Auswahl der wissenschaftlichen Literatur zum Thema „FAT10“
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Zeitschriftenartikel zum Thema "FAT10"
Hipp, Mark Steffen, Birte Kalveram, Shahri Raasi, Marcus Groettrup und Gunter Schmidtke. „FAT10, a Ubiquitin-Independent Signal for Proteasomal Degradation“. Molecular and Cellular Biology 25, Nr. 9 (01.05.2005): 3483–91. http://dx.doi.org/10.1128/mcb.25.9.3483-3491.2005.
Der volle Inhalt der QuelleSchnell, Leonie, Alina Zubrod, Nicola Catone, Johanna Bialas und Annette Aichem. „Tumor necrosis factor mediates USE1-independent FAT10ylation under inflammatory conditions“. Life Science Alliance 6, Nr. 11 (21.08.2023): e202301985. http://dx.doi.org/10.26508/lsa.202301985.
Der volle Inhalt der QuelleJia, Yue, Ping Ji und Samuel W. French. „The Role of FAT10 in Alcoholic Hepatitis Pathogenesis“. Biomedicines 8, Nr. 7 (01.07.2020): 189. http://dx.doi.org/10.3390/biomedicines8070189.
Der volle Inhalt der QuelleMah, Mei Min, Nicola Roverato und Marcus Groettrup. „Regulation of Interferon Induction by the Ubiquitin-Like Modifier FAT10“. Biomolecules 10, Nr. 6 (23.06.2020): 951. http://dx.doi.org/10.3390/biom10060951.
Der volle Inhalt der QuelleArshad, Maria, Nazefah Abdul Hamid, Mun Chiang Chan, Fuad Ismail, Geok Chin Tan, Francesco Pezzella und Ka-Liong Tan. „NUB1 and FAT10 Proteins as Potential Novel Biomarkers in Cancer: A Translational Perspective“. Cells 10, Nr. 9 (24.08.2021): 2176. http://dx.doi.org/10.3390/cells10092176.
Der volle Inhalt der QuelleCanaan, Allon, Xiaofeng Yu, Carmen J. Booth, Jin Lian, Isaac Lazar, Serwa L. Gamfi, Katrina Castille et al. „FAT10/Diubiquitin-Like Protein-Deficient Mice Exhibit Minimal Phenotypic Differences“. Molecular and Cellular Biology 26, Nr. 13 (01.07.2006): 5180–89. http://dx.doi.org/10.1128/mcb.00966-05.
Der volle Inhalt der QuelleSchregle, Richard, Stefanie Mueller, Daniel F. Legler, Jérémie Rossy, Wolfgang A. Krueger und Marcus Groettrup. „FAT10 localises in dendritic cell aggresome-like induced structures and contributes to their disassembly“. Journal of Cell Science 133, Nr. 14 (16.06.2020): jcs240085. http://dx.doi.org/10.1242/jcs.240085.
Der volle Inhalt der QuelleBoehm, Annika N., Johanna Bialas, Nicola Catone, Almudena Sacristan-Reviriego, Jacqueline van der Spuy, Marcus Groettrup und Annette Aichem. „The ubiquitin-like modifier FAT10 inhibits retinal PDE6 activity and mediates its proteasomal degradation“. Journal of Biological Chemistry 295, Nr. 42 (14.08.2020): 14402–18. http://dx.doi.org/10.1074/jbc.ra120.013873.
Der volle Inhalt der QuelleSaxena, Kritika, Nicola Domenico Roverato, Melody Reithmann, Mei Min Mah, Richard Schregle, Gunter Schmidtke, Ivan Silbern, Henning Urlaub und Annette Aichem. „FAT10 is phosphorylated by IKKβ to inhibit the antiviral type-I interferon response“. Life Science Alliance 7, Nr. 1 (08.11.2023): e202101282. http://dx.doi.org/10.26508/lsa.202101282.
Der volle Inhalt der QuelleYao, Yi, Weikun Jia, Xiaofei Zeng, Yali Wang, Qiuxia Hu, Shiran Yu, Dongsheng He und Ying Li. „FAT10 Combined with Miltefosine Inhibits Mitochondrial Apoptosis and Energy Metabolism in Hypoxia-Induced H9C2 Cells by Regulating the PI3K/AKT Signaling Pathway“. Evidence-Based Complementary and Alternative Medicine 2022 (18.08.2022): 1–10. http://dx.doi.org/10.1155/2022/4388919.
Der volle Inhalt der QuelleDissertationen zum Thema "FAT10"
Bialas, Johanna [Verfasser]. „The influence of FAT10 on the ubiquitin pathway and The search for FAT10-specific E3 ligases / Johanna Bialas“. Konstanz : KOPS Universität Konstanz, 2018. http://d-nb.info/1215032919/34.
Der volle Inhalt der QuelleRyu, Stella [Verfasser]. „Investigation of the FAT10 conjugation pathway / Stella Ryu“. Konstanz : Bibliothek der Universität Konstanz, 2012. http://d-nb.info/105034880X/34.
Der volle Inhalt der QuelleAhmad, Faiz [Verfasser]. „The Search for Deconjugating Enzymes of FAT10 / Faiz Ahmad“. Konstanz : Bibliothek der Universität Konstanz, 2016. http://d-nb.info/1159513368/34.
Der volle Inhalt der QuelleBürger, Stefanie [Verfasser]. „The Ubiquitin-like modifier FAT10 in tolerance induction / Stefanie Bürger“. Konstanz : Bibliothek der Universität Konstanz, 2013. http://d-nb.info/1110770529/34.
Der volle Inhalt der QuelleSchwab, Ricarda [Verfasser]. „Investigation of the interaction of FAT10 and VCP (p97) / Ricarda Schwab“. Konstanz : Bibliothek der Universität Konstanz, 2015. http://d-nb.info/1144178703/34.
Der volle Inhalt der QuelleMah, Mei Min [Verfasser]. „The Role of FAT10 in Regulating the Interferon Response / Mei Min Mah“. Konstanz : KOPS Universität Konstanz, 2019. http://d-nb.info/1202012833/34.
Der volle Inhalt der QuelleSpinnenhirn, Valentina [Verfasser]. „Functional analysis of the ubiquitin-like modifier FAT10 in autophagy / Valentina Spinnenhirn“. Konstanz : Bibliothek der Universität Konstanz, 2015. http://d-nb.info/1112604391/34.
Der volle Inhalt der QuelleKluge, Kathrin Christiane [Verfasser]. „Characterisation of the Interaction between FAT10 and its Substrate Protein p62 / Kathrin Christiane Kluge“. Konstanz : Bibliothek der Universität Konstanz, 2014. http://d-nb.info/1112745238/34.
Der volle Inhalt der QuelleSchregle, Richard [Verfasser]. „The Ubiquitin-like Modifier FAT10 in Dendritic Cell Aggresome-like Induced Structures / Richard Schregle“. Konstanz : KOPS Universität Konstanz, 2018. http://d-nb.info/121985266X/34.
Der volle Inhalt der QuelleBernard, Lucie. „Rôle de FAT10 dans la sénescence des hépatocytes et le développement de la NASH“. Electronic Thesis or Diss., Université de Lille (2022-....), 2023. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2023/2023ULILS039.pdf.
Der volle Inhalt der QuelleThe accumulation of senescent hepatocytes has been identified as a key factor in the progression of non-alcoholic fatty liver diseases (NAFLDs), which correspond to a spectrum of chronic liver pathologies, ranging from simple steatosis to the development of non-alcoholic steatohepatitis (NASH), cirrhosis or even hepatocellular carcinoma (HCC). However, the mechanisms and actors involved in the regulation of senescence during NASH are still poorly described. The objective of this thesis was therefore to study the mechanisms controlling hepatocyte senescence during the development of NASH. Using transcriptomic and protein analyses, we have shown in the livers of patients and mice that the protein FAT10 (human leukocyte antigen-F Adjacent Transcript 10), also called UBD (Ubiquitin D), is induced during NASH. However, FAT10 is an ubiquitin-like protein that interacts with different partners playing a role in metabolism and senescence, we therefore hypothesized that FAT10 could be involved in the development of NASH, as well as in the induction and spread of hepatocyte senescence. First, we showed in the livers of NASH patients a positive correlation between the expression of FAT10 and the severity of the disease. Conversely, FAT10 expression decreases when the disease regresses. We showed specifically in hepatocytes of NASH mice that the expression of Fat10 negatively correlates with lipid metabolism pathways, and that interestingly, the decrease of Fat10 expression in NASH mice hepatocytes decreases hepatic steatosis, by reducing the size and number of lipid droplets. Secondly, we showed a positive correlation between the expression of FAT10 and of senescence genes in the livers of NASH patients. This correlation is found specifically in hepatocytes in mice. Furthermore, in this mouse model of NASH, Fat10 expression positively correlates with liver SA-β-Gal (Senescence Associated-β-Galactosidase) activity. In vitro, the induction of senescence in human hepatocytes by an irradiation or a treatment with H2O2 induces FAT10 protein as a SASP (Senescence Associated Secretory Phenotype) actor. Interestingly, FAT10 inhibition in this model promotes the induction and propagation of senescence, through an increase of SA-β-Gal activity, an induction of SASP genes, an accelerated cell proliferation arrest, an induction of the DNA damage response system and a greater accumulation of lipid droplets. Conversely, stable overexpression of FAT10 in senescent hepatocytes accelerates the loss of senescent status (decreased SA-β-Gal activity), and promotes the senescence escape and the acquisition of a pro-cancerous phenotype. In the end, all of these data suggest that the induction of FAT10 within hepatocytes during the development of NASH promotes the progression of the disease, on one hand by altering lipid metabolism within steatotic hepatocytes, and on the other hand by gradually promoting the escape of senescent hepatocytes, which could lead to the development of HCC
Bücher zum Thema "FAT10"
Nayak, R. V., N. A. Mousa und International Joint Power Generation Conference (1990 Boston, Mass.). Combustion Modeling and Burner Replacement Strategies/Fact10/No G00523: Presented at the 1990 International Joint Power Generation Conference, Boston, ... 21-25, 1990 (Fact (Series), Vol. 10,). Amer Society of Mechanical, 1992.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "FAT10"
Pelzer, Christiane, und Marcus Groettrup. „FAT10“. In Subcellular Biochemistry, 238–46. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6676-6_19.
Der volle Inhalt der QuelleAichem, Annette, und Marcus Groettrup. „Detection and Analysis of FAT10 Modification“. In Methods in Molecular Biology, 125–32. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-474-2_7.
Der volle Inhalt der QuelleLukasiak, Sebastian, Kai Breuhahn, Claudia Schiller, Gunter Schmidtke und Marcus Groettrup. „Quantitative Analysis of Gene Expression Relative to 18S rRNA in Carcinoma Samples Using the LightCycler® Instrument and a SYBR GreenI-based Assay: Determining FAT10 mRNA Levels in Hepatocellular Carcinoma“. In Methods in Molecular Biology, 59–72. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-040-3_5.
Der volle Inhalt der QuelleAichem, Annette, Annika N. Boehm, Nicola Catone, Gunter Schmidtke und Marcus Groettrup. „Analysis of modification and proteolytic targeting by the ubiquitin-like modifier FAT10“. In Methods in Enzymology, 229–56. Elsevier, 2019. http://dx.doi.org/10.1016/bs.mie.2018.12.040.
Der volle Inhalt der QuelleAdams, Susan. „"And the Sun Refused to Shine"“. In Final Acts: The End of Life: Hospice and Palliative Care. Baywood Publishing Company, Inc., 2013. http://dx.doi.org/10.2190/fatc10.
Der volle Inhalt der QuelleB. Pathak, Anand, und Satyam Satyarthi. „Head Neck Squamous Cell Cancer Genomics: Oncogenes, Tumor Suppressor Genes and Clinical Implications“. In Molecular Mechanisms in Cancer. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101044.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "FAT10"
Noymai, Anukool, Urachada Ketprom und Chaichana Mitrpant. „Increasing memory in FAT16 removable media of RFID handheld reader“. In 2008 5th International Conference on Electrical Engineering/Electronics, Computer, Telecommunications and Information Technology (ECTI-CON). IEEE, 2008. http://dx.doi.org/10.1109/ecticon.2008.4600538.
Der volle Inhalt der QuelleIrshad, Khushboo, Chitrangda Srivastava, Nargis Malik, Yakhlesh Gupta, Vaishali Suri, Swati Mahajan, Deepak Gupta et al. „Abstract 3175: FAT1 and the immunosuppressive milieu in glioblastoma tumors“. In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-3175.
Der volle Inhalt der QuelleDikshit, Bhawana, Parthaprasad Chattopadhyay, Subrata Sinha und Kunzang Chosdol. „Abstract 4102: FAT1: A novel regulator of cancer and inflammation.“ In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4102.
Der volle Inhalt der QuelleSrivastava, Chitrangda, Khushboo Irshad, Parthaprasad Chattopadhyay, Chitra Sarkar, Ashish Suri, Subrata Sinha und Kunzang Chosdol. „Abstract 3534: FAT1: A potential target of NFkB (RelA) in GBM“. In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3534.
Der volle Inhalt der QuelleHalimah, Nova Nur. „KARAKTERISASI SENSOR HY-SRF05 DAN LOAD CELL SINGLE-POINT SEBAGAI PARAMETER PENGUKURAN ANTROPOMETRI PADA SISTEM PEMANTAUAN STATUS GIZI BAYI“. In SEMINAR NASIONAL FISIKA 2016 UNJ. PRODI Pendidikan Fisika dan Fisika UNJ, 2024. http://dx.doi.org/10.21009/03.1201.fa10.
Der volle Inhalt der QuelleArafahnti, Bestari Laksmi, Umiatin Umiatin und Heru Prasetio. „PENGARUH ENERGI LINAC TERHADAP RESPON FILM DOSIMETRI GAFCHROMIC“. In SEMINAR NASIONAL FISIKA 2016 UNJ. PRODI Pendidikan Fisika dan Fisika UNJ, 2023. http://dx.doi.org/10.21009/03.1101.fa10.
Der volle Inhalt der QuelleGupta, Y., SS Shivajirao, K. Irshad, B. Dikshit, T. Srivastav, PP Chattopadhyay, S. Sinha und K. Chosdol. „PO-125 FAT1 on salvador-warts-hippo (SWH) pathway in human glioblastoma“. In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.166.
Der volle Inhalt der QuelleKrasteva, V. M., G. H. Sigel, S. L. Semjonov, M. M. Bubnov und M. I. Belovolov. „Pr3+ -doped Ge-S-I glasses and fibers for PDFA applications“. In Optical Amplifiers and Their Applications. Washington, D.C.: OSA, 1997. http://dx.doi.org/10.1364/oaa.1997.faw10.
Der volle Inhalt der QuelleConnor, Ashton A., Jordan Lerner-Ellis, Mohammad R. Akbari, Cezary Cybulski, J. Lubinski, Caroline Badouel, Helen McNeill, James G. Dowty, Mark Clendenning und Daniel D. Buchanan. „Abstract A23: Rare variants in the FAT1 gene may predispose to familial colorectal cancer“. In Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-a23.
Der volle Inhalt der QuelleKasahara, Shunji, und Ryo Yamamoto. „HIGH-RESOLUTION LASER SPECTROSCOPY OF THE S1 ← S0 TRANSITION OF Cl-NAPHTHALENES“. In 70th International Symposium on Molecular Spectroscopy. Urbana, Illinois: University of Illinois at Urbana-Champaign, 2015. http://dx.doi.org/10.15278/isms.2015.fa10.
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