Bibliografie tematiche / FAT10

Letteratura scientifica selezionata sul tema "FAT10"

Autore: Grafiati

Pubblicato: 15 giugno 2024

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Articoli di riviste sul tema "FAT10":

Hipp, Mark Steffen, Birte Kalveram, Shahri Raasi, Marcus Groettrup e Gunter Schmidtke. "FAT10, a Ubiquitin-Independent Signal for Proteasomal Degradation". Molecular and Cellular Biology 25, n. 9 (1 maggio 2005): 3483–91. http://dx.doi.org/10.1128/mcb.25.9.3483-3491.2005.

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ABSTRACT FAT10 is a small ubiquitin-like modifier that is encoded in the major histocompatibility complex and is synergistically inducible by tumor necrosis factor alpha and gamma interferon. It is composed of two ubiquitin-like domains and possesses a free C-terminal diglycine motif that is required for the formation of FAT10 conjugates. Here we show that unconjugated FAT10 and a FAT10 conjugate were rapidly degraded by the proteasome at a similar rate. Fusion of FAT10 to the N terminus of very long-lived proteins enhanced their degradation rate as potently as fusion with ubiquitin did. FAT10-green fluorescent protein fusion proteins were not cleaved but entirely degraded, suggesting that FAT10-specific deconjugating enzymes were not present in the analyzed cell lines. Interestingly, the prevention of ubiquitylation of FAT10 by mutation of all lysines or by expression in ubiquitylation-deficient cells did not affect FAT10 degradation. Thus, conjugation with FAT10 is an alternative and ubiquitin-independent targeting mechanism for degradation by the proteasome, which, in contrast to polyubiquitylation, is cytokine inducible and irreversible.

Schnell, Leonie, Alina Zubrod, Nicola Catone, Johanna Bialas e Annette Aichem. "Tumor necrosis factor mediates USE1-independent FAT10ylation under inflammatory conditions". Life Science Alliance 6, n. 11 (21 agosto 2023): e202301985. http://dx.doi.org/10.26508/lsa.202301985.

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The ubiquitin-like modifier FAT10 is up-regulated in many different cell types by IFNγ and TNFα (TNF) and directly targets proteins for proteasomal degradation. FAT10 gets covalently conjugated to its conjugation substrates by the E1 activating enzyme UBA6, the E2 conjugating enzyme USE1, and E3 ligases including Parkin. To date, USE1 was supposed to be the only E2 enzyme for FAT10ylation, and we show here that a knockout of USE1 strongly diminished FAT10 conjugation. Remarkably, under inflammatory conditions in the presence of TNF, FAT10 conjugation appears to be independent of USE1. We report on the identification of additional E2 conjugating enzymes, which were previously not associated with FAT10. We confirm their capacity to be charged with FAT10 onto their active site cysteine, and to rescue FAT10 conjugation in the absence of USE1. This finding strongly widens the field of FAT10 research by pointing to multiple, so far unknown pathways for the conjugation of FAT10, disclosing novel possibilities for pharmacological interventions to regulate FAT10 conjugation under inflammatory conditions and/or viral infections.

Jia, Yue, Ping Ji e Samuel W. French. "The Role of FAT10 in Alcoholic Hepatitis Pathogenesis". Biomedicines 8, n. 7 (1 luglio 2020): 189. http://dx.doi.org/10.3390/biomedicines8070189.

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FAT10 expression is highly up-regulated by pro-inflammatory cytokines IFNγ and TNFα in all cell types and tissues. Increased FAT10 expression may induce increasing mitotic non-disjunction and chromosome instability, leading to tumorigenesis. In this review, we summarized others’ and our work on FAT10 expression in liver biopsy samples from patients with alcoholic hepatitis (AH). FAT10 is essential to maintain the function of liver cell protein quality control and Mallory–Denk body (MDB) formation. FAT10 overexpression in AH leads to balloon degeneration and MDB aggregation formation, all of which is prevented in fat10-/- mice. FAT10 causes the proteins’ accumulation, overexpression, and forming MDBs through modulating 26s proteasome’s proteases. The pathway that increases FAT10 expression includes TNFα/IFNγ and the interferon sequence response element (ISRE), followed by NFκB and STAT3, which were all up-regulated in AH. FAT10 was only reported in human and mouse specimens but plays critical role for the development of alcoholic hepatitis. Flavanone derivatives of milk thistle inhibit TNFα/IFNγ, NFκB, and STAT3, then inhibit the expression of FAT10. NFκB is the key nodal hub of the IFNα/TNFα-response genes. Studies on Silibinin and other milk thistle derivatives to treat AH confirms that overexpressed FAT10 is the major key molecule in these networks.

Mah, Mei Min, Nicola Roverato e Marcus Groettrup. "Regulation of Interferon Induction by the Ubiquitin-Like Modifier FAT10". Biomolecules 10, n. 6 (23 giugno 2020): 951. http://dx.doi.org/10.3390/biom10060951.

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The revelation that the human major histocompatibility complex (MHC) class I locus encodes a ubiquitin-like protein designated HLA-F adjacent transcript 10 (FAT10) or ubiquitin D (UBD) has attracted increasing attention to the function of this protein. Interestingly, the pro-inflammatory cytokines interferon (IFN)-γ and tumor necrosis factor (TNF) α synergize to strongly induce FAT10 expression, thereby suggesting a role of FAT10 in the immune response. Recent reports that FAT10 downregulates type I interferon production while it upregulates IFN-γ pose mechanistic questions on how FAT10 differentially regulates interferon induction. Several covalent and non-covalent binding partners of FAT10 involved in signal transduction pathways leading to IFN synthesis have been identified. After introducing FAT10, we review here recent insights into how FAT10 affects proteins in the interferon pathways, like the virus-responsive pattern recognition receptor RIG-I, the ubiquitin ligase ZNF598, and the deubiquitylating enzyme OTUB1. Moreover, we outline the consequences of FAT10 deficiency on interferon synthesis and viral expansion in mice and human cells. We discuss the need for covalent isopeptide linkage of FAT10 to the involved target proteins and the concomitant targeting for proteasomal degradation. After years of investigating the elusive biological functions of this fascinating ubiquitin-like modifier, we review the emerging evidence for a novel role of FAT10 in interferon regulation.

Arshad, Maria, Nazefah Abdul Hamid, Mun Chiang Chan, Fuad Ismail, Geok Chin Tan, Francesco Pezzella e Ka-Liong Tan. "NUB1 and FAT10 Proteins as Potential Novel Biomarkers in Cancer: A Translational Perspective". Cells 10, n. 9 (24 agosto 2021): 2176. http://dx.doi.org/10.3390/cells10092176.

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Cancer increases the global disease burden substantially, but it remains a challenge to manage it. The search for novel biomarkers is essential for risk assessment, diagnosis, prognosis, prediction of treatment response, and cancer monitoring. This paper examined NEDD8 ultimate buster-1 (NUB1) and F-adjacent transcript 10 (FAT10) proteins as novel biomarkers in cancer. This literature review is based on the search of the electronic database, PubMed. NUB1 is an interferon-inducible protein that mediates apoptotic and anti-proliferative actions in cancer, while FAT10 is a ubiquitin-like modifier that promotes cancer. The upregulated expression of both NUB1 and FAT10 has been observed in various cancers. NUB1 protein binds to FAT10 non-covalently to promote FAT10 degradation. An overexpressed FAT10 stimulates nuclear factor-kappa β, activates the inflammatory pathways, and induces the proliferation of cancer. The FAT10 protein interacts with the mitotic arrest deficient 2 protein, causing chromosomal instability and breast tumourigenesis. FAT10 binds to the proliferating cell nuclear antigen protein and inhibits the DNA damage repair response. In addition, FAT10 involves epithelial–mesenchymal transition, invasion, apoptosis, and multiplication in hepatocellular carcinoma. Our knowledge about them is still limited. There is a need to further develop NUB1 and FAT10 as novel biomarkers.

Canaan, 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, n. 13 (1 luglio 2006): 5180–89. http://dx.doi.org/10.1128/mcb.00966-05.

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ABSTRACT The FAT10 gene encodes a diubiquitin-like protein containing two tandem head-to-tail ubiquitin-like domains. There is a high degree of similarity between murine and human FAT10 sequences at both the mRNA and protein levels. In various cell lines, FAT10 expression was shown to be induced by gamma interferon or by tumor necrosis factor alpha. In addition, FAT10 expression was found to be up-regulated in some Epstein-Barr virus-infected B-cell lines, in activated dendritic cells, and in several epithelial tumors. However, forced expression of FAT10 in cultured cells was also found to produce apoptotic cell death. Overall, these findings suggest that FAT10 may modulate cellular growth or cellular viability. Here we describe the steps to generate, by genetic targeting, a FAT10 gene knockout mouse model. The FAT10 knockout homozygous mice are viable and fertile. No gross lesions or obvious histological differences were found in these mutated mice. Examination of lymphocyte populations from spleen, thymus, and bone marrow did not reveal any abnormalities. However, flow cytometry analysis demonstrated that the lymphocytes of FAT10 knockout mice were, on average, more prone to spontaneous apoptotic death. Physiologically, these mice demonstrated a high level of sensitivity toward endotoxin challenge. These findings indicate that FAT10 may function as a survival factor.

Schregle, Richard, Stefanie Mueller, Daniel F. Legler, Jérémie Rossy, Wolfgang A. Krueger e Marcus Groettrup. "FAT10 localises in dendritic cell aggresome-like induced structures and contributes to their disassembly". Journal of Cell Science 133, n. 14 (16 giugno 2020): jcs240085. http://dx.doi.org/10.1242/jcs.240085.

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ABSTRACTDendritic cell (DC) aggresome-like induced structures (DALIS) are protein aggregates of polyubiquitylated proteins that form transiently during DC maturation. DALIS scatter randomly throughout the cytosol and serve as antigen storage sites synchronising DC maturation and antigen presentation. Maturation of DCs is accompanied by the induction of the ubiquitin-like modifier FAT10 (also known as UBD), which localises to aggresomes, structures that are similar to DALIS. FAT10 is conjugated to substrate proteins and serves as a signal for their rapid and irreversible degradation by the 26S proteasome similar to, yet independently of ubiquitin, thereby contributing to antigen presentation. Here, we have investigated whether FAT10 is involved in the formation and turnover of DALIS, and whether proteins accumulating in DALIS can be modified through conjunction to FAT10 (FAT10ylated). We found that FAT10 localises to DALIS in maturing DCs and that this localisation occurs independently of its conjugation to substrates. Additionally, we investigated the DALIS turnover in FAT10-deficient and -proficient DCs, and observed FAT10-mediated disassembly of DALIS. Thus, we report further evidence that FAT10 is involved in antigen processing, which may provide a functional rationale as to why FAT10 is selectively induced upon DC maturation.

Boehm, Annika N., Johanna Bialas, Nicola Catone, Almudena Sacristan-Reviriego, Jacqueline van der Spuy, Marcus Groettrup e Annette Aichem. "The ubiquitin-like modifier FAT10 inhibits retinal PDE6 activity and mediates its proteasomal degradation". Journal of Biological Chemistry 295, n. 42 (14 agosto 2020): 14402–18. http://dx.doi.org/10.1074/jbc.ra120.013873.

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The retina-specific chaperone aryl hydrocarbon interacting protein-like 1 (AIPL1) is essential for the correct assembly of phosphodiesterase 6 (PDE6), which is a pivotal effector enzyme for phototransduction and vision because it hydrolyzes cGMP. AIPL1 interacts with the cytokine-inducible ubiquitin-like modifier FAT10, which gets covalently conjugated to hundreds of proteins and targets its conjugation substrates for proteasomal degradation, but whether FAT10 affects PDE6 function or turnover is unknown. Here, we show that FAT10 mRNA is expressed in human retina and identify rod PDE6 as a retina-specific substrate of FAT10 conjugation. We found that AIPL1 stabilizes the FAT10 monomer and the PDE6-FAT10 conjugate. Additionally, we elucidated the functional consequences of PDE6 FAT10ylation. On the one hand, we demonstrate that FAT10 targets PDE6 for proteasomal degradation by formation of a covalent isopeptide linkage. On the other hand, FAT10 inhibits PDE6 cGMP hydrolyzing activity by noncovalently interacting with the PDE6 GAFa and catalytic domains. Therefore, FAT10 may contribute to loss of PDE6 and, as a consequence, degeneration of retinal cells in eye diseases linked to inflammation and inherited blindness-causing mutations in AIPL1.

Saxena, Kritika, Nicola Domenico Roverato, Melody Reithmann, Mei Min Mah, Richard Schregle, Gunter Schmidtke, Ivan Silbern, Henning Urlaub e Annette Aichem. "FAT10 is phosphorylated by IKKβ to inhibit the antiviral type-I interferon response". Life Science Alliance 7, n. 1 (8 novembre 2023): e202101282. http://dx.doi.org/10.26508/lsa.202101282.

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IFN-I secretion provides a rapid host defense against infection with RNA viruses. Within the host cell, viral RNA triggers the activation of the RIG-I signaling pathway, leading to the production of IFN-I. Because an exaggerated IFN-I response causes severe tissue damage, RIG-I signaling is tightly regulated. One of the factors that control the IFN-I response is the ubiquitin-like modifier FAT10, which is induced by TNF and IFNγ and targets covalently FAT10-linked proteins for proteasomal degradation. However, the mechanism of how FAT10 modulates IFN-I secretion remains to be fully elucidated. Here, we provide strong evidence that FAT10 is phosphorylated by IκB kinase β (IKKβ) upon TNF stimulation and during influenza A virus infection on several serine and threonine residues. FAT10 phosphorylation increases the binding of FAT10 to the TRAF3-deubiquitylase OTUB1 and its FAT10-mediated activation. Consequently, FAT10 phosphorylation results in a low ubiquitylation state of TRAF3, which is unable to maintain interferon regulatory factor 3 phosphorylation and downstream induction of IFN-I. Taken together, we reveal a mechanism of how phosphorylation of FAT10 limits the production of tissue-destructive IFN-I in inflammation.

Yao, Yi, Weikun Jia, Xiaofei Zeng, Yali Wang, Qiuxia Hu, Shiran Yu, Dongsheng He e 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 agosto 2022): 1–10. http://dx.doi.org/10.1155/2022/4388919.

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Hypoxia-induced cardiomyocyte apoptosis is the main contributor to heart diseases. Human leukocyte antigen F-associated transcript 10 (FAT10), the small ubiquitin-like protein family subtype involved in apoptosis, is expressed in the heart and exhibits cardioprotective functions. This study explored the impact of FAT10 on hypoxia-induced cardiomyocyte apoptosis and the involved mechanisms. The cardiomyocyte cell line H9C2 was cultivated in hypoxia-inducing conditions (94% N2, 5% CO2, and 1% O2) and the expression of FAT10 in hypoxia-stimulated H9C2 cells was identified. For this, FAT10 overexpression/interference vectors were exposed to transfection into H9C2 cells with/without the PI3K/AKT inhibitor, miltefosine. The results indicated that hypoxia exposure decreased the FAT10 expression, suppressed H9C2 cell growth, disrupted mitochondrial metabolism, and promoted H9C2 cell apoptosis and oxidative stress. However, these impacts were reversed by the FAT10 overexpression. In addition, the inhibition of PI3K/AKT in FAT10-overexpressing cells suppressed cell proliferation, impaired mitochondrial metabolism, and promoted apoptosis and oxidative stress response. The findings demonstrated that FAT10 inhibited mitochondrial apoptosis and energy metabolism in hypoxia-stimulated H9C2 cells through the PI3K/AKT pathway. This finding can be utilized for developing therapeutic targets for treating heart disorders associated with hypoxia-induced apoptosis.

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Tesi sul tema "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.

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Ryu, Stella [Verfasser]. "Investigation of the FAT10 conjugation pathway / Stella Ryu". Konstanz : Bibliothek der Universität Konstanz, 2012. http://d-nb.info/105034880X/34.

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Ahmad, Faiz [Verfasser]. "The Search for Deconjugating Enzymes of FAT10 / Faiz Ahmad". Konstanz : Bibliothek der Universität Konstanz, 2016. http://d-nb.info/1159513368/34.

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Bürger, Stefanie [Verfasser]. "The Ubiquitin-like modifier FAT10 in tolerance induction / Stefanie Bürger". Konstanz : Bibliothek der Universität Konstanz, 2013. http://d-nb.info/1110770529/34.

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Schwab, 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.

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Mah, 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.

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Spinnenhirn, 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.

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Kluge, 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.

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Schregle, 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.

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Bernard, 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.

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L'accumulation d'hépatocytes sénescents a été identifiée comme un facteur clé dans la progression des maladies du foie gras non alcooliques (NAFLDs), qui correspondent à un spectre de pathologies hépatiques chroniques, allant de la simple stéatose jusqu'au développement d'une stéato-hépatite non alcoolique (NASH), d'une cirrhose voire d'un carcinome hépatocellulaire (HCC). Cependant, les mécanismes et acteurs participant à la régulation de la sénescence au cours de la NASH sont encore peu décrits. L'objectif de cette thèse a donc été d'étudier les mécanismes contrôlant la sénescence des hépatocytes au cours du développement de la NASH. Grâce à des analyses transcriptomiques et protéiques, nous avons montré dans les foies de patients et de souris que la protéine FAT10 (human leukocyte antigen-F Adjacent Transcript 10), aussi appelée UBD (Ubiquitine D), est induite au cours de la NASH. Or, FAT10 est une protéine ubiquitin-like qui interagit avec différents partenaires jouant un rôle dans le métabolisme et la sénescence, nous avons donc émis l'hypothèse que FAT10 pourrait être impliquée dans le développement de la NASH, ainsi que dans l'induction et la propagation de la sénescence des hépatocytes. Dans un premier temps, nous avons montré dans les foies de patients NASH une corrélation positive entre l'expression de FAT10 et la gravité de la maladie. A l'inverse, l'expression de FAT10 diminue lorsque la maladie régresse. Nous avons montré spécifiquement dans les hépatocytes de souris NASH que l'expression de Fat10 corrèle négativement avec les voies du métabolisme des lipides, et que de manière intéressante, la diminution de l'expression de Fat10 dans les hépatocytes des souris NASH diminue la stéatose hépatique, en réduisant la taille et le nombre des gouttelettes lipidiques. Dans un second temps, nous avons montré une corrélation positive entre l'expression de FAT10 et celle des gènes de la sénescence au sein des foies de patients NASH. Cette corrélation est retrouvée spécifiquement dans les hépatocytes chez la souris atteinte de NASH. De plus, dans ce modèle murin, l'expression de Fat10 corrèle positivement avec l'activité SA-β-Gal (Senescence Associated-β-Galactosidase) du foie. In vitro, l'induction de la sénescence dans les hépatocytes humains par une irradiation ou un traitement à l'H2O2 permet d'induire la protéine FAT10 en tant qu'acteur du SASP (Senescence Associated Secretory Phenotype). De manière intéressante, l'inhibition de FAT10 dans ce modèle favorise l'induction et la propagation de la sénescence, par une augmentation de l'activité SA-β-Gal, une induction des gènes du SASP, un arrêt de la prolifération cellulaire accélérée, une induction des acteurs de la réponse aux dommages à l'ADN et une accumulation plus importante de gouttelettes lipidiques. A l'inverse, la surexpression stable de FAT10 dans les hépatocytes sénescents accélère la perte du statut sénescent (diminution de l'activité SA-β-Gal), et promeut l'échappement et l'acquisition d'un phénotype pro-cancéreux par les hépatocytes. Au final, ces données suggèrent que l'induction de FAT10 au sein des hépatocytes lors du développement de la NASH favorise la progression de la maladie, d'une part en altérant le métabolisme des lipides au sein des hépatocytes stéatosés, et d'autre part en favorisant progressivement l'échappement des hépatocytes sénescents à leur phénotype, ce qui pourrait conduire au développement de l'HCC
The 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

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Libri sul tema "FAT10":

Nayak, R. V., N. A. Mousa e 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.

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Capitoli di libri sul tema "FAT10":

Pelzer, Christiane, e 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.

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Aichem, Annette, e 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.

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Lukasiak, Sebastian, Kai Breuhahn, Claudia Schiller, Gunter Schmidtke e 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.

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Aichem, Annette, Annika N. Boehm, Nicola Catone, Gunter Schmidtke e 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.

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Adams, 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.

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B. Pathak, Anand, e 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.

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Abstract (sommario):

Head Neck Squamous Cell Cancer is genomically heterogenous. Common somatic mutations involve TP53, CDKN2A, FAT1, NOTCH1, PIK3CA, KMT2D and NSD1, less frequently others. Epigenetic changes also contribute to HNSCC biology. Alterations in tumor suppressor genes is a major oncogenic event in HNSCC. Genomic heterogeneity exists between different subsites within head neck region and also between the primary and metastatic disease. Intratumor heterogeneity has also been recognized. Based on key genomic alterations, four major molecular subtypes have been identified. Multi-omics analysis has provided further insights into HNSCC biology and shed light on EGFR pathway and immunogenomics. Corelative genomics of tumor cells, stromal cells and immune cells have led to emergence of distinct immune molecular subtypes of HNSCC. Major tumor suppressor genes and oncogenes have a correlation with prognosis, survival and treatment resistance. EGFR pathway is in focus for renewed understanding of resistance to EGFR targeted treatments and novel ways to target EGFR pathways. Increasingly genomic data is being leveraged towards clinical use including HNSCC prevention, prediction of metastases, survival and prognostication, fine tuning use of surgery, chemotherapy and radiation therapy, identifying patients for using immunotherapy, predicting drug resistance and gaining new information from radiological studies. Several novel targeted therapies are being pursued in clinical trials. Molecular co targeting strategies are being developed. Understanding the way tumor suppressor genes and oncogenes shape HNSCC biology and clinical behavior is bringing the much-needed therapeutic breakthrough in this tough to treat disease.

Atti di convegni sul tema "FAT10":

Noymai, Anukool, Urachada Ketprom e 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.

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Irshad, 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.

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Dikshit, Bhawana, Parthaprasad Chattopadhyay, Subrata Sinha e 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.

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Srivastava, Chitrangda, Khushboo Irshad, Parthaprasad Chattopadhyay, Chitra Sarkar, Ashish Suri, Subrata Sinha e 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.

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Halimah, 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.

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Arafahnti, Bestari Laksmi, Umiatin Umiatin e 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.

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Gupta, Y., SS Shivajirao, K. Irshad, B. Dikshit, T. Srivastav, PP Chattopadhyay, S. Sinha e 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.

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Krasteva, V. M., G. H. Sigel, S. L. Semjonov, M. M. Bubnov e 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.

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Connor, Ashton A., Jordan Lerner-Ellis, Mohammad R. Akbari, Cezary Cybulski, J. Lubinski, Caroline Badouel, Helen McNeill, James G. Dowty, Mark Clendenning e 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.

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Kasahara, Shunji, e 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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