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  • 1
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    Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-20
    Description: Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR). In situ binding and organ culture studies indicate that EDA-A1 and EDA-A2 are differentially expressed and play a role in epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, M -- Wang, L C -- Hymowitz, S G -- Schilbach, S -- Lee, J -- Goddard, A -- de Vos, A M -- Gao, W Q -- Dixit, V M -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039935" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Binding Sites ; Cell Line ; DNA-Binding Proteins/metabolism ; Ectodermal Dysplasia/genetics ; Ectodysplasins ; Epidermis/embryology/*metabolism ; Humans ; *I-kappa B Proteins ; In Situ Hybridization ; Ligands ; Membrane Proteins/*chemistry/*metabolism ; Mice ; Models, Molecular ; Molecular Sequence Data ; Morphogenesis ; NF-kappa B/metabolism ; Phosphorylation ; Point Mutation ; Protein Conformation ; Proteins/metabolism ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 6 ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    DNA topoisomerase IIbeta and neural development (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-30
    Description: DNA topoisomerase IIbeta is shown to have an unsuspected and critical role in neural development. Neurogenesis was normal in IIbeta mutant mice, but motor axons failed to contact skeletal muscles, and sensory axons failed to enter the spinal cord. Despite an absence of innervation, clusters of acetylcholine receptors were concentrated in the central region of skeletal muscles, thereby revealing patterning mechanisms that are autonomous to skeletal muscle. The defects in motor axon growth in IIbeta mutant mice resulted in a breathing impairment and death of the pups shortly after birth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, X -- Li, W -- Prescott, E D -- Burden, S J -- Wang, J C -- NS10537/NS/NINDS NIH HHS/ -- NS27963/NS/NINDS NIH HHS/ -- NS36193/NS/NINDS NIH HHS/ -- R01 NS036193/NS/NINDS NIH HHS/ -- R01 NS036193-02/NS/NINDS NIH HHS/ -- R01 NS041311/NS/NINDS NIH HHS/ -- R01 NS041311-03/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):131-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skirball Institute of Molecular Medicine, New York University Medical School, 540 First Avenue, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cell Lineage ; Cues ; DNA Repair ; DNA Topoisomerases, Type II/genetics/*metabolism ; DNA-Binding Proteins ; Diaphragm/chemistry/embryology/innervation ; Embryonic and Fetal Development ; Gene Targeting ; Intercostal Muscles/innervation ; Mice ; Mice, Knockout ; Motor Neurons/physiology/ultrastructure ; Muscle, Skeletal/embryology/*innervation ; Neuromuscular Junction/*embryology/growth & development ; Neurons, Afferent/physiology/ultrastructure ; Presynaptic Terminals/ultrastructure ; Receptors, Cholinergic/analysis ; Skin/innervation ; Spinal Cord/embryology/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    NAADP mobilizes calcium from acidic organelles through two-pore channels (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-04-24
    Description: Ca(2+) mobilization from intracellular stores represents an important cell signalling process that is regulated, in mammalian cells, by inositol-1,4,5-trisphosphate (InsP(3)), cyclic ADP ribose and nicotinic acid adenine dinucleotide phosphate (NAADP). InsP(3) and cyclic ADP ribose cause the release of Ca(2+) from sarcoplasmic/endoplasmic reticulum stores by the activation of InsP(3) and ryanodine receptors (InsP(3)Rs and RyRs). In contrast, the nature of the intracellular stores targeted by NAADP and the molecular identity of the NAADP receptors remain controversial, although evidence indicates that NAADP mobilizes Ca(2+) from lysosome-related acidic compartments. Here we show that two-pore channels (TPCs) comprise a family of NAADP receptors, with human TPC1 (also known as TPCN1) and chicken TPC3 (TPCN3) being expressed on endosomal membranes, and human TPC2 (TPCN2) on lysosomal membranes when expressed in HEK293 cells. Membranes enriched with TPC2 show high affinity NAADP binding, and TPC2 underpins NAADP-induced Ca(2+) release from lysosome-related stores that is subsequently amplified by Ca(2+)-induced Ca(2+) release by InsP(3)Rs. Responses to NAADP were abolished by disrupting the lysosomal proton gradient and by ablating TPC2 expression, but were only attenuated by depleting endoplasmic reticulum Ca(2+) stores or by blocking InsP(3)Rs. Thus, TPCs form NAADP receptors that release Ca(2+) from acidic organelles, which can trigger further Ca(2+) signals via sarcoplasmic/endoplasmic reticulum. TPCs therefore provide new insights into the regulation and organization of Ca(2+) signals in animal cells, and will advance our understanding of the physiological role of NAADP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2761823/" 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/PMC2761823/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Calcraft, Peter J -- Ruas, Margarida -- Pan, Zui -- Cheng, Xiaotong -- Arredouani, Abdelilah -- Hao, Xuemei -- Tang, Jisen -- Rietdorf, Katja -- Teboul, Lydia -- Chuang, Kai-Ting -- Lin, Peihui -- Xiao, Rui -- Wang, Chunbo -- Zhu, Yingmin -- Lin, Yakang -- Wyatt, Christopher N -- Parrington, John -- Ma, Jianjie -- Evans, A Mark -- Galione, Antony -- Zhu, Michael X -- 070772/Wellcome Trust/United Kingdom -- FS/05/050/British Heart Foundation/United Kingdom -- P30 NS045758/NS/NINDS NIH HHS/ -- P30 NS045758-05/NS/NINDS NIH HHS/ -- P30 NS045758-059003/NS/NINDS NIH HHS/ -- P30-NS045758/NS/NINDS NIH HHS/ -- R01 DK081654/DK/NIDDK NIH HHS/ -- R01 DK081654-01A1/DK/NIDDK NIH HHS/ -- R01 NS042183/NS/NINDS NIH HHS/ -- R01 NS042183-04/NS/NINDS NIH HHS/ -- R21 NS056942/NS/NINDS NIH HHS/ -- R21 NS056942-01/NS/NINDS NIH HHS/ -- England -- Nature. 2009 May 28;459(7246):596-600. doi: 10.1038/nature08030. Epub 2009 Apr 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Integrative Physiology, College of Medicine and Veterinary Medicine, University of Edinburgh, Hugh Robson Building, Edinburgh EH8 9XD, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19387438" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/genetics/*metabolism ; *Calcium Signaling/drug effects ; Cell Line ; Chickens ; Humans ; Hydrogen-Ion Concentration ; Insulin-Secreting Cells/drug effects/metabolism ; Mice ; Mice, Knockout ; Molecular Sequence Data ; NADP/*analogs & derivatives/metabolism/pharmacology ; Organelles/drug effects/*metabolism ; Protein Binding
    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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  • 4
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    Quantitative reactivity profiling predicts functional cysteines in proteomes (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-11-19
    Description: Cysteine is the most intrinsically nucleophilic amino acid in proteins, where its reactivity is tuned to perform diverse biochemical functions. The absence of a consensus sequence that defines functional cysteines in proteins has hindered their discovery and characterization. Here we describe a proteomics method to profile quantitatively the intrinsic reactivity of cysteine residues en masse directly in native biological systems. Hyper-reactivity was a rare feature among cysteines and it was found to specify a wide range of activities, including nucleophilic and reductive catalysis and sites of oxidative modification. Hyper-reactive cysteines were identified in several proteins of uncharacterized function, including a residue conserved across eukaryotic phylogeny that we show is required for yeast viability and is involved in iron-sulphur protein biogenesis. We also demonstrate that quantitative reactivity profiling can form the basis for screening and functional assignment of cysteines in computationally designed proteins, where it discriminated catalytically active from inactive cysteine hydrolase designs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058684/" 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/PMC3058684/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weerapana, Eranthie -- Wang, Chu -- Simon, Gabriel M -- Richter, Florian -- Khare, Sagar -- Dillon, Myles B D -- Bachovchin, Daniel A -- Mowen, Kerri -- Baker, David -- Cravatt, Benjamin F -- CA087660/CA/NCI NIH HHS/ -- MH084512/MH/NIMH NIH HHS/ -- R01 CA087660/CA/NCI NIH HHS/ -- R01 CA087660-09/CA/NCI NIH HHS/ -- R01 GM085117/GM/NIGMS NIH HHS/ -- R01 GM090294/GM/NIGMS NIH HHS/ -- R01 GM090294-02/GM/NIGMS NIH HHS/ -- R37 CA087660/CA/NCI NIH HHS/ -- R37 CA087660-10/CA/NCI NIH HHS/ -- U54 MH084512/MH/NIMH NIH HHS/ -- U54 MH084512-030004/MH/NIMH NIH HHS/ -- England -- Nature. 2010 Dec 9;468(7325):790-5. doi: 10.1038/nature09472. Epub 2010 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21085121" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biocatalysis ; Cell Line, Tumor ; Conserved Sequence ; Cysteine/analysis/*metabolism ; Humans ; Hydrolases/chemistry/metabolism ; Iron-Sulfur Proteins/biosynthesis ; Liver/metabolism ; Mice ; Myocardium/metabolism ; Nuclear Proteins/chemistry/metabolism ; Oxidation-Reduction ; Protein Engineering ; Protein Hydrolysates ; Protein-Arginine N-Methyltransferases/chemistry/metabolism ; Proteins/*chemistry/*metabolism ; Proteome/*chemistry/*metabolism ; Proteomics/methods ; Repressor Proteins/chemistry/metabolism ; Saccharomyces cerevisiae/genetics/metabolism ; Saccharomyces cerevisiae Proteins/chemistry/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Tet2 is required to resolve inflammation by recruiting Hdac2 to specifically repress IL-6 (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-08-20
    Description: Epigenetic modifiers have fundamental roles in defining unique cellular identity through the establishment and maintenance of lineage-specific chromatin and methylation status. Several DNA modifications such as 5-hydroxymethylcytosine (5hmC) are catalysed by the ten eleven translocation (Tet) methylcytosine dioxygenase family members, and the roles of Tet proteins in regulating chromatin architecture and gene transcription independently of DNA methylation have been gradually uncovered. However, the regulation of immunity and inflammation by Tet proteins independent of their role in modulating DNA methylation remains largely unknown. Here we show that Tet2 selectively mediates active repression of interleukin-6 (IL-6) transcription during inflammation resolution in innate myeloid cells, including dendritic cells and macrophages. Loss of Tet2 resulted in the upregulation of several inflammatory mediators, including IL-6, at late phase during the response to lipopolysaccharide challenge. Tet2-deficient mice were more susceptible to endotoxin shock and dextran-sulfate-sodium-induced colitis, displaying a more severe inflammatory phenotype and increased IL-6 production compared to wild-type mice. IkappaBzeta, an IL-6-specific transcription factor, mediated specific targeting of Tet2 to the Il6 promoter, further indicating opposite regulatory roles of IkappaBzeta at initial and resolution phases of inflammation. For the repression mechanism, independent of DNA methylation and hydroxymethylation, Tet2 recruited Hdac2 and repressed transcription of Il6 via histone deacetylation. We provide mechanistic evidence for the gene-specific transcription repression activity of Tet2 via histone deacetylation and for the prevention of constant transcription activation at the chromatin level for resolving inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4697747/" 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/PMC4697747/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Qian -- Zhao, Kai -- Shen, Qicong -- Han, Yanmei -- Gu, Yan -- Li, Xia -- Zhao, Dezhi -- Liu, Yiqi -- Wang, Chunmei -- Zhang, Xiang -- Su, Xiaoping -- Liu, Juan -- Ge, Wei -- Levine, Ross L -- Li, Nan -- Cao, Xuetao -- P30 CA008748/CA/NCI NIH HHS/ -- R01 CA173636/CA/NCI NIH HHS/ -- England -- Nature. 2015 Sep 17;525(7569):389-93. doi: 10.1038/nature15252. Epub 2015 Aug 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Key Laboratory of Medical Molecular Biology &Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China. ; National Key Laboratory of Medical Immunology &Institute of Immunology, Second Military Medical University, Shanghai 200433, China. ; Human Oncology and Pathogenesis Program and Leukemia Service, Department of Medicine, Memorial Sloan-Kettering Cancer, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26287468" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Chromatin/chemistry/genetics/metabolism ; Colitis/enzymology/immunology/metabolism ; DNA Methylation ; DNA-Binding Proteins/deficiency/*metabolism ; Dendritic Cells/cytology/metabolism ; Down-Regulation/genetics ; Epigenesis, Genetic ; Female ; HEK293 Cells ; Histone Deacetylase 2/*metabolism ; Histones/chemistry/metabolism ; Humans ; I-kappa B Proteins/metabolism ; Inflammation/enzymology/immunology/*metabolism ; Interleukin-6/*antagonists & inhibitors/*biosynthesis/genetics/immunology ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins/deficiency/*metabolism ; Transcription, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Promoting axon regeneration in the adult CNS by modulation of the PTEN/mTOR pathway (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-08
    Description: The failure of axons to regenerate is a major obstacle for functional recovery after central nervous system (CNS) injury. Removing extracellular inhibitory molecules results in limited axon regeneration in vivo. To test for the role of intrinsic impediments to axon regrowth, we analyzed cell growth control genes using a virus-assisted in vivo conditional knockout approach. Deletion of PTEN (phosphatase and tensin homolog), a negative regulator of the mammalian target of rapamycin (mTOR) pathway, in adult retinal ganglion cells (RGCs) promotes robust axon regeneration after optic nerve injury. In wild-type adult mice, the mTOR activity was suppressed and new protein synthesis was impaired in axotomized RGCs, which may contribute to the regeneration failure. Reactivating this pathway by conditional knockout of tuberous sclerosis complex 1, another negative regulator of the mTOR pathway, also leads to axon regeneration. Thus, our results suggest the manipulation of intrinsic growth control pathways as a therapeutic approach to promote axon regeneration after CNS injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652400/" 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/PMC2652400/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Kevin Kyungsuk -- Liu, Kai -- Hu, Yang -- Smith, Patrice D -- Wang, Chen -- Cai, Bin -- Xu, Bengang -- Connolly, Lauren -- Kramvis, Ioannis -- Sahin, Mustafa -- He, Zhigang -- R01 NS051788/NS/NINDS NIH HHS/ -- R01 NS051788-04/NS/NINDS NIH HHS/ -- R01 NS058956/NS/NINDS NIH HHS/ -- R01 NS058956-02/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):963-6. doi: 10.1126/science.1161566.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉F. M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988856" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Axotomy ; Carrier Proteins/*metabolism ; Cell Survival ; Mice ; Mice, Knockout ; Nerve Crush ; *Nerve Regeneration ; Optic Nerve ; PTEN Phosphohydrolase/genetics/*metabolism ; Phosphotransferases (Alcohol Group Acceptor)/*metabolism ; Protein Biosynthesis ; Retinal Ganglion Cells/metabolism/physiology ; Ribosomal Protein S6/metabolism ; *Signal Transduction ; TOR Serine-Threonine Kinases ; Tumor Suppressor Proteins/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-14
    Description: Dendritic cells (DCs) play a vital role in initiating robust immunity against pathogens as well as maintaining immunological tolerance to self antigens. However, the intracellular signaling networks that program DCs to become tolerogenic remain unknown. We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells. Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease. Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732486/" 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/PMC3732486/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manicassamy, Santhakumar -- Reizis, Boris -- Ravindran, Rajesh -- Nakaya, Helder -- Salazar-Gonzalez, Rosa Maria -- Wang, Yi-Chong -- Pulendran, Bali -- HHSN266 200700006C/PHS HHS/ -- N01 AI50019/AI/NIAID NIH HHS/ -- N01 AI50025/AI/NIAID NIH HHS/ -- R01 AI048638/AI/NIAID NIH HHS/ -- R01 AI056499/AI/NIAID NIH HHS/ -- R01 DK057665/DK/NIDDK NIH HHS/ -- R01DK057665,/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- R37AI48638,/AI/NIAID NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19AI057266,/AI/NIAID NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- U54AI057157/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):849-53. doi: 10.1126/science.1188510.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, GA 30329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/metabolism ; Dendritic Cells/*immunology/metabolism ; Gene Expression Profiling ; *Inflammation ; Inflammatory Bowel Diseases/*immunology ; Intestinal Mucosa/cytology/*immunology/metabolism ; Macrophages/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; *Self Tolerance ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Tretinoin/metabolism ; Wnt Proteins/metabolism ; beta Catenin/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Akt-mediated regulation of autophagy and tumorigenesis through Beclin 1 phosphorylation (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-01
    Description: Aberrant signaling through the class I phosphatidylinositol 3-kinase (PI3K)-Akt axis is frequent in human cancer. Here, we show that Beclin 1, an essential autophagy and tumor suppressor protein, is a target of the protein kinase Akt. Expression of a Beclin 1 mutant resistant to Akt-mediated phosphorylation increased autophagy, reduced anchorage-independent growth, and inhibited Akt-driven tumorigenesis. Akt-mediated phosphorylation of Beclin 1 enhanced its interactions with 14-3-3 and vimentin intermediate filament proteins, and vimentin depletion increased autophagy and inhibited Akt-driven transformation. Thus, Akt-mediated phosphorylation of Beclin 1 functions in autophagy inhibition, oncogenesis, and the formation of an autophagy-inhibitory Beclin 1/14-3-3/vimentin intermediate filament complex. These findings have broad implications for understanding the role of Akt signaling and intermediate filament proteins in autophagy and cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507442/" 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/PMC3507442/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Richard C -- Wei, Yongjie -- An, Zhenyi -- Zou, Zhongju -- Xiao, Guanghua -- Bhagat, Govind -- White, Michael -- Reichelt, Julia -- Levine, Beth -- K08 CA164047/CA/NCI NIH HHS/ -- P30 CA142543/CA/NCI NIH HHS/ -- R01 CA071443/CA/NCI NIH HHS/ -- R01 CA084254/CA/NCI NIH HHS/ -- R01 CA109618/CA/NCI NIH HHS/ -- R01 CA129451/CA/NCI NIH HHS/ -- R01 CA84254-S1/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):956-9. doi: 10.1126/science.1225967. Epub 2012 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23112296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins/genetics/*metabolism ; *Autophagy ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/*metabolism ; Fibroblasts/metabolism/pathology ; HeLa Cells ; Humans ; Membrane Proteins/genetics/*metabolism ; Mice ; Phosphorylation ; Proto-Oncogene Proteins c-akt/genetics/*metabolism ; RNA, Small Interfering/genetics ; Rats ; Transduction, Genetic ; Vimentin/genetics ; Xenograft Model Antitumor Assays
    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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    Gastric cancer originating from bone marrow-derived cells (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-30
    Description: Epithelial cancers are believed to originate from transformation of tissue stem cells. However, bone marrow-derived cells (BMDCs), which are frequently recruited to sites of tissue injury and inflammation, might also represent a potential source of malignancy. We show that although acute injury, acute inflammation, or transient parietal cell loss within the stomach do not lead to BMDC recruitment, chronic infection of C57BL/6 mice with Helicobacter, a known carcinogen, induces repopulation of the stomach with BMDCs. Subsequently, these cells progress through metaplasia and dysplasia to intraepithelial cancer. These findings suggest that epithelial cancers can originate from marrow-derived sources and thus have broad implications for the multistep model of cancer progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Houghton, Jeanmarie -- Stoicov, Calin -- Nomura, Sachiyo -- Rogers, Arlin B -- Carlson, Jane -- Li, Hanchen -- Cai, Xun -- Fox, James G -- Goldenring, James R -- Wang, Timothy C -- CA95103/CA/NCI NIH HHS/ -- K22 CA90518/CA/NCI NIH HHS/ -- R01 CA87958/CA/NCI NIH HHS/ -- R01 DK58/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2004 Nov 26;306(5701):1568-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA. jeanmarie.houghton@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15567866" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bone Marrow Cells/*cytology ; Bone Marrow Transplantation ; Carcinoma in Situ/pathology ; Cell Differentiation ; Cell Fusion ; Disease Progression ; Female ; Gastric Mucosa/chemistry/pathology ; Gastritis/*pathology ; Helicobacter Infections/*pathology ; *Helicobacter felis ; Keratins/analysis ; Male ; Mesenchymal Stromal Cells/physiology ; Metaplasia ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mucins/analysis ; Muscle Proteins/analysis ; Parietal Cells, Gastric/physiology ; Peptides/analysis ; Phenotype ; Stem Cells/*physiology ; Stomach Neoplasms/*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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  • 10
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    Evolution of human BCR-ABL1 lymphoblastic leukaemia-initiating cells (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-01-21
    Description: Many tumours are composed of genetically diverse cells; however, little is known about how diversity evolves or the impact that diversity has on functional properties. Here, using xenografting and DNA copy number alteration (CNA) profiling of human BCR-ABL1 lymphoblastic leukaemia, we demonstrate that genetic diversity occurs in functionally defined leukaemia-initiating cells and that many diagnostic patient samples contain multiple genetically distinct leukaemia-initiating cell subclones. Reconstructing the subclonal genetic ancestry of several samples by CNA profiling demonstrated a branching multi-clonal evolution model of leukaemogenesis, rather than linear succession. For some patient samples, the predominant diagnostic clone repopulated xenografts, whereas in others it was outcompeted by minor subclones. Reconstitution with the predominant diagnosis clone was associated with more aggressive growth properties in xenografts, deletion of CDKN2A and CDKN2B, and a trend towards poorer patient outcome. Our findings link clonal diversity with leukaemia-initiating-cell function and underscore the importance of developing therapies that eradicate all intratumoral subclones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Notta, Faiyaz -- Mullighan, Charles G -- Wang, Jean C Y -- Poeppl, Armando -- Doulatov, Sergei -- Phillips, Letha A -- Ma, Jing -- Minden, Mark D -- Downing, James R -- Dick, John E -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2011 Jan 20;469(7330):362-7. doi: 10.1038/nature09733.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Stem Cell and Developmental Biology, Campbell Family Institute for Cancer Research/Ontario Cancer Institute, Toronto, Ontario M5G 1L7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21248843" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival ; Clone Cells/*metabolism/*pathology ; Cyclin-Dependent Kinase Inhibitor p15/deficiency/genetics ; DNA Copy Number Variations/genetics ; Disease Progression ; *Evolution, Molecular ; Fusion Proteins, bcr-abl/*genetics ; Genes, p16 ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Models, Biological ; Neoplasm Transplantation ; Oligonucleotide Array Sequence Analysis ; Philadelphia Chromosome ; Polymorphism, Single Nucleotide/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/*pathology ; Survival Rate ; Transplantation, Heterologous
    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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