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  • 1
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    BTB-ZF factors recruit the E3 ligase cullin 3 to regulate lymphoid effector programs (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-23
    Description: The differentiation of several T- and B-cell effector programs in the immune system is directed by signature transcription factors that induce rapid epigenetic remodelling. Here we report that promyelocytic leukaemia zinc finger (PLZF), the BTB-zinc finger (BTB-ZF) transcription factor directing the innate-like effector program of natural killer T-cell thymocytes, is prominently associated with cullin 3 (CUL3), an E3 ubiquitin ligase previously shown to use BTB domain-containing proteins as adaptors for substrate binding. PLZF transports CUL3 to the nucleus, where the two proteins are associated within a chromatin-modifying complex. Furthermore, PLZF expression results in selective ubiquitination changes of several components of this complex. CUL3 was also found associated with the BTB-ZF transcription factor BCL6, which directs the germinal-centre B cell and follicular T-helper cell programs. Conditional CUL3 deletion in mice demonstrated an essential role for CUL3 in the development of PLZF- and BCL6-dependent lineages. We conclude that distinct lineage-specific BTB-ZF transcription factors recruit CUL3 to alter the ubiquitination pattern of their associated chromatin-modifying complex. We propose that this new function is essential to direct the differentiation of several T- and B-cell effector programs, and may also be involved in the oncogenic role of PLZF and BCL6 in leukaemias and lymphomas.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504649/" 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/PMC3504649/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mathew, Rebecca -- Seiler, Michael P -- Scanlon, Seth T -- Mao, Ai-ping -- Constantinides, Michael G -- Bertozzi-Villa, Clara -- Singer, Jeffrey D -- Bendelac, Albert -- 5R01GM082940/GM/NIGMS NIH HHS/ -- P30 DK042086/DK/NIDDK NIH HHS/ -- R01 AI038339/AI/NIAID NIH HHS/ -- R01 GM082940/GM/NIGMS NIH HHS/ -- R01AI038339/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Nov 22;491(7425):618-21. doi: 10.1038/nature11548. Epub 2012 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Committee on Immunology, Department of Pathology, The Howard Hughes Medical Institute, University of Chicago, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23086144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/cytology/*metabolism ; Cell Differentiation ; Cell Line ; Cullin Proteins/chemistry/genetics/*metabolism ; DNA-Binding Proteins/metabolism ; Kruppel-Like Transcription Factors/*metabolism ; Mice ; Protein Binding ; Protein Transport ; T-Lymphocytes/cytology/*metabolism ; Ubiquitination ; *Zinc Fingers
    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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    ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-28
    Description: Malnutrition affects up to one billion people in the world and is a major cause of mortality. In many cases, malnutrition is associated with diarrhoea and intestinal inflammation, further contributing to morbidity and death. The mechanisms by which unbalanced dietary nutrients affect intestinal homeostasis are largely unknown. Here we report that deficiency in murine angiotensin I converting enzyme (peptidyl-dipeptidase A) 2 (Ace2), which encodes a key regulatory enzyme of the renin-angiotensin system (RAS), results in highly increased susceptibility to intestinal inflammation induced by epithelial damage. The RAS is known to be involved in acute lung failure, cardiovascular functions and SARS infections. Mechanistically, ACE2 has a RAS-independent function, regulating intestinal amino acid homeostasis, expression of antimicrobial peptides, and the ecology of the gut microbiome. Transplantation of the altered microbiota from Ace2 mutant mice into germ-free wild-type hosts was able to transmit the increased propensity to develop severe colitis. ACE2-dependent changes in epithelial immunity and the gut microbiota can be directly regulated by the dietary amino acid tryptophan. Our results identify ACE2 as a key regulator of dietary amino acid homeostasis, innate immunity, gut microbial ecology, and transmissible susceptibility to colitis. These results provide a molecular explanation for how amino acid malnutrition can cause intestinal inflammation and diarrhoea.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hashimoto, Tatsuo -- Perlot, Thomas -- Rehman, Ateequr -- Trichereau, Jean -- Ishiguro, Hiroaki -- Paolino, Magdalena -- Sigl, Verena -- Hanada, Toshikatsu -- Hanada, Reiko -- Lipinski, Simone -- Wild, Birgit -- Camargo, Simone M R -- Singer, Dustin -- Richter, Andreas -- Kuba, Keiji -- Fukamizu, Akiyoshi -- Schreiber, Stefan -- Clevers, Hans -- Verrey, Francois -- Rosenstiel, Philip -- Penninger, Josef M -- England -- Nature. 2012 Jul 25;487(7408):477-81. doi: 10.1038/nature11228.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, 1030 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22837003" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biocatalysis ; Colitis/drug therapy/*etiology/*microbiology/pathology ; Dextran Sulfate ; Diarrhea/complications ; Dietary Proteins/metabolism/pharmacology ; Female ; Gene Deletion ; Genetic Predisposition to Disease ; Germ-Free Life ; Homeostasis ; Immunity, Innate ; Intestines/*microbiology/pathology ; Male ; Malnutrition/*complications/metabolism ; *Metagenome ; Mice ; Models, Biological ; Niacinamide/metabolism/pharmacology/therapeutic use ; Peptidyl-Dipeptidase A/deficiency/genetics/*metabolism ; Renin-Angiotensin System/physiology ; TOR Serine-Threonine Kinases/metabolism ; Trinitrobenzenesulfonic Acid ; Tryptophan/*metabolism/pharmacology/therapeutic use
    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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