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  • 1
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    Dynamic involvement of ATG5 in cellular stress responses (2014)
    Springer Nature
    Details
    Publication Date: 2014-10-24
    Description: Dynamic involvement of ATG5 in cellular stress responses Cell Death and Disease 5, e1478 (October 2014). doi:10.1038/cddis.2014.428 Authors: H H Lin, S-M Lin, Y Chung, S Vonderfecht, J M Camden, P Flodby, Z Borok, K H Limesand, N Mizushima & D K Ann
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 2
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    Autophagy fights disease through cellular self-digestion (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-02-29
    Description: Autophagy, or cellular self-digestion, is a cellular pathway involved in protein and organelle degradation, with an astonishing number of connections to human disease and physiology. For example, autophagic dysfunction is associated with cancer, neurodegeneration, microbial infection and ageing. Paradoxically, although autophagy is primarily a protective process for the cell, it can also play a role in cell death. Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2670399/" 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/PMC2670399/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mizushima, Noboru -- Levine, Beth -- Cuervo, Ana Maria -- Klionsky, Daniel J -- R01 AG021904/AG/NIA NIH HHS/ -- R01 AG021904-06/AG/NIA NIH HHS/ -- R03 AG019834/AG/NIA NIH HHS/ -- R03 AG019834-02/AG/NIA NIH HHS/ -- R21 AG025355/AG/NIA NIH HHS/ -- R21 AG025355-02/AG/NIA NIH HHS/ -- England -- Nature. 2008 Feb 28;451(7182):1069-75. doi: 10.1038/nature06639.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Cell Biology, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18305538" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Autophagy/immunology/*physiology ; Cell Death ; Cell Survival ; Humans ; Immunity, Innate/immunology ; Neoplasms/pathology ; Neurodegenerative Diseases/pathology
    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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    Autophagy in thymic epithelium shapes the T-cell repertoire and is essential for tolerance (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-08-15
    Description: Recognition of self-antigen-derived epitopes presented by major histocompatibility complex class II (MHC II) molecules on thymic epithelial cells (TECs) is critical for the generation of a functional and self-tolerant CD4 T-cell repertoire. Whereas haematopoietic antigen-presenting cells generate MHC-II-peptide complexes predominantly through the processing of endocytosed polypeptides, it remains unknown if and how TECs use unconventional pathways of antigen presentation. Here we address the role of macroautophagy, a process that has recently been shown to allow for endogenous MHC II loading, in T-cell repertoire selection in the mouse thymus. In contrast to most other tissues, TECs had a high constitutive level of autophagy. Genetic interference with autophagy specifically in TECs led to altered selection of certain MHC-II-restricted T-cell specificities and resulted in severe colitis and multi-organ inflammation. Our findings indicate that autophagy focuses the MHC-II-peptide repertoire of TECs on their intracellular milieu, which notably comprises a wide array of otherwise strictly 'tissue-specific' self antigens. In doing so, it contributes to T-cell selection and is essential for the generation of a self-tolerant T-cell repertoire.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nedjic, Jelena -- Aichinger, Martin -- Emmerich, Jan -- Mizushima, Noboru -- Klein, Ludger -- England -- Nature. 2008 Sep 18;455(7211):396-400. doi: 10.1038/nature07208. Epub 2008 Aug 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Institute of Molecular Pathology, Doktor Bohr Gasse 7, 1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18701890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cell Differentiation ; Chimera/immunology ; Colitis/genetics/immunology/metabolism ; Epithelial Cells/cytology/immunology ; Epithelium/*immunology ; Female ; Histocompatibility Antigens/immunology ; Immune Tolerance/*immunology ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/deficiency/genetics ; Receptors, Antigen, T-Cell/immunology ; Stromal Cells/cytology ; T-Lymphocytes/*cytology/*immunology ; Thymus Gland/*cytology/*immunology/transplantation
    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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    A key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-10-14
    Description: Susceptibility to Crohn's disease, a complex inflammatory disease involving the small intestine, is controlled by over 30 loci. One Crohn's disease risk allele is in ATG16L1, a gene homologous to the essential yeast autophagy gene ATG16 (ref. 2). It is not known how ATG16L1 or autophagy contributes to intestinal biology or Crohn's disease pathogenesis. To address these questions, we generated and characterized mice that are hypomorphic for ATG16L1 protein expression, and validated conclusions on the basis of studies in these mice by analysing intestinal tissues that we collected from Crohn's disease patients carrying the Crohn's disease risk allele of ATG16L1. Here we show that ATG16L1 is a bona fide autophagy protein. Within the ileal epithelium, both ATG16L1 and a second essential autophagy protein ATG5 are selectively important for the biology of the Paneth cell, a specialized epithelial cell that functions in part by secretion of granule contents containing antimicrobial peptides and other proteins that alter the intestinal environment. ATG16L1- and ATG5-deficient Paneth cells exhibited notable abnormalities in the granule exocytosis pathway. In addition, transcriptional analysis revealed an unexpected gain of function specific to ATG16L1-deficient Paneth cells including increased expression of genes involved in peroxisome proliferator-activated receptor (PPAR) signalling and lipid metabolism, of acute phase reactants and of two adipocytokines, leptin and adiponectin, known to directly influence intestinal injury responses. Importantly, Crohn's disease patients homozygous for the ATG16L1 Crohn's disease risk allele displayed Paneth cell granule abnormalities similar to those observed in autophagy-protein-deficient mice and expressed increased levels of leptin protein. Thus, ATG16L1, and probably the process of autophagy, have a role within the intestinal epithelium of mice and Crohn's disease patients by selective effects on the cell biology and specialized regulatory properties of Paneth cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695978/" 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/PMC2695978/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cadwell, Ken -- Liu, John Y -- Brown, Sarah L -- Miyoshi, Hiroyuki -- Loh, Joy -- Lennerz, Jochen K -- Kishi, Chieko -- Kc, Wumesh -- Carrero, Javier A -- Hunt, Steven -- Stone, Christian D -- Brunt, Elizabeth M -- Xavier, Ramnik J -- Sleckman, Barry P -- Li, Ellen -- Mizushima, Noboru -- Stappenbeck, Thaddeus S -- Virgin, Herbert W 4th -- AI062773/AI/NIAID NIH HHS/ -- DK43351/DK/NIDDK NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-13/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30 DK043351-18/DK/NIDDK NIH HHS/ -- P30 DK052574-09/DK/NIDDK NIH HHS/ -- P30 DK52574/DK/NIDDK NIH HHS/ -- R01 AI062773/AI/NIAID NIH HHS/ -- R01 AI062773-01A1/AI/NIAID NIH HHS/ -- R01 AI062832/AI/NIAID NIH HHS/ -- R01 AI062832-04/AI/NIAID NIH HHS/ -- T32 AR007279/AR/NIAMS NIH HHS/ -- T32 AR007279-30/AR/NIAMS NIH HHS/ -- T32 AR07279/AR/NIAMS NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- U54 AI057160-010005/AI/NIAID NIH HHS/ -- U54 AI057160-05S10018/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Nov 13;456(7219):259-63. doi: 10.1038/nature07416. Epub 2008 Oct 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18849966" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Autophagy/*genetics ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Crohn Disease/genetics/pathology ; Exocytosis/genetics ; Homozygote ; Humans ; Mice ; Mice, Inbred C57BL ; Mutation ; Paneth Cells/*metabolism/pathology
    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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  • 5
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    Autophagy-dependent viral recognition by plasmacytoid dendritic cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: Plasmacytoid dendritic cells (pDCs) detect viruses in the acidified endosomes by means of Toll-like receptors (TLRs). Yet, pDC responses to certain single-stranded RNA (ssRNA) viruses occur only after live viral infection. We present evidence here that the recognition of such viruses by TLR7 requires transport of cytosolic viral replication intermediates into the lysosome by the process of autophagy. In addition, autophagy was found to be required for the production of interferon-alpha by pDCs. These results support a key role for autophagy in mediating ssRNA virus detection and interferon-alpha secretion by pDCs and suggest that cytosolic replication intermediates of viruses serve as pathogen signatures recognized by TLR7.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Heung Kyu -- Lund, Jennifer M -- Ramanathan, Balaji -- Mizushima, Noboru -- Iwasaki, Akiko -- AI054359/AI/NIAID NIH HHS/ -- AI064705/AI/NIAID NIH HHS/ -- AI07019/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 9;315(5817):1398-401. Epub 2007 Feb 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Dendritic Cells/*immunology/physiology/*virology ; Endosomes/immunology/virology ; Female ; Immunity, Innate ; Interferon-alpha/metabolism ; Interleukin-12/metabolism ; Lysosomes/virology ; Male ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Transgenic ; Phagosomes/physiology/ultrastructure ; RNA, Viral/*immunology/metabolism ; Rhabdoviridae Infections/*immunology ; Toll-Like Receptor 7/*immunology ; Vesicular stomatitis Indiana virus/*immunology/physiology ; Virus Replication
    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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    Escape of intracellular Shigella from autophagy (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-04
    Description: The degradation of undesirable cellular components or organelles, including invading microbes, by autophagy is crucial for cell survival. Here, Shigella, an invasive bacteria, was found to be able to escape autophagy by secreting IcsB by means of the type III secretion system. Mutant bacteria lacking IcsB were trapped by autophagy during multiplication within the host cells. IcsB did not directly inhibit autophagy. Rather, Shigella VirG, a protein required for intracellular actin-based motility, induced autophagy by binding to the autophagy protein, Atg5. In nonmutant Shigella, this binding is competitively inhibited by IcsB binding to VirG.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogawa, Michinaga -- Yoshimori, Tamotsu -- Suzuki, Toshihiko -- Sagara, Hiroshi -- Mizushima, Noboru -- Sasakawa, Chihiro -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):727-31. Epub 2004 Dec 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15576571" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Bacterial Proteins/genetics/*metabolism ; Cell Line ; DNA-Binding Proteins/*metabolism ; Humans ; Mice ; Mice, Knockout ; Microscopy, Electron ; Microtubule-Associated Proteins/metabolism ; Phagosomes/metabolism/*microbiology/ultrastructure ; Protein Binding ; Recombinant Fusion Proteins/metabolism ; Shigella flexneri/genetics/growth & development/metabolism/*pathogenicity ; Transcription Factors/*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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  • 7
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    Autophagy defends cells against invading group A Streptococcus (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-11-06
    Description: We found that the autophagic machinery could effectively eliminate pathogenic group A Streptococcus (GAS) within nonphagocytic cells. After escaping from endosomes into the cytoplasm, GAS became enveloped by autophagosome-like compartments and were killed upon fusion of these compartments with lysosomes. In autophagy-deficient Atg5-/- cells, GAS survived, multiplied, and were released from the cells. Thus, the autophagic machinery can act as an innate defense system against invading pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakagawa, Ichiro -- Amano, Atsuo -- Mizushima, Noboru -- Yamamoto, Akitsugu -- Yamaguchi, Hitomi -- Kamimoto, Takahiro -- Nara, Atsuki -- Funao, Junko -- Nakata, Masanobu -- Tsuda, Kayoko -- Hamada, Shigeyuki -- Yoshimori, Tamotsu -- New York, N.Y. -- Science. 2004 Nov 5;306(5698):1037-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita-Osaka 565-0871, Japan. ichiro@dent.osaka-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15528445" target="_blank"〉PubMed〈/a〉
    Keywords: Autophagy/*physiology ; Colony Count, Microbial ; HeLa Cells ; Humans ; Immunity, Innate ; Lysosomes/physiology ; Streptococcus pyogenes/*immunology
    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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    Autophagy in immunity and inflammation (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-01-21
    Description: Autophagy is an essential, homeostatic process by which cells break down their own components. Perhaps the most primordial function of this lysosomal degradation pathway is adaptation to nutrient deprivation. However, in complex multicellular organisms, the core molecular machinery of autophagy - the 'autophagy proteins' - orchestrates diverse aspects of cellular and organismal responses to other dangerous stimuli such as infection. Recent developments reveal a crucial role for the autophagy pathway and proteins in immunity and inflammation. They balance the beneficial and detrimental effects of immunity and inflammation, and thereby may protect against infectious, autoimmune and inflammatory diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131688/" 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/PMC3131688/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, Beth -- Mizushima, Noboru -- Virgin, Herbert W -- R01 AI054483/AI/NIAID NIH HHS/ -- R01 AI084887/AI/NIAID NIH HHS/ -- R01 CA096511/CA/NCI NIH HHS/ -- R01 CA109618/CA/NCI NIH HHS/ -- R01 CA109618-07/CA/NCI NIH HHS/ -- U54 AI057156/AI/NIAID NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jan 20;469(7330):323-35. doi: 10.1038/nature09782.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9113, USA. beth.levine@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21248839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/*immunology/physiology ; Cell Membrane/metabolism ; Humans ; Immunity/*immunology/physiology ; Immunity, Innate/immunology/physiology ; Infection/immunology/microbiology/parasitology/virology ; Inflammation/*immunology/microbiology/*pathology ; Phagosomes/immunology/microbiology/parasitology/virology
    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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  • 9
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    Autophagy is essential for preimplantation development of mouse embryos (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-05
    Description: After fertilization, maternal proteins in oocytes are degraded and new proteins encoded by the zygotic genome are synthesized. We found that autophagy, a process for the degradation of cytoplasmic constituents in the lysosome, plays a critical role during this period. Autophagy was triggered by fertilization and up-regulated in early mouse embryos. Autophagy-defective oocytes derived from oocyte-specific Atg5 (autophagy-related 5) knockout mice failed to develop beyond the four- and eight-cell stages if they were fertilized by Atg5-null sperm, but could develop if they were fertilized by wild-type sperm. Protein synthesis rates were reduced in the autophagy-null embryos. Thus, autophagic degradation within early embryos is essential for preimplantation development in mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsukamoto, Satoshi -- Kuma, Akiko -- Murakami, Mirei -- Kishi, Chieko -- Yamamoto, Akitsugu -- Mizushima, Noboru -- New York, N.Y. -- Science. 2008 Jul 4;321(5885):117-20. doi: 10.1126/science.1154822.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Cell Biology, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18599786" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Blastocyst/*physiology ; Cells, Cultured ; *Embryonic Development ; Female ; Fertilization ; Lysosomes/physiology/ultrastructure ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Microtubule-Associated Proteins/genetics/metabolism ; Oocytes/physiology ; Parthenogenesis ; Phagosomes/physiology/ultrastructure ; Pregnancy ; Protein Biosynthesis ; Proteins/metabolism ; Recombinant Fusion Proteins/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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  • 10
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    Component parts of the World Heat Flow Data Collection
    PANGAEA
    Details
    Publication Date: 2023-05-12
    Keywords: Area/locality; Conductivity, average; Depth, bottom/max; ELEVATION; Heat flow; LATITUDE; LONGITUDE; Number; Sample, optional label/labor no; Temperature gradient
    Type: Dataset
    Format: text/tab-separated-values, 7 data points
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