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  • 1
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    Hedgehog/Wnt feedback supports regenerative proliferation of epithelial stem cells in bladder (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-11
    Description: Epithelial integrity in metazoan organs is maintained through the regulated proliferation and differentiation of organ-specific stem and progenitor cells. Although the epithelia of organs such as the intestine regenerate constantly and thus remain continuously proliferative, other organs, such as the mammalian urinary bladder, shift from near-quiescence to a highly proliferative state in response to epithelial injury. The cellular and molecular mechanisms underlying this injury-induced mode of regenerative response are poorly defined. Here we show in mice that the proliferative response to bacterial infection or chemical injury within the bladder is regulated by signal feedback between basal cells of the urothelium and the stromal cells that underlie them. We demonstrate that these basal cells include stem cells capable of regenerating all cell types within the urothelium, and are marked by expression of the secreted protein signal Sonic hedgehog (Shh). On injury, Shh expression in these basal cells increases and elicits increased stromal expression of Wnt protein signals, which in turn stimulate the proliferation of both urothelial and stromal cells. The heightened activity of this signal feedback circuit and the associated increase in cell proliferation appear to be required for restoration of urothelial function and, in the case of bacterial injury, may help clear and prevent further spread of infection. Our findings provide a conceptual framework for injury-induced epithelial regeneration in endodermal organs, and may provide a basis for understanding the roles of signalling pathways in cancer growth and metastasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3676169/" 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/PMC3676169/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, Kunyoo -- Lee, John -- Guo, Nini -- Kim, James -- Lim, Agnes -- Qu, Lishu -- Mysorekar, Indira U -- Beachy, Philip A -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Apr 7;472(7341):110-4. doi: 10.1038/nature09851. Epub 2011 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Institute for Stem Cell Biology and Regenerative Medicine, Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA. kunyoos@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21389986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Cell Proliferation ; Epithelial Cells/*cytology/metabolism ; Feedback, Physiological ; Female ; Fibroblast Growth Factors/metabolism ; Hedgehog Proteins/*metabolism ; Kruppel-Like Transcription Factors/genetics/metabolism ; Mice ; Organoids/cytology ; Regeneration/*physiology ; Signal Transduction ; Stem Cells/*cytology/metabolism ; Stromal Cells/cytology/metabolism ; Urinary Bladder/*cytology/drug effects/injuries/metabolism ; Urinary Bladder Diseases/chemically induced/metabolism/microbiology/pathology ; Uropathogenic Escherichia coli/physiology ; Urothelium/cytology ; Wnt Proteins/*metabolism
    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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  • 2
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    Phosphorylation of NLRC4 is critical for inflammasome activation (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-08-14
    Description: NLRC4 is a cytosolic member of the NOD-like receptor family that is expressed in innate immune cells. It senses indirectly bacterial flagellin and type III secretion systems, and responds by assembling an inflammasome complex that promotes caspase-1 activation and pyroptosis. Here we use knock-in mice expressing NLRC4 with a carboxy-terminal 3xFlag tag to identify phosphorylation of NLRC4 on a single, evolutionarily conserved residue, Ser 533, following infection of macrophages with Salmonella enterica serovar Typhimurium (also known as Salmonella typhimurium). Western blotting with a NLRC4 phospho-Ser 533 antibody confirmed that this post-translational modification occurs only in the presence of stimuli known to engage NLRC4 and not the related protein NLRP3 or AIM2. Nlrc4(-/-) macrophages reconstituted with NLRC4 mutant S533A, unlike those reconstituted with wild-type NLRC4, did not activate caspase-1 and pyroptosis in response to S. typhimurium, indicating that S533 phosphorylation is critical for NLRC4 inflammasome function. Conversely, phosphomimetic NLRC4 S533D caused rapid macrophage pyroptosis without infection. Biochemical purification of the NLRC4-phosphorylating activity and a screen of kinase inhibitors identified PRKCD (PKCdelta) as a candidate NLRC4 kinase. Recombinant PKCdelta phosphorylated NLRC4 S533 in vitro, immunodepletion of PKCdelta from macrophage lysates blocked NLRC4 S533 phosphorylation in vitro, and Prkcd(-/-) macrophages exhibited greatly attenuated caspase-1 activation and IL-1beta secretion specifically in response to S. typhimurium. Phosphorylation-defective NLRC4 S533A failed to recruit procaspase-1 and did not assemble inflammasome specks during S. typhimurium infection, so phosphorylation of NLRC4 S533 probably drives conformational changes necessary for NLRC4 inflammasome activity and host innate immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qu, Yan -- Misaghi, Shahram -- Izrael-Tomasevic, Anita -- Newton, Kim -- Gilmour, Laurie L -- Lamkanfi, Mohamed -- Louie, Salina -- Kayagaki, Nobuhiko -- Liu, Jinfeng -- Komuves, Laszlo -- Cupp, James E -- Arnott, David -- Monack, Denise -- Dixit, Vishva M -- England -- Nature. 2012 Oct 25;490(7421):539-42. doi: 10.1038/nature11429. Epub 2012 Aug 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22885697" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CARD Signaling Adaptor Proteins/chemistry/deficiency/genetics/*metabolism ; Calcium-Binding Proteins/chemistry/deficiency/genetics/*metabolism ; Caspase 1/metabolism ; Enzyme Activation ; Gene Knock-In Techniques ; Humans ; Immunity, Innate/immunology ; Inflammasomes/*metabolism ; Interleukin-1beta/immunology/secretion ; Macrophages/immunology ; Mice ; Molecular Sequence Data ; Phosphorylation ; Protein Conformation ; Protein Kinase C-delta/deficiency/genetics/metabolism ; Salmonella typhimurium/immunology ; Sequence Alignment
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Non-canonical inflammasome activation targets caspase-11 (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-18
    Description: Caspase-1 activation by inflammasome scaffolds comprised of intracellular nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) and the adaptor ASC is believed to be essential for production of the pro-inflammatory cytokines interleukin (IL)-1beta and IL-18 during the innate immune response. Here we show, with C57BL/6 Casp11 gene-targeted mice, that caspase-11 (also known as caspase-4) is critical for caspase-1 activation and IL-1beta production in macrophages infected with Escherichia coli, Citrobacter rodentium or Vibrio cholerae. Strain 129 mice, like Casp11(-/-) mice, exhibited defects in IL-1beta production and harboured a mutation in the Casp11 locus that attenuated caspase-11 expression. This finding is important because published targeting of the Casp1 gene was done using strain 129 embryonic stem cells. Casp1 and Casp11 are too close in the genome to be segregated by recombination; consequently, the published Casp1(-/-) mice lack both caspase-11 and caspase-1. Interestingly, Casp11(-/-) macrophages secreted IL-1beta normally in response to ATP and monosodium urate, indicating that caspase-11 is engaged by a non-canonical inflammasome. Casp1(-/-)Casp11(129mt/129mt) macrophages expressing caspase-11 from a C57BL/6 bacterial artificial chromosome transgene failed to secrete IL-1beta regardless of stimulus, confirming an essential role for caspase-1 in IL-1beta production. Caspase-11 rather than caspase-1, however, was required for non-canonical inflammasome-triggered macrophage cell death, indicating that caspase-11 orchestrates both caspase-1-dependent and -independent outputs. Caspase-1 activation by non-canonical stimuli required NLRP3 and ASC, but caspase-11 processing and cell death did not, implying that there is a distinct activator of caspase-11. Lastly, loss of caspase-11 rather than caspase-1 protected mice from a lethal dose of lipopolysaccharide. These data highlight a unique pro-inflammatory role for caspase-11 in the innate immune response to clinically significant bacterial infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kayagaki, Nobuhiko -- Warming, Soren -- Lamkanfi, Mohamed -- Vande Walle, Lieselotte -- Louie, Salina -- Dong, Jennifer -- Newton, Kim -- Qu, Yan -- Liu, Jinfeng -- Heldens, Sherry -- Zhang, Juan -- Lee, Wyne P -- Roose-Girma, Merone -- Dixit, Vishva M -- England -- Nature. 2011 Oct 16;479(7371):117-21. doi: 10.1038/nature10558.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech Inc., South San Francisco, California 94080, USA. kayagaki@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22002608" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 1/metabolism ; Caspases/genetics/*metabolism ; Citrobacter rodentium/immunology ; Enzyme Activation ; Escherichia coli/immunology ; Immunity, Innate/immunology ; Inflammasomes/*metabolism ; Interleukin-1beta/biosynthesis/secretion ; Lipopolysaccharides/adverse effects/immunology ; Macrophages/immunology/secretion ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Vibrio cholerae/immunology
    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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    Nanoparticle biointerfacing by platelet membrane cloaking (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-09-17
    Description: Development of functional nanoparticles can be encumbered by unanticipated material properties and biological events, which can affect nanoparticle effectiveness in complex, physiologically relevant systems. Despite the advances in bottom-up nanoengineering and surface chemistry, reductionist functionalization approaches remain inadequate in replicating the complex interfaces present in nature and cannot avoid exposure of foreign materials. Here we report on the preparation of polymeric nanoparticles enclosed in the plasma membrane of human platelets, which are a unique population of cellular fragments that adhere to a variety of disease-relevant substrates. The resulting nanoparticles possess a right-side-out unilamellar membrane coating functionalized with immunomodulatory and adhesion antigens associated with platelets. Compared to uncoated particles, the platelet membrane-cloaked nanoparticles have reduced cellular uptake by macrophage-like cells and lack particle-induced complement activation in autologous human plasma. The cloaked nanoparticles also display platelet-mimicking properties such as selective adhesion to damaged human and rodent vasculatures as well as enhanced binding to platelet-adhering pathogens. In an experimental rat model of coronary restenosis and a mouse model of systemic bacterial infection, docetaxel and vancomycin, respectively, show enhanced therapeutic efficacy when delivered by the platelet-mimetic nanoparticles. The multifaceted biointerfacing enabled by the platelet membrane cloaking method provides a new approach in developing functional nanoparticles for disease-targeted delivery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Che-Ming J -- Fang, Ronnie H -- Wang, Kuei-Chun -- Luk, Brian T -- Thamphiwatana, Soracha -- Dehaini, Diana -- Nguyen, Phu -- Angsantikul, Pavimol -- Wen, Cindy H -- Kroll, Ashley V -- Carpenter, Cody -- Ramesh, Manikantan -- Qu, Vivian -- Patel, Sherrina H -- Zhu, Jie -- Shi, William -- Hofman, Florence M -- Chen, Thomas C -- Gao, Weiwei -- Zhang, Kang -- Chien, Shu -- Zhang, Liangfang -- R01DK095168/DK/NIDDK NIH HHS/ -- R01EY25090/EY/NEI NIH HHS/ -- R01HL108735/HL/NHLBI NIH HHS/ -- R25CA153915/CA/NCI NIH HHS/ -- England -- Nature. 2015 Oct 1;526(7571):118-21. doi: 10.1038/nature15373. Epub 2015 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of NanoEngineering, University of California, San Diego, La Jolla, California 92093, USA. ; Moores Cancer Center, University of California, San Diego, La Jolla, California 92093, USA. ; Department of Bioengineering, University of California, San Diego, La Jolla, California 92093, USA. ; Institute of Engineering in Medicine, University of California, San Diego, La Jolla, California 92093, USA. ; Shiley Eye Institute, University of California, San Diego, La Jolla, California 92093, USA. ; Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA. ; Veterans Administration Healthcare System, San Diego, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26374997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/*administration & dosage/pharmacokinetics ; Blood Platelets/*cytology ; Blood Vessels/cytology/metabolism/pathology ; Cell Membrane/*metabolism ; Collagen/chemistry/immunology ; Complement Activation/immunology ; Coronary Restenosis/blood/drug therapy/metabolism ; Disease Models, Animal ; Drug Delivery Systems/*methods ; Humans ; Macrophages/immunology ; Male ; Mice ; Nanoparticles/*administration & dosage/*chemistry ; *Platelet Adhesiveness ; Polymers/chemistry ; Rats ; Rats, Sprague-Dawley ; Staphylococcal Infections/blood/drug therapy/metabolism/microbiology ; Staphylococcus aureus/cytology/metabolism ; Taxoids/administration & dosage/pharmacokinetics ; Unilamellar Liposomes/chemistry ; Vancomycin/administration & dosage/pharmacokinetics
    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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    Aging stem cells. A Werner syndrome stem cell model unveils heterochromatin alterations as a driver of human aging (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-05-02
    Description: Werner syndrome (WS) is a premature aging disorder caused by WRN protein deficiency. Here, we report on the generation of a human WS model in human embryonic stem cells (ESCs). Differentiation of WRN-null ESCs to mesenchymal stem cells (MSCs) recapitulates features of premature cellular aging, a global loss of H3K9me3, and changes in heterochromatin architecture. We show that WRN associates with heterochromatin proteins SUV39H1 and HP1alpha and nuclear lamina-heterochromatin anchoring protein LAP2beta. Targeted knock-in of catalytically inactive SUV39H1 in wild-type MSCs recapitulates accelerated cellular senescence, resembling WRN-deficient MSCs. Moreover, decrease in WRN and heterochromatin marks are detected in MSCs from older individuals. Our observations uncover a role for WRN in maintaining heterochromatin stability and highlight heterochromatin disorganization as a potential determinant of human aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4494668/" 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/PMC4494668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Weiqi -- Li, Jingyi -- Suzuki, Keiichiro -- Qu, Jing -- Wang, Ping -- Zhou, Junzhi -- Liu, Xiaomeng -- Ren, Ruotong -- Xu, Xiuling -- Ocampo, Alejandro -- Yuan, Tingting -- Yang, Jiping -- Li, Ying -- Shi, Liang -- Guan, Dee -- Pan, Huize -- Duan, Shunlei -- Ding, Zhichao -- Li, Mo -- Yi, Fei -- Bai, Ruijun -- Wang, Yayu -- Chen, Chang -- Yang, Fuquan -- Li, Xiaoyu -- Wang, Zimei -- Aizawa, Emi -- Goebl, April -- Soligalla, Rupa Devi -- Reddy, Pradeep -- Esteban, Concepcion Rodriguez -- Tang, Fuchou -- Liu, Guang-Hui -- Belmonte, Juan Carlos Izpisua -- F32 AG047770/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2015 Jun 5;348(6239):1160-3. doi: 10.1126/science.aaa1356. Epub 2015 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China. ; Biodynamic Optical Imaging Center, College of Life Sciences, Peking University, Beijing 100871, China. ; Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. ; State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China. ; Diagnosis and Treatment Center for Oral Disease, the 306th Hospital of the PLA, Beijing, China. ; Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; College of Life Sciences, Peking University, Beijing 100871, China. ; The Center for Anti-aging and Regenerative Medicine, Shenzhen University, Shenzhen 518060, China. ; Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. Universidad Catolica San Antonio de Murcia, Campus de los Jeronimos s/n, 30107 Guadalupe, Murcia, Spain. ; Biodynamic Optical Imaging Center, College of Life Sciences, Peking University, Beijing 100871, China. Ministry of Education Key Laboratory of Cell Proliferation and Differentiation, Beijing 100871, China. Center for Molecular and Translational Medicine (CMTM), Beijing 100101, China. Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China. ghliu@ibp.ac.cn tangfuchou@pku.edu.cn belmonte@salk.edu. ; National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China. The Center for Anti-aging and Regenerative Medicine, Shenzhen University, Shenzhen 518060, China. Center for Molecular and Translational Medicine (CMTM), Beijing 100101, China. Beijing Institute for Brain Disorders, Beijing 100069, China. ghliu@ibp.ac.cn tangfuchou@pku.edu.cn belmonte@salk.edu. ; Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. ghliu@ibp.ac.cn tangfuchou@pku.edu.cn belmonte@salk.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25931448" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/*metabolism ; Animals ; *Cell Aging ; Cell Differentiation ; Centromere/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; DNA-Binding Proteins/metabolism ; Epigenesis, Genetic ; Exodeoxyribonucleases/genetics/*metabolism ; Gene Knockout Techniques ; HEK293 Cells ; Heterochromatin/chemistry/*metabolism ; Humans ; Membrane Proteins/metabolism ; Mesenchymal Stromal Cells/*metabolism ; Methyltransferases/genetics/metabolism ; Mice ; Models, Biological ; RecQ Helicases/genetics/*metabolism ; Repressor Proteins/genetics/metabolism ; Werner Syndrome/genetics/*metabolism
    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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  • 6
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    Rfx6 directs islet formation and insulin production in mice and humans (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-02-12
    Description: Insulin from the beta-cells of the pancreatic islets of Langerhans controls energy homeostasis in vertebrates, and its deficiency causes diabetes mellitus. During embryonic development, the transcription factor neurogenin 3 (Neurog3) initiates the differentiation of the beta-cells and other islet cell types from pancreatic endoderm, but the genetic program that subsequently completes this differentiation remains incompletely understood. Here we show that the transcription factor Rfx6 directs islet cell differentiation downstream of Neurog3. Mice lacking Rfx6 failed to generate any of the normal islet cell types except for pancreatic-polypeptide-producing cells. In human infants with a similar autosomal recessive syndrome of neonatal diabetes, genetic mapping and subsequent sequencing identified mutations in the human RFX6 gene. These studies demonstrate a unique position for Rfx6 in the hierarchy of factors that coordinate pancreatic islet development in both mice and humans. Rfx6 could prove useful in efforts to generate beta-cells for patients with diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896718/" 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/PMC2896718/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Stuart B -- Qu, Hui-Qi -- Taleb, Nadine -- Kishimoto, Nina Y -- Scheel, David W -- Lu, Yang -- Patch, Ann-Marie -- Grabs, Rosemary -- Wang, Juehu -- Lynn, Francis C -- Miyatsuka, Takeshi -- Mitchell, John -- Seerke, Rina -- Desir, Julie -- Vanden Eijnden, Serge -- Abramowicz, Marc -- Kacet, Nadine -- Weill, Jacques -- Renard, Marie-Eve -- Gentile, Mattia -- Hansen, Inger -- Dewar, Ken -- Hattersley, Andrew T -- Wang, Rennian -- Wilson, Maria E -- Johnson, Jeffrey D -- Polychronakos, Constantin -- German, Michael S -- P30 DK063720/DK/NIDDK NIH HHS/ -- P30 DK063720-045954/DK/NIDDK NIH HHS/ -- P30 DK063720-045955/DK/NIDDK NIH HHS/ -- P30 DK063720-045956/DK/NIDDK NIH HHS/ -- P30 DK063720-045957/DK/NIDDK NIH HHS/ -- P30 DK063720-045958/DK/NIDDK NIH HHS/ -- P30 DK063720-05/DK/NIDDK NIH HHS/ -- R01 DK021344/DK/NIDDK NIH HHS/ -- R01 DK021344-26/DK/NIDDK NIH HHS/ -- U19 DK061245/DK/NIDDK NIH HHS/ -- U19 DK061245-04/DK/NIDDK NIH HHS/ -- U19 DK061245-049001/DK/NIDDK NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Feb 11;463(7282):775-80. doi: 10.1038/nature08748.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Diabetes Center, University of California San Francisco, San Francisco, California 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20148032" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/deficiency/genetics/metabolism ; *Cell Differentiation ; DNA Mutational Analysis ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Diabetes Mellitus/congenital/genetics/metabolism/pathology ; Embryo, Mammalian/metabolism ; Female ; Fetus/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genes, Recessive/genetics ; Genetic Testing ; Humans ; Infant, Newborn ; Insulin/*biosynthesis ; Islets of Langerhans/*cytology/embryology/*metabolism ; Male ; Mice ; NIH 3T3 Cells ; Nerve Tissue Proteins/deficiency/genetics/metabolism ; Organ Specificity ; Syndrome ; Transcription Factors/deficiency/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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