee, Christopher -- Crooijmans, Richard P M A -- Dawson, Harry D -- Dehais, Patrice -- De Sapio, Fioravante -- Dibbits, Bert -- Drou, Nizar -- Du, Zhi-Qiang -- Eversole, Kellye -- Fadista, Joao -- Fairley, Susan -- Faraut, Thomas -- Faulkner, Geoffrey J -- Fowler, Katie E -- Fredholm, Merete -- Fritz, Eric -- Gilbert, James G R -- Giuffra, Elisabetta -- Gorodkin, Jan -- Griffin, Darren K -- Harrow, Jennifer L -- Hayward, Alexander -- Howe, Kerstin -- Hu, Zhi-Liang -- Humphray, Sean J -- Hunt, Toby -- Hornshoj, Henrik -- Jeon, Jin-Tae -- Jern, Patric -- Jones, Matthew -- Jurka, Jerzy -- Kanamori, Hiroyuki -- Kapetanovic, Ronan -- Kim, Jaebum -- Kim, Jae-Hwan -- Kim, Kyu-Won -- Kim, Tae-Hun -- Larson, Greger -- Lee, Kyooyeol -- Lee, Kyung-Tai -- Leggett, Richard -- Lewin, Harris A -- Li, Yingrui -- Liu, Wansheng -- Loveland, Jane E -- Lu, Yao -- Lunney, Joan K -- Ma, Jian -- Madsen, Ole -- Mann, Katherine -- Matthews, Lucy -- McLaren, Stuart -- Morozumi, Takeya -- Murtaugh, Michael P -- Narayan, Jitendra -- Nguyen, Dinh Truong -- Ni, Peixiang -- Oh, Song-Jung -- Onteru, Suneel -- Panitz, Frank -- Park, Eung-Woo -- Park, Hong-Seog -- Pascal, Geraldine -- Paudel, Yogesh -- Perez-Enciso, Miguel -- Ramirez-Gonzalez, Ricardo -- Reecy, James M -- Rodriguez-Zas, Sandra -- Rohrer, Gary A -- Rund, Lauretta -- Sang, Yongming -- Schachtschneider, Kyle -- Schraiber, Joshua G -- Schwartz, John -- Scobie, Linda -- Scott, Carol -- Searle, Stephen -- Servin, Bertrand -- Southey, Bruce R -- Sperber, Goran -- Stadler, Peter -- Sweedler, Jonathan V -- Tafer, Hakim -- Thomsen, Bo -- Wali, Rashmi -- Wang, Jian -- Wang, Jun -- White, Simon -- Xu, Xun -- Yerle, Martine -- Zhang, Guojie -- Zhang, Jianguo -- Zhang, Jie -- Zhao, Shuhong -- Rogers, Jane -- Churcher, Carol -- Schook, Lawrence B -- 095908/Wellcome Trust/United Kingdom -- 249894/European Research Council/International -- 5 P41 LM006252/LM/NLM NIH HHS/ -- 5 P41LM006252/LM/NLM NIH HHS/ -- BB/E010520/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E010520/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E010768/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E011640/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G004013/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H005935/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/I025328/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0900950/Medical Research Council/United Kingdom -- P20-RR017686/RR/NCRR NIH HHS/ -- P30 DA018310/DA/NIDA NIH HHS/ -- R13 RR020283A/RR/NCRR NIH HHS/ -- R13 RR032267A/RR/NCRR NIH HHS/ -- R21 DA027548/DA/NIDA NIH HHS/ -- R21 HG006464/HG/NHGRI NIH HHS/ -- T32 AI083196/AI/NIAID NIH HHS/ -- England -- Nature. 2012 Nov 15;491(7424):393-8. doi: 10.1038/nature11622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Animal Breeding and Genomics Centre, Wageningen University, De Elst 1, 6708 WD, Wageningen, The Netherlands. martien.groenen@wur.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23151582" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Demography ; Genome/*genetics ; Models, Animal ; Molecular Sequence Data ; *Phylogeny ; Population Dynamics ; Sus scrofa/*classification/*genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Co-opting sulphur-carrier proteins from primary metabolic pathways for 2-thiosugar biosynthesis (2014)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2014-05-13
    Beschreibung: Sulphur is an essential element for life and is ubiquitous in living systems. Yet how the sulphur atom is incorporated into many sulphur-containing secondary metabolites is poorly understood. For bond formation between carbon and sulphur in primary metabolites, the major ionic sulphur sources are the persulphide and thiocarboxylate groups on sulphur-carrier (donor) proteins. Each group is post-translationally generated through the action of a specific activating enzyme. In all reported bacterial cases, the gene encoding the enzyme that catalyses the carbon-sulphur bond formation reaction and that encoding the cognate sulphur-carrier protein exist in the same gene cluster. To study the production of the 2-thiosugar moiety in BE-7585A, an antibiotic from Amycolatopsis orientalis, we identified a putative 2-thioglucose synthase, BexX, whose protein sequence and mode of action seem similar to those of ThiG, the enzyme that catalyses thiazole formation in thiamine biosynthesis. However, no gene encoding a sulphur-carrier protein could be located in the BE-7585A cluster. Subsequent genome sequencing uncovered a few genes encoding sulphur-carrier proteins that are probably involved in the biosynthesis of primary metabolites but only one activating enzyme gene in the A. orientalis genome. Further experiments showed that this activating enzyme can adenylate each of these sulphur-carrier proteins and probably also catalyses the subsequent thiolation, through its rhodanese domain. A proper combination of these sulphur-delivery systems is effective for BexX-catalysed 2-thioglucose production. The ability of BexX to selectively distinguish sulphur-carrier proteins is given a structural basis using X-ray crystallography. This study is, to our knowledge, the first complete characterization of thiosugar formation in nature and also demonstrates the receptor promiscuity of the A. orientalis sulphur-delivery system. Our results also show that co-opting the sulphur-delivery machinery of primary metabolism for the biosynthesis of sulphur-containing natural products is probably a general strategy found in nature.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4082789/" 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/PMC4082789/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sasaki, Eita -- Zhang, Xuan -- Sun, He G -- Lu, Mei-yeh Jade -- Liu, Tsung-lin -- Ou, Albert -- Li, Jeng-yi -- Chen, Yu-hsiang -- Ealick, Steven E -- Liu, Hung-wen -- DK67081/DK/NIDDK NIH HHS/ -- GM035906/GM/NIGMS NIH HHS/ -- GM103403/GM/NIGMS NIH HHS/ -- GM103485/GM/NIGMS NIH HHS/ -- P41 GM103403/GM/NIGMS NIH HHS/ -- P41 GM103485/GM/NIGMS NIH HHS/ -- R01 DK067081/DK/NIDDK NIH HHS/ -- R01 GM035906/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Jun 19;510(7505):427-31. doi: 10.1038/nature13256. Epub 2014 May 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Texas at Austin, Austin, Texas 78712, USA. ; Department of Chemistry and Chemical Biology, Cornell University, Ithaca, New York 14853, USA. ; Division of Medicinal Chemistry, College of Pharmacy, University of Texas at Austin, Austin, Texas 78712, USA. ; 1] Biodiversity Research Center, Academia Sinica, Taipei 115, Taiwan [2] Genomics Research Center, Academia Sinica, Taipei 115, Taiwan. ; 1] Genomics Research Center, Academia Sinica, Taipei 115, Taiwan [2] Institute of Bioinformatics and Biosignal Transduction, National Cheng-Kung University, Tainan 701, Taiwan. ; Genomics Research Center, Academia Sinica, Taipei 115, Taiwan. ; Biodiversity Research Center, Academia Sinica, Taipei 115, Taiwan. ; 1] Department of Chemistry, University of Texas at Austin, Austin, Texas 78712, USA [2] Division of Medicinal Chemistry, College of Pharmacy, University of Texas at Austin, Austin, Texas 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24814342" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actinomycetales/*enzymology/*genetics/metabolism ; Carrier Proteins/chemistry/*metabolism ; Catalytic Domain ; Genome, Bacterial/genetics ; Ligases/*chemistry/genetics/metabolism ; Models, Molecular ; Molecular Sequence Data ; Protein Structure, Tertiary ; Sulfur/*metabolism ; Thiosugars/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    Control of nonapoptotic developmental cell death in Caenorhabditis elegans by a polyglutamine-repeat protein (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2012-03-01
    Beschreibung: Death is a vital developmental cell fate. In Caenorhabditis elegans, programmed death of the linker cell, which leads gonadal elongation, proceeds independently of caspases and apoptotic effectors. To identify genes promoting linker-cell death, we performed a genome-wide RNA interference screen. We show that linker-cell death requires the gene pqn-41, encoding an endogenous polyglutamine-repeat protein. pqn-41 functions cell-autonomously and is expressed at the onset of linker-cell death. pqn-41 expression is controlled by the mitogen-activated protein kinase kinase SEK-1, which functions in parallel to the zinc-finger protein LIN-29 to promote cellular demise. Linker-cell death is morphologically similar to cell death associated with normal vertebrate development and polyglutamine-induced neurodegeneration. Our results may therefore provide molecular inroads to understanding nonapoptotic cell death in metazoan development and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858082/" 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/PMC3858082/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blum, Elyse S -- Abraham, Mary C -- Yoshimura, Satoshi -- Lu, Yun -- Shaham, Shai -- CA09673/CA/NCI NIH HHS/ -- R01 HD042680/HD/NICHD NIH HHS/ -- R01HD042680/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2012 Feb 24;335(6071):970-3. doi: 10.1126/science.1215156.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22363008" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Caenorhabditis elegans/*cytology/genetics/growth & development/*metabolism ; Caenorhabditis elegans Proteins/chemistry/*genetics/*metabolism ; *Cell Death ; Cell Nucleus/ultrastructure ; Cell Survival ; DNA-Binding Proteins/genetics/metabolism ; Gene Expression Regulation ; Genes, Helminth ; Genome, Helminth ; MAP Kinase Kinase 4/genetics/metabolism ; Male ; Molecular Sequence Data ; Mutant Proteins/chemistry/metabolism ; Peptides/chemistry ; Protein Structure, Tertiary ; RNA Interference ; Sequence Deletion ; Transcription Factors/genetics/metabolism ; Transgenes
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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