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  • Animals  (10)
  • 2005-2009  (10)
  • 2000-2004
  • 1925-1929
  • 2008  (10)
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  • 1
    Publikationsdatum: 2008-10-25
    Beschreibung: BAX is a pro-apoptotic protein of the BCL-2 family that is stationed in the cytosol until activated by a diversity of stress stimuli to induce cell death. Anti-apoptotic proteins such as BCL-2 counteract BAX-mediated cell death. Although an interaction site that confers survival functionality has been defined for anti-apoptotic proteins, an activation site has not been identified for BAX, rendering its explicit trigger mechanism unknown. We previously developed stabilized alpha-helix of BCL-2 domains (SAHBs) that directly initiate BAX-mediated mitochondrial apoptosis. Here we demonstrate by NMR analysis that BIM SAHB binds BAX at an interaction site that is distinct from the canonical binding groove characterized for anti-apoptotic proteins. The specificity of the human BIM-SAHB-BAX interaction is highlighted by point mutagenesis that disrupts functional activity, confirming that BAX activation is initiated at this novel structural location. Thus, we have now defined a BAX interaction site for direct activation, establishing a new target for therapeutic modulation of apoptosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597110/" 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/PMC2597110/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gavathiotis, Evripidis -- Suzuki, Motoshi -- Davis, Marguerite L -- Pitter, Kenneth -- Bird, Gregory H -- Katz, Samuel G -- Tu, Ho-Chou -- Kim, Hyungjin -- Cheng, Emily H-Y -- Tjandra, Nico -- Walensky, Loren D -- 5P01CA92625/CA/NCI NIH HHS/ -- 5R01CA125562/CA/NCI NIH HHS/ -- 5R01CA50239/CA/NCI NIH HHS/ -- K99 HL095929/HL/NHLBI NIH HHS/ -- K99 HL095929-01A1/HL/NHLBI NIH HHS/ -- K99 HL095929-02/HL/NHLBI NIH HHS/ -- R00 HL095929/HL/NHLBI NIH HHS/ -- R01 CA050239/CA/NCI NIH HHS/ -- R01 CA125562/CA/NCI NIH HHS/ -- R01 CA125562-02/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1076-81. doi: 10.1038/nature07396.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric Oncology and the Program in Cancer Chemical Biology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948948" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins/chemistry/metabolism ; BH3 Interacting Domain Death Agonist Protein/metabolism ; Cell Line ; *Gene Expression Regulation ; Humans ; Membrane Proteins/chemistry/metabolism ; Mice ; Mutagenesis, Site-Directed ; Mutation/genetics ; Nuclear Magnetic Resonance, Biomolecular ; Protein Binding ; Proto-Oncogene Proteins/chemistry/metabolism ; Sequence Alignment ; bcl-2-Associated X Protein/chemistry/*metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 2008-12-19
    Beschreibung: Palmitoylation regulates diverse aspects of neuronal protein trafficking and function. Here a global characterization of rat neural palmitoyl-proteomes identifies most of the known neural palmitoyl proteins-68 in total, plus more than 200 new palmitoyl-protein candidates, with further testing confirming palmitoylation for 21 of these candidates. The new palmitoyl proteins include neurotransmitter receptors, transporters, adhesion molecules, scaffolding proteins, as well as SNAREs and other vesicular trafficking proteins. Of particular interest is the finding of palmitoylation for a brain-specific Cdc42 splice variant. The palmitoylated Cdc42 isoform (Cdc42-palm) differs from the canonical, prenylated form (Cdc42-prenyl), both with regard to localization and function: Cdc42-palm concentrates in dendritic spines and has a special role in inducing these post-synaptic structures. Furthermore, assessing palmitoylation dynamics in drug-induced activity models identifies rapidly induced changes for Cdc42 as well as for other synaptic palmitoyl proteins, suggesting that palmitoylation may participate broadly in the activity-driven changes that shape synapse morphology and function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2610860/" 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/PMC2610860/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Rujun -- Wan, Junmei -- Arstikaitis, Pamela -- Takahashi, Hideto -- Huang, Kun -- Bailey, Aaron O -- Thompson, James X -- Roth, Amy F -- Drisdel, Renaldo C -- Mastro, Ryan -- Green, William N -- Yates, John R 3rd -- Davis, Nicholas G -- El-Husseini, Alaa -- DA019695/DA/NIDA NIH HHS/ -- DA13602/DA/NIDA NIH HHS/ -- GM65525/GM/NIGMS NIH HHS/ -- NS043782/NS/NINDS NIH HHS/ -- P01 DA019695/DA/NIDA NIH HHS/ -- P01 DA019695-01A20001/DA/NIDA NIH HHS/ -- P01 DA019695-020001/DA/NIDA NIH HHS/ -- R01 DA013602/DA/NIDA NIH HHS/ -- R01 DA013602-01/DA/NIDA NIH HHS/ -- R01 DA013602-02/DA/NIDA NIH HHS/ -- R01 DA013602-02S1/DA/NIDA NIH HHS/ -- R01 DA013602-02S2/DA/NIDA NIH HHS/ -- R01 DA013602-03/DA/NIDA NIH HHS/ -- R01 DA013602-04/DA/NIDA NIH HHS/ -- R01 DA013602-05/DA/NIDA NIH HHS/ -- R01 NS032693/NS/NINDS NIH HHS/ -- R01 NS032693-08/NS/NINDS NIH HHS/ -- R01 NS043782/NS/NINDS NIH HHS/ -- R01 NS043782-01A2/NS/NINDS NIH HHS/ -- R01 NS043782-02/NS/NINDS NIH HHS/ -- R01 NS043782-03/NS/NINDS NIH HHS/ -- R01 NS043782-04/NS/NINDS NIH HHS/ -- R01 NS043782-05/NS/NINDS NIH HHS/ -- R56 NS043782/NS/NINDS NIH HHS/ -- R56 NS043782-06/NS/NINDS NIH HHS/ -- RR011823/RR/NCRR NIH HHS/ -- England -- Nature. 2008 Dec 18;456(7224):904-9. doi: 10.1038/nature07605.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Brain Research Centre, University of British Columbia, Vancouver V6T 1Z3, British Columbia, Canada. rkang@interchange.ubc.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19092927" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alternative Splicing/genetics ; Animals ; Cells, Cultured ; Cerebral Cortex/cytology/embryology ; Dendrites/metabolism ; *Lipoylation ; Models, Neurological ; Neurons/*metabolism ; Organ Specificity ; Proteome/metabolism ; *Proteomics ; Rats ; Synapses/*metabolism ; cdc42 GTP-Binding Protein/genetics/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 2008-03-26
    Beschreibung: Tribolium castaneum is a member of the most species-rich eukaryotic order, a powerful model organism for the study of generalized insect development, and an important pest of stored agricultural products. We describe its genome sequence here. This omnivorous beetle has evolved the ability to interact with a diverse chemical environment, as shown by large expansions in odorant and gustatory receptors, as well as P450 and other detoxification enzymes. Development in Tribolium is more representative of other insects than is Drosophila, a fact reflected in gene content and function. For example, Tribolium has retained more ancestral genes involved in cell-cell communication than Drosophila, some being expressed in the growth zone crucial for axial elongation in short-germ development. Systemic RNA interference in T. castaneum functions differently from that in Caenorhabditis elegans, but nevertheless offers similar power for the elucidation of gene function and identification of targets for selective insect control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tribolium Genome Sequencing Consortium -- Richards, Stephen -- Gibbs, Richard A -- Weinstock, George M -- Brown, Susan J -- Denell, Robin -- Beeman, Richard W -- Gibbs, Richard -- Bucher, Gregor -- Friedrich, Markus -- Grimmelikhuijzen, Cornelis J P -- Klingler, Martin -- Lorenzen, Marce -- Roth, Siegfried -- Schroder, Reinhard -- Tautz, Diethard -- Zdobnov, Evgeny M -- Muzny, Donna -- Attaway, Tony -- Bell, Stephanie -- Buhay, Christian J -- Chandrabose, Mimi N -- Chavez, Dean -- Clerk-Blankenburg, Kerstin P -- Cree, Andrew -- Dao, Marvin -- Davis, Clay -- Chacko, Joseph -- Dinh, Huyen -- Dugan-Rocha, Shannon -- Fowler, Gerald -- Garner, Toni T -- Garnes, Jeffrey -- Gnirke, Andreas -- Hawes, Alica -- Hernandez, Judith -- Hines, Sandra -- Holder, Michael -- Hume, Jennifer -- Jhangiani, Shalini N -- Joshi, Vandita -- Khan, Ziad Mohid -- Jackson, LaRonda -- Kovar, Christie -- Kowis, Andrea -- Lee, Sandra -- Lewis, Lora R -- Margolis, Jon -- Morgan, Margaret -- Nazareth, Lynne V -- Nguyen, Ngoc -- Okwuonu, Geoffrey -- Parker, David -- Ruiz, San-Juana -- Santibanez, Jireh -- Savard, Joel -- Scherer, Steven E -- Schneider, Brian -- Sodergren, Erica -- Vattahil, Selina -- Villasana, Donna -- White, Courtney S -- Wright, Rita -- Park, Yoonseong -- Lord, Jeff -- Oppert, Brenda -- Brown, Susan -- Wang, Liangjiang -- Weinstock, George -- Liu, Yue -- Worley, Kim -- Elsik, Christine G -- Reese, Justin T -- Elhaik, Eran -- Landan, Giddy -- Graur, Dan -- Arensburger, Peter -- Atkinson, Peter -- Beidler, Jim -- Demuth, Jeffery P -- Drury, Douglas W -- Du, Yu-Zhou -- Fujiwara, Haruhiko -- Maselli, Vincenza -- Osanai, Mizuko -- Robertson, Hugh M -- Tu, Zhijian -- Wang, Jian-jun -- Wang, Suzhi -- Song, Henry -- Zhang, Lan -- Werner, Doreen -- Stanke, Mario -- Morgenstern, Burkhard -- Solovyev, Victor -- Kosarev, Peter -- Brown, Garth -- Chen, Hsiu-Chuan -- Ermolaeva, Olga -- Hlavina, Wratko -- Kapustin, Yuri -- Kiryutin, Boris -- Kitts, Paul -- Maglott, Donna -- Pruitt, Kim -- Sapojnikov, Victor -- Souvorov, Alexandre -- Mackey, Aaron J -- Waterhouse, Robert M -- Wyder, Stefan -- Kriventseva, Evgenia V -- Kadowaki, Tatsuhiko -- Bork, Peer -- Aranda, Manuel -- Bao, Riyue -- Beermann, Anke -- Berns, Nicola -- Bolognesi, Renata -- Bonneton, Francois -- Bopp, Daniel -- Butts, Thomas -- Chaumot, Arnaud -- Denell, Robin E -- Ferrier, David E K -- Gordon, Cassondra M -- Jindra, Marek -- Lan, Que -- Lattorff, H Michael G -- Laudet, Vincent -- von Levetsow, Cornelia -- Liu, Zhenyi -- Lutz, Rebekka -- Lynch, Jeremy A -- da Fonseca, Rodrigo Nunes -- Posnien, Nico -- Reuter, Rolf -- Schinko, Johannes B -- Schmitt, Christian -- Schoppmeier, Michael -- Shippy, Teresa D -- Simonnet, Franck -- Marques-Souza, Henrique -- Tomoyasu, Yoshinori -- Trauner, Jochen -- Van der Zee, Maurijn -- Vervoort, Michel -- Wittkopp, Nadine -- Wimmer, Ernst A -- Yang, Xiaoyun -- Jones, Andrew K -- Sattelle, David B -- Ebert, Paul R -- Nelson, David -- Scott, Jeffrey G -- Muthukrishnan, Subbaratnam -- Kramer, Karl J -- Arakane, Yasuyuki -- Zhu, Qingsong -- Hogenkamp, David -- Dixit, Radhika -- Jiang, Haobo -- Zou, Zhen -- Marshall, Jeremy -- Elpidina, Elena -- Vinokurov, Konstantin -- Oppert, Cris -- Evans, Jay -- Lu, Zhiqiang -- Zhao, Picheng -- Sumathipala, Niranji -- Altincicek, Boran -- Vilcinskas, Andreas -- Williams, Michael -- Hultmark, Dan -- Hetru, Charles -- Hauser, Frank -- Cazzamali, Giuseppe -- Williamson, Michael -- Li, Bin -- Tanaka, Yoshiaki -- Predel, Reinhard -- Neupert, Susanne -- Schachtner, Joachim -- Verleyen, Peter -- Raible, Florian -- Walden, Kimberly K O -- Angeli, Sergio -- Foret, Sylvain -- Schuetz, Stefan -- Maleszka, Ryszard -- Miller, Sherry C -- Grossmann, Daniela -- BBS/B/12067/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/12067/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- R01 GM058634/GM/NIGMS NIH HHS/ -- R01 HD029594/HD/NICHD NIH HHS/ -- R01 HD029594-16/HD/NICHD NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2008 Apr 24;452(7190):949-55. doi: 10.1038/nature06784. Epub 2008 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genome Sequencing Center, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA. stephenr@bcm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18362917" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Base Composition ; Body Patterning/genetics ; Cytochrome P-450 Enzyme System/genetics ; DNA Transposable Elements/genetics ; Genes, Insect/*genetics ; Genome, Insect/*genetics ; Growth and Development/genetics ; Humans ; Insecticides/pharmacology ; Neurotransmitter Agents/genetics ; Oogenesis/genetics ; Phylogeny ; Proteome/genetics ; RNA Interference ; Receptors, G-Protein-Coupled/genetics ; Receptors, Odorant/genetics ; Repetitive Sequences, Nucleic Acid/genetics ; Taste/genetics ; Telomere/genetics ; Tribolium/classification/embryology/*genetics/physiology ; Vision, Ocular/genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Publikationsdatum: 2008-06-13
    Beschreibung: MicroRNAs (miRNAs) are small non-coding RNAs that participate in the spatiotemporal regulation of messenger RNA and protein synthesis. Aberrant miRNA expression leads to developmental abnormalities and diseases, such as cardiovascular disorders and cancer; however, the stimuli and processes regulating miRNA biogenesis are largely unknown. The transforming growth factor beta (TGF-beta) and bone morphogenetic protein (BMP) family of growth factors orchestrates fundamental biological processes in development and in the homeostasis of adult tissues, including the vasculature. Here we show that induction of a contractile phenotype in human vascular smooth muscle cells by TGF-beta and BMPs is mediated by miR-21. miR-21 downregulates PDCD4 (programmed cell death 4), which in turn acts as a negative regulator of smooth muscle contractile genes. Surprisingly, TGF-beta and BMP signalling promotes a rapid increase in expression of mature miR-21 through a post-transcriptional step, promoting the processing of primary transcripts of miR-21 (pri-miR-21) into precursor miR-21 (pre-miR-21) by the DROSHA (also known as RNASEN) complex. TGF-beta- and BMP-specific SMAD signal transducers are recruited to pri-miR-21 in a complex with the RNA helicase p68 (also known as DDX5), a component of the DROSHA microprocessor complex. The shared cofactor SMAD4 is not required for this process. Thus, regulation of miRNA biogenesis by ligand-specific SMAD proteins is critical for control of the vascular smooth muscle cell phenotype and potentially for SMAD4-independent responses mediated by the TGF-beta and BMP signalling pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653422/" 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/PMC2653422/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, Brandi N -- Hilyard, Aaron C -- Lagna, Giorgio -- Hata, Akiko -- HD042149/HD/NICHD NIH HHS/ -- HL082854/HL/NHLBI NIH HHS/ -- HL086572/HL/NHLBI NIH HHS/ -- R01 HD042149/HD/NICHD NIH HHS/ -- R01 HD042149-05/HD/NICHD NIH HHS/ -- R01 HL082854/HL/NHLBI NIH HHS/ -- R01 HL082854-03/HL/NHLBI NIH HHS/ -- R21 HL086572/HL/NHLBI NIH HHS/ -- R21 HL086572-02/HL/NHLBI NIH HHS/ -- England -- Nature. 2008 Jul 3;454(7200):56-61. doi: 10.1038/nature07086. Epub 2008 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18548003" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apoptosis Regulatory Proteins/metabolism ; Bone Morphogenetic Protein 4 ; Bone Morphogenetic Proteins/metabolism/pharmacology ; Breast Neoplasms/genetics ; Cell Line ; Cercopithecus aethiops ; DEAD-box RNA Helicases/metabolism ; Gene Expression Regulation/drug effects ; Humans ; Ligands ; Mice ; MicroRNAs/biosynthesis/*metabolism ; Muscle, Smooth/metabolism ; Phenotype ; Protein Binding ; *RNA Processing, Post-Transcriptional ; RNA-Binding Proteins/metabolism ; Ribonuclease III/*metabolism ; Signal Transduction/drug effects ; Smad Proteins/*metabolism ; Transforming Growth Factor beta/metabolism/pharmacology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 2008-08-01
    Beschreibung: Percolation theory is most commonly associated with the slow flow of liquid through a porous medium, with applications to the physical sciences. Epidemiological applications have been anticipated for disease systems where the host is a plant or volume of soil, and hence is fixed in space. However, no natural examples have been reported. The central question of interest in percolation theory, the possibility of an infinite connected cluster, corresponds in infectious disease to a positive probability of an epidemic. Archived records of plague (infection with Yersinia pestis) in populations of great gerbils (Rhombomys opimus) in Kazakhstan have been used to show that epizootics only occur when more than about 0.33 of the burrow systems built by the host are occupied by family groups. The underlying mechanism for this abundance threshold is unknown. Here we present evidence that it is a percolation threshold, which arises from the difference in scale between the movements that transport infectious fleas between family groups and the vast size of contiguous landscapes colonized by gerbils. Conventional theory predicts that abundance thresholds for the spread of infectious disease arise when transmission between hosts is density dependent such that the basic reproduction number (R(0)) increases with abundance, attaining 1 at the threshold. Percolation thresholds, however, are separate, spatially explicit thresholds that indicate long-range connectivity in a system and do not coincide with R(0) = 1. Abundance thresholds are the theoretical basis for attempts to manage infectious disease by reducing the abundance of susceptibles, including vaccination and the culling of wildlife. This first natural example of a percolation threshold in a disease system invites a re-appraisal of other invasion thresholds, such as those for epidemic viral infections in African lions (Panthera leo), and of other disease systems such as bovine tuberculosis (caused by Mycobacterium bovis) in badgers (Meles meles).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S -- Trapman, P -- Leirs, H -- Begon, M -- Heesterbeek, J A P -- England -- Nature. 2008 Jul 31;454(7204):634-7. doi: 10.1038/nature07053.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Theoretical Epidemiology, Faculty of Veterinary Medicine, University of Utrecht, Yalelaan 7, 3584 CL Utrecht, The Netherlands. S.A.Davis@uu.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18668107" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Disease Outbreaks ; Gerbillinae/microbiology/parasitology ; Kazakhstan/epidemiology ; *Models, Biological ; Plague/epidemiology/parasitology/*transmission/veterinary ; Population Density ; Population Dynamics ; Rodent Diseases/epidemiology/parasitology/transmission ; Siphonaptera/microbiology/physiology ; Yersinia pestis/*physiology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    Publikationsdatum: 2008-06-27
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tomchik, Seth M -- Davis, Ronald L -- England -- Nature. 2008 Jun 26;453(7199):1192-4. doi: 10.1038/4531192a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18580936" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Drosophila melanogaster/enzymology/*physiology ; Humans ; Locomotion/physiology ; Memory/*physiology ; Models, Neurological ; Neurons/enzymology/metabolism ; Orientation/*physiology ; Ribosomal Protein S6 Kinases, 90-kDa/genetics/metabolism ; Space Perception/*physiology ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
    Publikationsdatum: 2008-12-06
    Beschreibung: A high-fat diet causes activation of the regulatory protein c-Jun NH2-terminal kinase 1 (JNK1) and triggers development of insulin resistance. JNK1 is therefore a potential target for therapeutic treatment of metabolic syndrome. We explored the mechanism of JNK1 signaling by engineering mice in which the Jnk1 gene was ablated selectively in adipose tissue. JNK1 deficiency in adipose tissue suppressed high-fat diet-induced insulin resistance in the liver. JNK1-dependent secretion of the inflammatory cytokine interleukin-6 by adipose tissue caused increased expression of liver SOCS3, a protein that induces hepatic insulin resistance. Thus, JNK1 activation in adipose tissue can cause insulin resistance in the liver.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643026/" 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/PMC2643026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabio, Guadalupe -- Das, Madhumita -- Mora, Alfonso -- Zhang, Zhiyou -- Jun, John Y -- Ko, Hwi Jin -- Barrett, Tamera -- Kim, Jason K -- Davis, Roger J -- DK52530/DK/NIDDK NIH HHS/ -- R01 CA065861/CA/NCI NIH HHS/ -- R01 CA065861-14/CA/NCI NIH HHS/ -- R01 DK080756/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1539-43. doi: 10.1126/science.1160794.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056984" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adipocytes/enzymology/*metabolism ; Adipose Tissue/enzymology/metabolism ; Animals ; Dietary Fats/administration & dosage ; Enzyme Activation ; Glucose/metabolism ; Insulin/metabolism ; Insulin Receptor Substrate Proteins/metabolism ; *Insulin Resistance ; Interleukin-6/administration & dosage/metabolism ; Liver/*metabolism ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 8/deficiency/genetics/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; *Signal Transduction ; *Stress, Physiological ; Suppressor of Cytokine Signaling Proteins/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2008-12-20
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fore, Leska S -- Karr, James R -- Fisher, William S -- Davis, Wayne S -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1788. doi: 10.1126/science.322.5909.1788a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19095922" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Anthozoa ; Conservation of Natural Resources/*legislation & jurisprudence ; *Seawater ; United States ; United States Environmental Protection Agency ; Water Pollution/*legislation & jurisprudence
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
    Publikationsdatum: 2008-09-27
    Beschreibung: Almost two decades after CFTR was identified as the gene responsible for cystic fibrosis (CF), we still lack answers to many questions about the pathogenesis of the disease, and it remains incurable. Mice with a disrupted CFTR gene have greatly facilitated CF studies, but the mutant mice do not develop the characteristic manifestations of human CF, including abnormalities of the pancreas, lung, intestine, liver, and other organs. Because pigs share many anatomical and physiological features with humans, we generated pigs with a targeted disruption of both CFTR alleles. Newborn pigs lacking CFTR exhibited defective chloride transport and developed meconium ileus, exocrine pancreatic destruction, and focal biliary cirrhosis, replicating abnormalities seen in newborn humans with CF. The pig model may provide opportunities to address persistent questions about CF pathogenesis and accelerate discovery of strategies for prevention and treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570747/" 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/PMC2570747/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogers, Christopher S -- Stoltz, David A -- Meyerholz, David K -- Ostedgaard, Lynda S -- Rokhlina, Tatiana -- Taft, Peter J -- Rogan, Mark P -- Pezzulo, Alejandro A -- Karp, Philip H -- Itani, Omar A -- Kabel, Amanda C -- Wohlford-Lenane, Christine L -- Davis, Greg J -- Hanfland, Robert A -- Smith, Tony L -- Samuel, Melissa -- Wax, David -- Murphy, Clifton N -- Rieke, August -- Whitworth, Kristin -- Uc, Aliye -- Starner, Timothy D -- Brogden, Kim A -- Shilyansky, Joel -- McCray, Paul B Jr -- Zabner, Joseph -- Prather, Randall S -- Welsh, Michael J -- AI076671/AI/NIAID NIH HHS/ -- DK54759/DK/NIDDK NIH HHS/ -- HL07638/HL/NHLBI NIH HHS/ -- HL51670/HL/NHLBI NIH HHS/ -- K08 AI076671/AI/NIAID NIH HHS/ -- K08 AI076671-01/AI/NIAID NIH HHS/ -- P01 HL051670/HL/NHLBI NIH HHS/ -- P01 HL051670-15/HL/NHLBI NIH HHS/ -- P30 DK054759/DK/NIDDK NIH HHS/ -- P30 DK054759-10/DK/NIDDK NIH HHS/ -- P30 DK054759-109004/DK/NIDDK NIH HHS/ -- R01 DK051315/DK/NIDDK NIH HHS/ -- T32 HL007638/HL/NHLBI NIH HHS/ -- T32 HL007638-23/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Sep 26;321(5897):1837-41. doi: 10.1126/science.1163600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18818360" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Animals, Newborn ; Chlorides/metabolism ; *Cystic Fibrosis/genetics/pathology/physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator/*genetics/metabolism ; *Disease Models, Animal ; Female ; Gallbladder/pathology ; Ileus/pathology/physiopathology ; Intestines/pathology ; Ion Transport ; Liver/pathology ; Liver Cirrhosis, Biliary/pathology ; Lung/pathology ; Male ; Pancreas, Exocrine/pathology ; Recombination, Genetic ; *Swine
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
    Publikationsdatum: 2008-05-03
    Beschreibung: Glycogen synthase kinase 3beta (GSK3beta) is involved in metabolism, neurodegeneration, and cancer. Inhibition of GSK3beta activity is the primary mechanism that regulates this widely expressed active kinase. Although the protein kinase Akt inhibits GSK3beta by phosphorylation at the N terminus, preventing Akt-mediated phosphorylation does not affect the cell-survival pathway activated through the GSK3beta substrate beta-catenin. Here, we show that p38 mitogen-activated protein kinase (MAPK) also inactivates GSK3beta by direct phosphorylation at its C terminus, and this inactivation can lead to an accumulation of beta-catenin. p38 MAPK-mediated phosphorylation of GSK3beta occurs primarily in the brain and thymocytes. Activation of beta-catenin-mediated signaling through GSK3beta inhibition provides a potential mechanism for p38 MAPK-mediated survival in specific tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597039/" 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/PMC2597039/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thornton, Tina M -- Pedraza-Alva, Gustavo -- Deng, Bin -- Wood, C David -- Aronshtam, Alexander -- Clements, James L -- Sabio, Guadalupe -- Davis, Roger J -- Matthews, Dwight E -- Doble, Bradley -- Rincon, Mercedes -- P20 RR021905/RR/NCRR NIH HHS/ -- P20 RR15557/RR/NCRR NIH HHS/ -- P20 RR16462/RR/NCRR NIH HHS/ -- R01 AI051454/AI/NIAID NIH HHS/ -- R01 AI051454-01A1/AI/NIAID NIH HHS/ -- R01 AI051454-02/AI/NIAID NIH HHS/ -- R01 AI051454-03/AI/NIAID NIH HHS/ -- R01 AI051454-04/AI/NIAID NIH HHS/ -- R01 AI051454-05/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 May 2;320(5876):667-70. doi: 10.1126/science.1156037.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine/Immunobiology Program, University of Vermont, Burlington, VT 05405-0068, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18451303" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain/enzymology ; Glycogen Synthase Kinase 3/*antagonists & inhibitors/immunology/metabolism ; Humans ; Mice ; Phosphorylation ; Protein Kinase Inhibitors/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Serine/metabolism ; Thymus Gland/cytology/enzymology ; beta Catenin/metabolism ; p38 Mitogen-Activated Protein Kinases/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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