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  • Animals  (10)
  • American Association for the Advancement of Science (AAAS)  (10)
  • Institute of Physics
  • Oxford University Press
  • Taylor & Francis
  • 2005-2009  (10)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (10)
  • Institute of Physics
  • Oxford University Press
  • Taylor & Francis
  • Nature Publishing Group (NPG)  (4)
Years
Year
  • 1
    Publication Date: 2006-11-25
    Description: The Dobzhansky-Muller model proposes that hybrid incompatibilities are caused by the interaction between genes that have functionally diverged in the respective hybridizing species. Here, we show that Lethal hybrid rescue (Lhr) has functionally diverged in Drosophila simulans and interacts with Hybrid male rescue (Hmr), which has functionally diverged in D. melanogaster, to cause lethality in F1 hybrid males. LHR localizes to heterochromatic regions of the genome and has diverged extensively in sequence between these species in a manner consistent with positive selection. Rapidly evolving heterochromatic DNA sequences may be driving the evolution of this incompatibility gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brideau, Nicholas J -- Flores, Heather A -- Wang, Jun -- Maheshwari, Shamoni -- Wang, Xu -- Barbash, Daniel A -- R01 GM074737-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 24;314(5803):1292-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17124320" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosome Mapping ; Crosses, Genetic ; Drosophila/*genetics/physiology ; Drosophila Proteins/chemistry/*genetics/metabolism ; Drosophila melanogaster/*genetics/physiology ; *Evolution, Molecular ; Female ; *Genes, Insect ; Genetic Speciation ; *Hybridization, Genetic ; Male ; Molecular Sequence Data ; Selection, Genetic ; Transformation, Genetic ; Transgenes
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  • 2
    Publication Date: 2006-01-28
    Description: The spread of H5N1 avian influenza viruses (AIVs) from China to Europe has raised global concern about their potential to infect humans and cause a pandemic. In spite of their substantial threat to human health, remarkably little AIV whole-genome information is available. We report here a preliminary analysis of the first large-scale sequencing of AIVs, including 2196 AIV genes and 169 complete genomes. We combine this new information with public AIV data to identify new gene alleles, persistent genotypes, compensatory mutations, and a potential virulence determinant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Obenauer, John C -- Denson, Jackie -- Mehta, Perdeep K -- Su, Xiaoping -- Mukatira, Suraj -- Finkelstein, David B -- Xu, Xiequn -- Wang, Jinhua -- Ma, Jing -- Fan, Yiping -- Rakestraw, Karen M -- Webster, Robert G -- Hoffmann, Erich -- Krauss, Scott -- Zheng, Jie -- Zhang, Ziwei -- Naeve, Clayton W -- AI95357/AI/NIAID NIH HHS/ -- CA 21765/CA/NCI NIH HHS/ -- R01 GM061739/GM/NIGMS NIH HHS/ -- R01 GM069916/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1576-80. Epub 2006 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hartwell Center for Bioinformatics and Biotechnology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/virology ; Computational Biology ; *Genes, Viral ; Genome, Viral ; Humans ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza A Virus, H2N2 Subtype/genetics ; Influenza A Virus, H3N2 Subtype/genetics ; Influenza A Virus, H3N8 Subtype/genetics ; Influenza A Virus, H5N1 Subtype/chemistry/*genetics/pathogenicity ; Influenza A Virus, H5N2 Subtype/genetics ; Influenza A Virus, H7N7 Subtype/genetics ; Influenza A Virus, H9N2 Subtype/genetics ; Influenza A virus/chemistry/*genetics/isolation & purification/pathogenicity ; Influenza in Birds/virology ; Influenza, Human/virology ; Molecular Sequence Data ; Mutation ; Phylogeny ; RNA, Viral/genetics ; Reassortant Viruses/genetics ; Sequence Analysis, DNA ; Viral Nonstructural Proteins/*chemistry/genetics ; Viral Proteins/chemistry/genetics ; Virulence Factors/*chemistry/genetics
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  • 3
    Publication Date: 2006-02-25
    Description: Apoptosis in the immune system is critical for maintaining self-tolerance and preventing autoimmunity. Nevertheless, inhibiting apoptosis in lymphocytes is not alone sufficient to break self-tolerance, suggesting the involvement of other cell types. We investigated whether apoptosis in dendritic cells (DCs) helps regulate self-tolerance by generating transgenic mice expressing the baculoviral caspase inhibitor, p35, in DCs (DC-p35). DC-p35 mice displayed defective DC apoptosis, resulting in their accumulation and, in turn, chronic lymphocyte activation and systemic autoimmune manifestations. The observation that a defect in DC apoptosis can independently lead to autoimmunity is consistent with a central role for these cells in maintaining immune self-tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Min -- Wang, Yui-Hsi -- Wang, Yihong -- Huang, Li -- Sandoval, Hector -- Liu, Yong-Jun -- Wang, Jin -- New York, N.Y. -- Science. 2006 Feb 24;311(5764):1160-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Baylor College of Medicine, Houston, TX 77030, USA. minc@bcm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16497935" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Aging ; Animals ; Antibodies, Antinuclear/analysis ; *Apoptosis ; *Autoimmunity ; B-Lymphocytes/immunology ; Caspase Inhibitors ; Cell Survival ; Dendritic Cells/*immunology/*physiology ; Kidney/immunology ; Lung/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; *Self Tolerance ; Spleen/immunology ; T-Lymphocytes/immunology ; Viral Proteins/genetics/metabolism
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  • 4
    Publication Date: 2008-05-24
    Description: beta-Arrestins have important roles in the regulation of seven-transmembrane receptors (7TMRs). Smoothened (Smo) is a 7TMR that mediates effects of Hedgehog on developmental processes and whose dysregulation may cause tumorigenesis. beta-Arrestins are required for endocytosis of Smo and signaling to Gli transcription factors. In mammalian cells, Smo-dependent signaling requires translocation to primary cilia. We demonstrated that beta-arrestins mediate the activity-dependent interaction of Smo and the kinesin motor protein Kif3A. This multimeric complex localized to primary cilia and was disrupted in cells transfected with beta-arrestin small interfering RNA. beta-Arrestin 1 or beta-arrestin 2 depletion prevented the localization of Smo to primary cilia and the Smo-dependent activation of Gli. These results suggest roles for beta-arrestins in mediating the intracellular transport of a 7TMR to its obligate subcellular location for signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587210/" 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/PMC2587210/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kovacs, Jeffrey J -- Whalen, Erin J -- Liu, Renshui -- Xiao, Kunhong -- Kim, Jihee -- Chen, Minyong -- Wang, Jiangbo -- Chen, Wei -- Lefkowitz, Robert J -- 5R01 CA113656-02/CA/NCI NIH HHS/ -- 5T32 AI007217-25/AI/NIAID NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- HL70631/HL/NHLBI NIH HHS/ -- R01 CA113656/CA/NCI NIH HHS/ -- R01 CA113656-02/CA/NCI NIH HHS/ -- R01 CA113656-03/CA/NCI NIH HHS/ -- R01 HL016037/HL/NHLBI NIH HHS/ -- R01 HL016037-35/HL/NHLBI NIH HHS/ -- R01 HL070631/HL/NHLBI NIH HHS/ -- R01 HL070631-04/HL/NHLBI NIH HHS/ -- T32 AI007217/AI/NIAID NIH HHS/ -- T32 AI007217-25/AI/NIAID NIH HHS/ -- T32 AI007217-26/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jun 27;320(5884):1777-81. doi: 10.1126/science.1157983. Epub 2008 May 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497258" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/genetics/*metabolism ; Cilia/*metabolism ; Hedgehog Proteins/metabolism ; Kinesin/*metabolism ; Mice ; Microscopy, Confocal ; Molecular Motor Proteins/*metabolism ; NIH 3T3 Cells ; Protein Transport ; RNA Interference ; Receptors, G-Protein-Coupled/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Transfection
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  • 5
    Publication Date: 2008-03-15
    Description: The diplomonad parasite Giardia intestinalis contains two functionally equivalent nuclei that are inherited independently during mitosis. Although presumed to be asexual, Giardia has low levels of allelic heterozygosity, indicating that the two nuclear genomes may exchange genetic material. Fluorescence in situ hybridization performed with probes to an episomal plasmid suggests that plasmids are transferred between nuclei in the cyst, and transmission electron micrographs demonstrate fusion between cyst nuclei. Green fluorescent protein fusions of giardial homologs of meiosis-specific genes localized to the nuclei of cysts, but not the vegetative trophozoite. These data suggest that the fusion of nuclei, or karyogamy, and subsequently somatic homologous recombination facilitated by the meiosis gene homologs, occur in the giardial cyst.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poxleitner, Marianne K -- Carpenter, Meredith L -- Mancuso, Joel J -- Wang, Chung-Ju R -- Dawson, Scott C -- Cande, W Zacheus -- 1F32GM078971/GM/NIGMS NIH HHS/ -- A1054693/PHS HHS/ -- New York, N.Y. -- Science. 2008 Mar 14;319(5869):1530-3. doi: 10.1126/science.1153752.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18339940" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/*physiology/ultrastructure ; Giardia lamblia/*genetics/growth & development/ultrastructure ; In Situ Hybridization, Fluorescence ; *Membrane Fusion ; Microscopy, Electron, Transmission ; Nuclear Envelope/physiology ; *Plasmids ; Protozoan Proteins/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Recombination, Genetic
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  • 6
    Publication Date: 2009-08-29
    Description: A single-base pair resolution silkworm genetic variation map was constructed from 40 domesticated and wild silkworms, each sequenced to approximately threefold coverage, representing 99.88% of the genome. We identified ~16 million single-nucleotide polymorphisms, many indels, and structural variations. We find that the domesticated silkworms are clearly genetically differentiated from the wild ones, but they have maintained large levels of genetic variability, suggesting a short domestication event involving a large number of individuals. We also identified signals of selection at 354 candidate genes that may have been important during domestication, some of which have enriched expression in the silk gland, midgut, and testis. These data add to our understanding of the domestication processes and may have applications in devising pest control strategies and advancing the use of silkworms as efficient bioreactors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3951477/" 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/PMC3951477/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xia, Qingyou -- Guo, Yiran -- Zhang, Ze -- Li, Dong -- Xuan, Zhaoling -- Li, Zhuo -- Dai, Fangyin -- Li, Yingrui -- Cheng, Daojun -- Li, Ruiqiang -- Cheng, Tingcai -- Jiang, Tao -- Becquet, Celine -- Xu, Xun -- Liu, Chun -- Zha, Xingfu -- Fan, Wei -- Lin, Ying -- Shen, Yihong -- Jiang, Lan -- Jensen, Jeffrey -- Hellmann, Ines -- Tang, Si -- Zhao, Ping -- Xu, Hanfu -- Yu, Chang -- Zhang, Guojie -- Li, Jun -- Cao, Jianjun -- Liu, Shiping -- He, Ningjia -- Zhou, Yan -- Liu, Hui -- Zhao, Jing -- Ye, Chen -- Du, Zhouhe -- Pan, Guoqing -- Zhao, Aichun -- Shao, Haojing -- Zeng, Wei -- Wu, Ping -- Li, Chunfeng -- Pan, Minhui -- Li, Jingjing -- Yin, Xuyang -- Li, Dawei -- Wang, Juan -- Zheng, Huisong -- Wang, Wen -- Zhang, Xiuqing -- Li, Songgang -- Yang, Huanming -- Lu, Cheng -- Nielsen, Rasmus -- Zhou, Zeyang -- Wang, Jian -- Xiang, Zhonghuai -- Wang, Jun -- R01 HG003229/HG/NHGRI NIH HHS/ -- R01 HG003229-05/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):433-6. doi: 10.1126/science.1176620. Epub 2009 Aug 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Key Sericultural Laboratory of Agricultural Ministry, College of Biotechnology, Southwest University, Chongqing 400715, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19713493" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bombyx/classification/*genetics ; Digestive System/metabolism ; Exocrine Glands/metabolism ; Female ; Gene Expression ; *Genes, Insect ; *Genetic Variation ; *Genome, Insect ; INDEL Mutation ; Linkage Disequilibrium ; Male ; Phylogeny ; Polymorphism, Single Nucleotide ; Principal Component Analysis ; Selection, Genetic ; *Sequence Analysis, DNA ; Testis/metabolism
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  • 7
    Publication Date: 2005-07-08
    Description: H5N1 avian influenza virus (AIV) has emerged as a pathogenic entity for a variety of species, including humans, in recent years. Here we report an outbreak among migratory birds on Lake Qinghaihu, China, in May and June 2005, in which more than a thousand birds were affected. Pancreatic necrosis and abnormal neurological symptoms were the major clinical features. Sequencing of the complete genomes of four H5N1 AIV strains revealed them to be reassortants related to a peregrine falcon isolate from Hong Kong and to have known highly pathogenic characteristics. Experimental animal infections reproduced typical highly pathogenic AIV infection symptoms and pathology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, J -- Xiao, H -- Lei, F -- Zhu, Q -- Qin, K -- Zhang, X-W -- Zhang, X-L -- Zhao, D -- Wang, G -- Feng, Y -- Ma, J -- Liu, W -- Wang, J -- Gao, G F -- New York, N.Y. -- Science. 2005 Aug 19;309(5738):1206. Epub 2005 Jul 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Veterinary Medicine, China Agricultural University, Beijing 100094, China. jhl@cau.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16000410" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animal Migration ; Animals ; Birds/virology ; Charadriiformes/*virology ; Chickens ; China/epidemiology ; Disease Outbreaks/*veterinary ; Geese/*virology ; Genome, Viral ; *Influenza A Virus, H5N1 Subtype ; Influenza A virus/classification/genetics/isolation & purification/*pathogenicity ; Influenza in Birds/*epidemiology/pathology/*virology ; Mice ; Molecular Sequence Data ; Phylogeny ; Reassortant Viruses/genetics/pathogenicity ; Virulence
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  • 8
    Publication Date: 2006-02-18
    Description: Lithium is commonly used to treat bipolar disorder, which is associated with altered circadian rhythm. Lithium is a potent inhibitor of glycogen synthase kinase 3 (GSK3), which regulates circadian rhythm in several organisms. In experiments with cultured cells, we show here that GSK3beta phosphorylates and stabilizes the orphan nuclear receptor Rev-erbalpha, a negative component of the circadian clock. Lithium treatment of cells leads to rapid proteasomal degradation of Rev-erbalpha and activation of clock gene Bmal1. A form of Rev-erbalpha that is insensitive to lithium interferes with the expression of circadian genes. Control of Rev-erbalpha protein stability is thus a critical component of the peripheral clock and a biological target of lithium therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, Lei -- Wang, Jing -- Klein, Peter S -- Lazar, Mitchell A -- DK 19525/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- MH058324/MH/NIMH NIH HHS/ -- R01 MH058324/MH/NIMH NIH HHS/ -- R01 MH058324-07/MH/NIMH NIH HHS/ -- R01 MH058324-08/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1002-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, and University of Pennsylvania School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484495" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Amino Acid Sequence ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Biological Clocks/*physiology ; Cell Line ; Cell Line, Tumor ; Circadian Rhythm/*physiology ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Down-Regulation ; Gene Expression Regulation ; Glycogen Synthase Kinase 3/antagonists & inhibitors/metabolism ; Humans ; Lithium Chloride/*pharmacology ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Phosphorylation ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex/metabolism ; Proteasome Inhibitors ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism
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  • 9
    Publication Date: 2009-07-11
    Description: Measurements of the abundance of common metabolites in cultured embryonic stem (ES) cells revealed an unusual state with respect to one-carbon metabolism. These findings led to the discovery of copious expression of the gene encoding threonine dehydrogenase (TDH) in ES cells. TDH-mediated catabolism of threonine takes place in mitochondria to generate glycine and acetyl-coenzyme A (CoA), with glycine facilitating one-carbon metabolism via the glycine cleavage system and acetyl-CoA feeding the tricarboxylic acid cycle. Culture media individually deprived of each of the 20 amino acids were applied to ES cells, leading to the discovery that ES cells are critically dependent on one amino acid--threonine. These observations show that ES cells exist in a high-flux backbone metabolic state comparable to that of rapidly growing bacterial cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4373593/" 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/PMC4373593/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Jian -- Alexander, Peter -- Wu, Leeju -- Hammer, Robert -- Cleaver, Ondine -- McKnight, Steven L -- R01 DK079862/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):435-9. doi: 10.1126/science.1173288. Epub 2009 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19589965" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Oxidoreductases/genetics/metabolism ; Animals ; Cells, Cultured ; Culture Media ; Embryo, Mammalian/metabolism ; Embryonic Development ; Embryonic Stem Cells/*metabolism ; HeLa Cells ; Humans ; Mice ; NIH 3T3 Cells ; Threonine/*metabolism ; Tissue Culture Techniques
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  • 10
    Publication Date: 2009-08-29
    Description: Akt signaling plays a central role in many biological functions, such as cell proliferation and apoptosis. Because Akt (also known as protein kinase B) resides primarily in the cytosol, it is not known how these signaling molecules are recruited to the plasma membrane and subsequently activated by growth factor stimuli. We found that the protein kinase Akt undergoes lysine-63 chain ubiquitination, which is important for Akt membrane localization and phosphorylation. TRAF6 was found to be a direct E3 ligase for Akt and was essential for Akt ubiquitination, membrane recruitment, and phosphorylation upon growth-factor stimulation. The human cancer-associated Akt mutant displayed an increase in Akt ubiquitination, in turn contributing to the enhancement of Akt membrane localization and phosphorylation. Thus, Akt ubiquitination is an important step for oncogenic Akt activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008763/" 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/PMC3008763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Wei-Lei -- Wang, Jing -- Chan, Chia-Hsin -- Lee, Szu-Wei -- Campos, Alejandro D -- Lamothe, Betty -- Hur, Lana -- Grabiner, Brian C -- Lin, Xin -- Darnay, Bryant G -- Lin, Hui-Kuan -- R01 CA149321/CA/NCI NIH HHS/ -- R01 CA149321-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 28;325(5944):1134-8. doi: 10.1126/science.1175065.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19713527" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Apoptosis ; Cell Line ; Cell Line, Tumor ; Cell Membrane/*metabolism ; Humans ; Insulin-Like Growth Factor I/pharmacology ; Interleukin-1beta/pharmacology ; Lipopolysaccharides/pharmacology ; Mice ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/chemistry/*metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 6/genetics/*metabolism ; Transplantation, Heterologous ; Ubiquitin-Protein Ligases/*metabolism ; Ubiquitination
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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