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Добірка наукової літератури з теми "TRIM18"

Автор: Grafiati

Опубліковано: 1 квітня 2023

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Статті в журналах з теми "TRIM18"

Yap, Melvyn W., Mark P. Dodding, and Jonathan P. Stoye. "Trim-Cyclophilin A Fusion Proteins Can Restrict Human Immunodeficiency Virus Type 1 Infection at Two Distinct Phases in the Viral Life Cycle." Journal of Virology 80, no. 8 (April 15, 2006): 4061–67. http://dx.doi.org/10.1128/jvi.80.8.4061-4067.2006.

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ABSTRACT The Trim5α protein from several primates restricts retroviruses in a capsid (CA)-dependent manner. In owl monkeys, the B30.2 domain of Trim5 has been replaced by cyclophilin A (CypA) following a retrotransposition. Restriction of human immunodeficiency virus type 1 (HIV-1) by the resulting Trim5-CypA fusion protein depends on CA binding to CypA, suggesting both that the B30.2 domain might be involved in CA binding and that the tripartite RING motif, B-BOX, and coiled coil (RBCC) motif domain can function independently of the B30.2 domain in restriction. To investigate the potential of RBCCs from other Trims to participate in restricting HIV-1, CypA was fused to the RBCC of Trim1, Trim18, and Trim19 and tested for restriction. Despite low identity within the RBCC domain, all fusion proteins were found to restrict HIV-1 but not the nonbinding G89V mutant, indicating that the overall structure of RBCC and not its primary sequence was important for the restriction function. The critical interaction between CA and Trim-CypA appears to take place soon after viral entry. Quantitative PCR analysis of viral reverse transcriptase products revealed that the different fusion proteins block HIV-1 at two distinct stages of its life cycle, either prior to reverse transcription or just before integration. With Trim1 and Trim18, this timing is dependent on the length of the Trim component of the fusion protein. These observations suggest that restriction factor binding can have different mechanistic consequences.

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Toka, Felix N., Kiera Dunaway, Matylda Mielcarska, Felicia Smaltz, and Magdalena Bossowska-Nowicka. "Expression pattern of TRIM genes in bovine macrophages stimulated with PAMPs." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 129.7. http://dx.doi.org/10.4049/jimmunol.198.supp.129.7.

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Abstract In mammals innate immune mechanisms form the first line of defence against invading pathogens. Detection of viruses early in infection relies on intracellular receptors that sense microbial molecular patterns, subsequently leading to gene transcription that eventually produces IFN type I and II. Type I and II IFNs act to prevent replication of viruses. Tripartite Motif-containing (TRIM) proteins belong to a superfamily of RING-domain E3 ubiquitin ligases. They represent a novel class of antiviral molecules involved in innate immunity. These enzymes function in a wide variety of important cellular processes, particularly in innate antiviral response mechanisms. We studied the expression profile of 46 TRIM genes in a bovine macrophage cell line BoMac using RT2 PCR. PAMPs were used to imitate 2 important groups of pathogens. PolyI:C was used in place of viral dsRNA, LPS was used in place of Gram-negative bacteria, Pam3CSK4 was used in place of Gram-positive and negative bacteria, PolyI:C-LyoVec was used in place of viral sRNA and CpG was used in place of bacterial and viral DNA. Of the 46 TRIM genes, only 8 bovine TRIM genes were upregulated following stimulation of BoMac with individual PAMPs. PolyI:C induce upregulation of TRIM21, TRIM25 and TRIM56. All three TRIMs are known for their antiviral activity in human cell lines and mice. Pam3CSK4 and LPS, both upregulated TRIM10. PolyI:C-LyoVec upregulated TRIM9, TRIM40 and TRIM55. TRIM40 is an anti-inflammatory molecule. CpG upregulated TRIM40 and TRIM29. High expression of TRIM29 is regarded as a poor prognostic in many tumors, but no antimicrobial role has been described yet for TRIM29. Data will be discussed in the context of antiviral role of TRIMs in bovine viral infections.

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Sebastian, Sarah, Christian Grütter, Caterina Strambio de Castillia, Thomas Pertel, Silvia Olivari, Markus G. Grütter та Jeremy Luban. "An Invariant Surface Patch on the TRIM5α PRYSPRY Domain Is Required for Retroviral Restriction but Dispensable for Capsid Binding". Journal of Virology 83, № 7 (19 січня 2009): 3365–73. http://dx.doi.org/10.1128/jvi.00432-08.

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ABSTRACT TRIM5α is a retrovirus restriction factor in the host cell cytoplasm that blocks infection before provirus establishment. Restriction activity requires capsid (CA)-specific recognition by the PRYSPRY domain of TRIM5α. To better understand the restriction mechanism, nine charge-cluster-to-triple-alanine mutants in the TRIM5α PRYSPRY domain were assessed for CA-specific restriction activity. Five mutants distributed along the TRIM5α PRYSPRY primary sequence disrupted restriction activity against N-tropic murine leukemia virus and equine infectious anemia virus. Modeling of the TRIM5α PRYSPRY domain based on the crystal structures of PRYSPRY-19q13.4.1, GUSTAVUS, and TRIM21 identified a surface patch where disruptive mutants clustered. All mutants in this patch retained CA-binding activity, a reticular distribution in the cytoplasm, and steady-state protein levels comparable to those of the wild type. Residues in the essential patch are conserved in TRIM5α orthologues and in closely related paralogues. The same surface patch in the TRIM18 and TRIM20 PRYSPRY domains is the site of mutants causing Opitz syndrome and familial Mediterranean fever. These results indicate that, in addition to CA-specific binding, the PRYSPRY domain possesses a second function, possibly binding of a cofactor, that is essential for retroviral restriction activity by TRIM5α.

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Margalit, Liad, Carmit Strauss, Ayellet Tal, and Sharon Schlesinger. "Trim24 and Trim33 Play a Role in Epigenetic Silencing of Retroviruses in Embryonic Stem Cells." Viruses 12, no. 9 (September 11, 2020): 1015. http://dx.doi.org/10.3390/v12091015.

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Embryonic stem cells (ESC) have the ability to epigenetically silence endogenous and exogenous retroviral sequences. Trim28 plays an important role in establishing this silencing, but less is known about the role other Trim proteins play. The Tif1 family is a sub-group of the Trim family, which possess histone binding ability in addition to the distinctive RING domain. Here, we have examined the interaction between three Tif1 family members, namely Trim24, Trim28 and Trim33, and their function in retroviral silencing. We identify a complex formed in ESC, comprised of these three proteins. We further show that when Trim33 is depleted, the complex collapses and silencing efficiency of both endogenous and exogenous sequences is reduced. Similar transcriptional activation takes place when Trim24 is depleted. Analysis of the H3K9me3 chromatin modification showed a decrease in this repressive mark, following both Trim24 and Trim33 depletion. As Trim28 is an identified binding partner of the H3K9 methyltransferase ESET, this further supports the involvement of Trim28 in the complex. The results presented here suggest that a complex of Tif1 family members, each of which possesses different specificity and efficiency, contributes to the silencing of retroviral sequences in ESC.

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Rybakowska, Paulina, Nina Wolska, Arkadiusz Klopocki, Kathy Sivils, Judith James, Harini Bagavant, and Umesh Deshmukh. "Multiple TRIM proteins are targets of autoimmune response in lupus and Sjogren's syndrome. (HUM7P.308)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 184.17. http://dx.doi.org/10.4049/jimmunol.192.supp.184.17.

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Abstract TRIM21 belongs to the large family of tripartite motif containing proteins, and is often targeted by autoantibodies in lupus and Sjogren’s syndrome. Considering the significant protein domain homology between different TRIM proteins, we hypothesized that additional TRIM proteins are targets of autoimmunity. Based on the literature, in this study we investigated autoantibody responses to TRIM38. While 9% of lupus patients (n=149) had anti-TRIM38 antibodies, the incidence in Sjogren’s syndrome patients (n=150) was 12%, and in controls (n=50) it was 4%. With respect to TRIM21, the incidence was 62%, 68%, and 4% respectively. In Sjogren’s syndrome patients, the presence of anti-TRIM38 antibodies was closely associated with the increased severity of dry eye parameters. Epitope mapping studies showed that anti-TRIM21 antibodies reacted with the RING, Coiled coil and PRY-SPRY domains of TRIM21, whereas anti-TRIM38 antibodies reacted only with the Coiled coil and PRY-SPRY domains of TRIM38. All anti-TRIM38 positive patients also had anti-TRIM21 antibodies. Affinity purified anti-TRIM21 antibodies from lupus patients did not immunoprecipitate TRIM38, indicating lack of cross-reactivity at B cell level. However, we observed T cell cross-reactivity between TRIM21298-312 and TRIM38302-316. Our study suggests that immune responses to TRIM proteins can evolve through epitope spreading and contribute towards exacerbating the pathogenesis in autoimmune disorders.

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Agarwal, Neeraj, Sebastien Rinaldetti, Bassem B. Cheikh, Qiong Zhou, Evan P. Hass, Robert T. Jones, Molishree Joshi, et al. "TRIM28 is a transcriptional activator of the mutant TERT promoter in human bladder cancer." Proceedings of the National Academy of Sciences 118, no. 38 (September 13, 2021): e2102423118. http://dx.doi.org/10.1073/pnas.2102423118.

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Bladder cancer (BC) has a 70% telomerase reverse transcriptase (TERT or hTERT in humans) promoter mutation prevalence, commonly at −124 base pairs, and this is associated with increased hTERT expression and poor patient prognosis. We inserted a green fluorescent protein (GFP) tag in the mutant hTERT promoter allele to create BC cells expressing an hTERT-GFP fusion protein. These cells were used in a fluorescence-activated cell sorting–based pooled CRISPR-Cas9 Kinome knockout genetic screen to identify tripartite motif containing 28 (TRIM28) and TRIM24 as regulators of hTERT expression. TRIM28 activates, while TRIM24 suppresses, hTERT transcription from the mutated promoter allele. TRIM28 is recruited to the mutant promoter where it interacts with TRIM24, which inhibits its activity. Phosphorylation of TRIM28 through the mTOR complex 1 (mTORC1) releases it from TRIM24 and induces hTERT transcription. TRIM28 expression promotes in vitro and in vivo BC cell growth and stratifies BC patient outcome. mTORC1 inhibition with rapamycin analog Ridaforolimus suppresses TRIM28 phosphorylation, hTERT expression, and cell viability. This study may lead to hTERT-directed cancer therapies with reduced effects on normal progenitor cells.

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Stevens, Rebecca V., Diego Esposito, and Katrin Rittinger. "Characterisation of class VI TRIM RING domains: linking RING activity to C-terminal domain identity." Life Science Alliance 2, no. 3 (April 26, 2019): e201900295. http://dx.doi.org/10.26508/lsa.201900295.

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TRIM E3 ubiquitin ligases regulate multiple cellular processes, and their dysfunction is linked to disease. They are characterised by a conserved N-terminal tripartite motif comprising a RING, B-box domains, and a coiled-coil region, with C-terminal domains often mediating substrate recruitment. TRIM proteins are grouped into 11 classes based on C-terminal domain identity. Class VI TRIMs, TRIM24, TRIM33, and TRIM28, have been described as transcriptional regulators, a function linked to their C-terminal plant homeodomain and bromodomain, and independent of their ubiquitination activity. It is unclear whether E3 ligase activity is regulated in family members where the C-terminal domains function independently. Here, we provide a detailed biochemical characterisation of the RING domains of class VI TRIMs and describe the solution structure of the TRIM28 RING. Our study reveals a lack of activity of the isolated RING domains, which may be linked to the absence of self-association. We propose that class VI TRIMs exist in an inactive state and require additional regulatory events to stimulate E3 ligase activity, ensuring that associated chromatin-remodelling factors are not injudiciously degraded.

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Zanchetta, Melania E., Luisa M. R. Napolitano, Danilo Maddalo, and Germana Meroni. "The E3 ubiquitin ligase MID1/TRIM18 promotes atypical ubiquitination of the BRCA2-associated factor 35, BRAF35." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1864, no. 10 (October 2017): 1844–54. http://dx.doi.org/10.1016/j.bbamcr.2017.07.014.

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McAvera, Roisin M., and Lisa J. Crawford. "TIF1 Proteins in Genome Stability and Cancer." Cancers 12, no. 8 (July 28, 2020): 2094. http://dx.doi.org/10.3390/cancers12082094.

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Genomic instability is a hallmark of cancer cells which results in excessive DNA damage. To counteract this, cells have evolved a tightly regulated DNA damage response (DDR) to rapidly sense DNA damage and promote its repair whilst halting cell cycle progression. The DDR functions predominantly within the context of chromatin and requires the action of chromatin-binding proteins to coordinate the appropriate response. TRIM24, TRIM28, TRIM33 and TRIM66 make up the transcriptional intermediary factor 1 (TIF1) family of chromatin-binding proteins, a subfamily of the large tripartite motif (TRIM) family of E3 ligases. All four TIF1 proteins are aberrantly expressed across numerous cancer types, and increasing evidence suggests that TIF1 family members can function to maintain genome stability by mediating chromatin-based responses to DNA damage. This review provides an overview of the TIF1 family in cancer, focusing on their roles in DNA repair, chromatin regulation and cell cycle regulation.

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Herquel, B., K. Ouararhni, K. Khetchoumian, M. Ignat, M. Teletin, M. Mark, G. Bechade, et al. "Transcription cofactors TRIM24, TRIM28, and TRIM33 associate to form regulatory complexes that suppress murine hepatocellular carcinoma." Proceedings of the National Academy of Sciences 108, no. 20 (April 29, 2011): 8212–17. http://dx.doi.org/10.1073/pnas.1101544108.

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Дисертації з теми "TRIM18"

Basu, Shrivastava Meenakshi. "Régulation de la stabilité de NFATc3 par SUMO et les E3 ubiquitine-ligases Trim39 et Trim17." Thesis, Montpellier, 2020. http://www.theses.fr/2020MONTT043.

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Les facteurs de transcription NFAT (facteur nucléaire des cellules T activées) jouent un rôle physiologique important dans le développement et le fonctionnement de nombreux organes, notamment dans le système immunitaire et le système nerveux. Par conséquent, leur dérégulation a été impliquée dans diverses maladies humaines telles que le cancer, les maladies neurodégénératives et les maladies auto-immunes. La régulation de l'activité de NFAT par translocation nucléo-cytoplasmique a été largement étudiée. En revanche, la régulation du niveau protéique de NFAT par le système ubiquitine-protéasome est encore mal comprise. Pourtant, les protéines NFAT ont une durée de vie courte et la régulation de leur stabilité est donc essentielle pour le contrôle de leur activité.Dans une étude précédente, mon groupe a montré que l'E3 ubiquitine-ligase Trim17 se lie à NFATc3 mais ne favorise pas son ubiquitination et tend plutôt à stabiliser la protéine. Les résultats préliminaires obtenus suggéraient que Trim39, un partenaire de Trim17, pourrait être une E3 ubiquitine-ligase pour NFATc3 et que la SUMOylation de NFATc3 modulait sa stabilité. L'objectif de ma thèse était donc de comprendre les mécanismes par lesquels Trim39, Trim17 et SUMO régulent la stabilité de NFATc3.Au cours de ma thèse, j'ai caractérisé Trim39 comme une E3 ubiquitine-ligase de NFATc3. En effet, mes résultats indiquent que la surexpression de Trim39, mais pas de son mutant inactif, induit l'ubiquitination de NFATc3 dans les cellules. En revanche, la déplétion de Trim39 endogène diminue le niveau d'ubiquitination de NFATc3. La protéine Trim39 recombinante induit directement l'ubiquitination de NFATc3 in vitro. De plus, la surexpression de Trim39 diminue les niveaux protéiques de NFATc3 alors que la déplétion de Trim39 les augmente. J'ai également montré que Trim17 inhibe l'ubiquitination de NFATc3 induite par Trim39, à la fois dans les cellules et in vitro. Trim17 agit à la fois en réduisant l'activité E3 ubiquitine-ligase intrinsèque de Trim39 et en empêchant l'interaction entre NFATc3 et Trim39. En outre, j'ai montré qu'un mutant de NFATc3 ne pouvant être SUMOylé est moins ubiquitiné et plus stable que la forme sauvage de NFATc3, ce qui suggère que la SUMOylation de NFATc3 est importante pour son ubiquitination et sa dégradation. En outre, j'ai identifié un motif d'interaction à SUMO (SIM) dans la séquence de Trim39, par lequel Trim39 lie les polymères de SUMO2. La mutation de ce SIM dans Trim39 ou des sites consensus de SUMOylation dans NFATc3 diminue l'interaction entre Trim39 et NFATc3, et l'ubiquitination de NFATc3 induite par Trim39. Ces résultats suggèrent fortement que Trim39 reconnaît et ubiquitine préférentiellement les formes SUMOylées de NFATc3 et agit donc comme une « E3 ubiquitine-ligase guidée par SUMO » (STUbL) pour NFATc3. Enfin, nous avons mesuré l'impact de ces mécanismes sur la fonction physiologique de NFATc3. J'ai tout d'abord montré que Trim39 diminue l'activité transcriptionnelle de NFATc3. En outre, à l'aide de cultures primaires de neurones granulaires du cervelet, nous avons montré que la mutation des sites de SUMOylation de NFATc3 et la déplétion de Trim39 endogène aggravent l'apoptose neuronale, probablement en stabilisant la protéine NFATc3. En conclusion, l’ensemble de mes données indiquent que Trim39 module l'apoptose neuronale en agissant comme une STUbL pour NFATc3 et en contrôlant sa stabilité
NFAT (Nuclear factor of activated T cells) transcription factors play important physiological roles in the development and function of many organs, notably in the immune system and nervous system. As a consequence, their dysregulation has been implicated in various human diseases such as cancer, neurodegenerative diseases, and auto-immune diseases. The regulation of NFAT activity by calcium-dependent nuclear-cytoplasmic shuttling has been extensively studied. In contrast, the regulation of NFAT protein level by the ubiquitin-proteasome system is still poorly understood. However, NFATs are short-lived proteins and regulation of their stability is critical for controlling their activity.In a previous study, my group has shown that the E3 ubiquitin-ligase Trim17 binds NFATc3 but does not promote its ubiquitination and rather stabilizes it. Preliminary results suggested that Trim39, a partner of Trim17, might be an E3 ubiquitin-ligase for NFATc3 and that SUMOylation of NFATc3 might modulate its stability. Therefore, the goal of my PhD was to understand the mechanisms through which Trim39, Trim17, and SUMO regulate the stability of NFATc3.During my PhD, I have characterized Trim39 as an E3 ubiquitin-ligase of NFATc3. Indeed, my results indicate that overexpression of Trim39, but not its inactive mutant, induces the ubiquitination of NFATc3 in cells. In contrast, silencing of endogenous Trim39 decreases the ubiquitination level of NFATc3. Recombinant Trim39 directly induces the ubiquitination of NFATc3 in vitro. Moreover, overexpression of Trim39 decreases the protein levels of NFATc3 whereas the silencing of Trim39 increases it. I have also shown that Trim17, which can bind Trim39, inhibits Trim39-mediated ubiquitination of NFATc3, both in cells and in vitro. Trim17 acts by both reducing the intrinsic E3 ubiquitin-ligase activity of Trim39 and by preventing the interaction between NFATc3 and Trim39. Furthermore, I found that a SUMOylation-deficient mutant of NFATc3 is less ubiquitinated and more stable than the wild type NFATc3, suggesting that SUMOylation of NFATc3 is important for its ubiquitination and degradation. Importantly, I identified one SUMO interacting motif (SIM) in the sequence of Trim39 through which Trim39 binds SUMO2 polymers via one of these SIMs. Mutation of this SIM in Trim39 or SUMOylation consensus sites in NFATc3 decreased the interaction between Trim39 and NFATc3, and the ubiquitination of NFATc3 mediated by Trim39. These results strongly suggest that Trim39 binds and ubiquitinates preferentially the SUMOylated forms of NFATc3 and therefore acts as a SUMO-targeted E3 ubiquitin-ligase (STUbL) for NFATc3. Finally, we have measured the impact of these mechanisms on the physiological function of NFATc3. I first found that Trim39 decreases the transcriptional activity of NFATc3. Furthermore, using primary cultures of cerebellar granule neurons as a model, we have shown that the mutation of the SUMOylation sites of NFATc3 and silencing of endogenous Trim39 enhances neuronal apoptosis, probably by stabilizing the NFATc3 protein. Taken together, these data indicate that Trim39 modulates neuronal apoptosis by acting as a STUbL for NFATc3 and by controlling its stability

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Buberl, Cilli Dana [Verfasser]. "Expressionsanalyse der putativen E3 Ligasen Trim23 und Trim7 in der frühen Neuralentwicklung von Xenopus laevis / Cilli Dana Buberl." Halle, 2017. http://d-nb.info/1137867698/34.

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Borle, Pawar Ankush [Verfasser], Norbert [Akademischer Betreuer] Frey, and Dennis [Gutachter] Schade. "Functional characterization of TRIM24 and TRIM32 proteins in the heart through their interaction with Dysbindin / Ankush Borle Pawar ; Gutachter: Dennis Schade ; Betreuer: Norbert Frey." Kiel : Universitätsbibliothek Kiel, 2019. http://d-nb.info/1220691259/34.

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Locke, Matthew. "TRIM32 in Genetic Disease." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.514962.

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VENUTO, SANTINA. "Dissecting the TRIM8 role in the pathogenesis of glioma." Doctoral thesis, Università degli Studi di Foggia, 2019. http://hdl.handle.net/11369/382357.

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I gliomi umani sono un gruppo eterogeneo di tumori cerebrali maligni primari, la cui patogenesi molecolare risulta ancora parzialmente sconosciuta. Pertanto, la comprensione dei meccanismi molecolari alla base della loro insorgenza e del loro decorso può portare a una migliore scelta di terapie appropriate e a migliori risultati prognostici, attraverso l'identificazione di nuovi geni specifici associati al glioma. Le proteine appartenenti alla famiglia “tripartite motif” (TRIM) sono coinvolte in diversi processi biologici, tra cui la regolazione trascrizionale, il controllo della progressione del ciclo cellulare, la proliferazione e il differenziamento cellulare. Alterazioni dell’espressione delle proteine TRIM sono associate a una varietà di patologie quali disturbi dello sviluppo, malattie infiammatorie e tumori. Tra le circa 80 proteine identificate appartenenti alla famiglia delle TRIM, TRIM8 è una E3 ubiquitina-ligasi coinvolta in vari processi patologici, quali ipertrofia, risposta antivirale, encefalopatia e sviluppo di diverse forme di cancro. Abbiamo recentemente identificato TRIM8 come un gene differenzialmente espresso nei gliomi, la cui espressione è correlata a un esito clinico sfavorevole nei pazienti con glioma. Per ottenere informazioni approfondite sulle funzioni di TRIM8, ne abbiamo studiato il “trascrittoma” e l' “interattoma” in cellule staminali neurali embrionali di topo, usando l’RNA-Sequencing e la spettrometria di massa, e successivamente analizzando i dati ottenuti mediante programmi bioinformatici. Sono state quindi eseguite analisi funzionali, biochimiche e cellulari, per esplorare il ruolo TRIM8 in differenti processi biologici. Il nostro studio ci ha permesso di identificare vie di segnale correlate alla neurotrasmissione e al sistema nervoso centrale (SNC), fornendo ulteriori prove dell'esistenza di una relazione funzionale tra TRIM8 e STAT3, con possibili implicazioni nello sviluppo e nella progressione del glioma. Abbiamo successivamente dimostrato che TRIM8 interagisce con KIFC1 e KIF11/Eg5, due importanti regolatori dell'assemblaggio del fuso mitotico e della riorganizzazione del citoscheletro. Approfondendo lo studio sul ruolo di TRIM8 nel processo mitotico, abbiamo verificato che TRIM8 localizza a livello del fuso mitotico durante la progressione della mitosi e svolge un ruolo chiave nella separazione dei centrosomi all’inizio della divisione mitotica, con un conseguente ritardo nella progressione della mitosi e un impatto sulla stabilità cromosomica. I nostri risultati confermano il ruolo di TRIM8 nelle funzioni cerebrali attraverso la deregolazione di geni appartenenti al pathway JAK-STAT e coinvolti in diverse funzioni del SNC. Inoltre, abbiamo identificato la funzione fisiologica di TRIM8 nello sviluppo del fuso mitotico, evidenziando un ruolo emergente di TRIM8 nella regolazione della mitosi.
Human gliomas are a heterogeneous group of primary malignant brain tumors, whose molecular pathogenesis is not yet solved. Therefore, understanding the molecular mechanisms underlying their aggressive behavior may lead to better management, appropriate therapies, and good outcomes through the identification of novel specific glioma-associated genes. Members of the tripartite motif (TRIM) proteins family are involved in many biological processes, including transcriptional regulation, cell proliferation and differentiation and cell cycle progression. Alterations of TRIM proteins are associated with a variety of pathologies like developmental disorders, inflammatory diseases and cancers. Among TRIMs protein family, TRIM8 encodes an E3 ubiquitin ligase involved in various pathological processes, including hypertrophy, antiviral defense, encephalopathy, and cancer development. We have identified TRIM8 as a gene aberrantly expressed in gliomas, whose expression correlates with unfavorable clinical outcome in glioma patients. To gain insights into the TRIM8 functions, we profiled the TRIM8 transcriptome and interactome in primary mouse embryonic neural stem cells using RNA-sequencing and proteomics, followed by bioinformatics analysis. Functional analysis, including biochemical and cellular assays were then performed to explore TRIM8 roles in different pathways. Our study firstly identified enriched pathways related to the neurotransmission and to the central nervous system (CNS) functions, providing additional evidence about the existence of a functional interactive crosstalk between TRIM8 and STAT3 with possible implications in the development and progression of glioma. Then, we found that TRIM8 interacts with KIFC1 and KIF11/Eg5, two master regulators of mitotic spindle assembly and cytoskeleton reorganization. Exploring the TRIM8 role in the mitotic spindle machinery, we showed that TRIM8 localizes at the mitotic spindle during mitosis and plays a role in centrosome separation at the beginning of mitosis with a subsequent delay of the mitotic progression and impact on chromosomal stability. Our results substantiate the role of TRIM8 in the brain functions through the deregulation of genes involved in different CNS-related pathways, including JAK-STAT. Moreover, we provided insights on the physiological function of TRIM8 in the mitotic spindle machinery, pointing to an emerging role for TRIM8 in the regulation of mitosis

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Crichton, Jennifer E. "The Role of the E3-ubiquitin Ligase Trim17 in the Mitochondrial Cell Death Pathway." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23715.

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The upregulation of apoptosis is a hallmark of several neurodegenerative disorders including ischemic stroke. In neurons, as in other cell types, Bax and tBid are critical regulators of the intrinsic pathway upstream of mitochondrial outer membrane permeabilization (MOMP) and caspase activation. The characterization of the molecular events that occur during the early stages is therefore extremely important from a therapeutic standpoint. Here I show that two independent genetic pilot screens looking for novel regulators of Bax activation identified a common hit in the E3 ubiquitin ligase Trim17. Knockdown of Trim17 was found to protect against tBid-induced death in primary cortical neurons and allowed for the maintenance of mitochondrial function and oxidative phosphorylation under this apoptotic stress. The RING-domain of Trim17 was found to interact with Opa1 in mouse brain extracts. Furthermore, Opa1 co-immunoprecipitated with exogenously expressed full-length Trim17 from HEK293 cells. Knockdown of Trim17 in neurons increased Opa1 protein levels under steady-state conditions. These results suggest that Trim17 regulates Bax-dependent apoptosis in neurons via the modulation of Opa1 levels.

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Simpson, Shmona. "Genetic, structural, and functional exploration of the restrictive capacity of TRIM proteins against immunodeficiency viruses." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:1af588ba-603a-4f39-9443-bb1a95d983f5.

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HIV-2 differs from HIV-1 in that many infected people experience normal survival, whilst only 20% progress rapidly to AIDS. Understanding mechanisms of delayed HIV-2 disease progression could provide new insights into HIV control. The Caio Community Cohort was established in Guinea-Bissau in the setting of high HIV-2 prevalence. This thesis investigates the role of polymorphic host restriction factors of the TRIM family in HIV-2 outcome. TRIM proteins are a family of E3 ubiquitin-ligases, where closely-related TRIM5α and TRIM22 are thought to inhibit HIV-1 transcription, uncoating and budding. There was an association between TRIM5α amino acid substitution R136Q and reduced HIV-2 viral load/prolonged survival. Conversely, P479L was enriched among HIV-2 infected participants and progressors with CD4+ T cell decline. TRIM22 was highly polymorphic in this cohort, revealing three novel coding variants. Although most substitutions were located in the putative virus-interacting PRYSPRY domain, two in the coiled-coil, D155N and R242T, showed significant and divergent associations with survival. R242T was enriched in HIV-2 infected participants, who progressed to death at twice the rate of wild-type controls. In silico studies predicted D282, D360, and R321 of TRIM22 to be highly conserved, exposed residues, for which polymorphisms would be deleterious. When aligned with sequences from the potent HIV-1 restriction factor, rhesus macaque TRIM5α, TRIM22 substitutions R321K, T415I, and D360Y were spatially relevant to residues involved in HIV-1 restriction. The role of TRIM22 in HIV restriction was supported by in vitro pilot studies showing that TRIM22 was upregulated by HIV-1 infection in a lymphoid cell line and co-localised with the HIV-1 capsid protein p24. Overexpression of TRIM22 resulted in the restriction of VSV-G pseudotyped HIV-1 and SIVmac. The R242T substitution diminished TRIM22's restriction of HIV-1 and SIVmac: protein analysis suggested that this may be due to the inability of the R242T mutant to fully dimerise.

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Guimarães, Dimitrius Santiago Passos Simões Fróes. "Caracterização bioquímica e celular da proteína TRIM49." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17131/tde-10042018-112409/.

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A autofagia é o processo de degradação de estruturas celulares através do seu direcionamento ao lisossomo. As proteínas TRIMs reconhecem as -cargas? autofágicas e reúnem o complexo de nucleação do fagóforo, contudo se desconhece a função de cada domínio e a importância da atividade de E3 ligase para a sua atividade. A proteína TRIM49 clonada e expressa em E. coli ou em células humanas HEK293T não apresentou atividade de E3 ubiquitina ligase in vitro e reduziu os níveis totais de ubiquitinação in vivo, indicando que não é um E3 ubiquitina ligase. Células desafiadas com Htt74Q apresentaram menores níveis de citotoxicidade quando co-transfectadas com TRIM49 selvagem, mas não com os mutantes do domínio RING ou SPRY, indicando os dois domínios são necessários para sua atividade celular. A proteína selvagem se colocaliza com o marcador autofágico LC3, após o bloqueio da autofagia com bafilomicina A1. Os resultados indicam que a TRIM49 pode atuar na degradação intracelular de proteínas, por um mecanismo não dependente de atividade de E3 ligase.
Autophagy is the process of degradation of intracellular proteins through their directioning to the lysosome. TRIM proteins can directely recognize autophagic cargo and also act as a hub for the phagophore nucleation complex, however the function of each domain and the role of the E3 ligase activity in this process is unknown. The TRIM49 protein cloned and expressed in E. coli or in human cells HEK23T showed no ubiquitin E3 ligase activity in vitro and cells transfected with the wild type protein showed lower levels of polyubiquitinated proteins, indicating that TRIM49 is not a bona fide E3 ubiquitin ligase. Cells challenged with Htt74Q presented lower cytotoxicity levels when cotransfected with wild type TRIM49, when compared with the RING domain mutant or with the truncated protein lacking the SPRY domain, indicating that both domains are required for its cellular activity. The wild type protein colocalizes with the autophagic marker LC3 after treatment with the autophagy inhibitor bafilomycin A1. Taken together, these results indicate that the TRIM49 protein plays a role in protein degradation independently of a E3 ligase activity.

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Bartsch, Frederike [Verfasser], and Elke [Akademischer Betreuer] Cario. "Funktion und Regulation von TRIM58 in der myeloischen Immunabwehr / Frederike Bartsch ; Betreuer: Elke Cario." Duisburg, 2019. http://d-nb.info/1196008418/34.

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McGuire, Cy Christopher. "Evaluation of PGR properties of TRIMAX in cotton." Texas A&M University, 2005. http://hdl.handle.net/1969.1/2605.

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Pesticides comprise a large portion of production inputs in cotton. Reducing or enhancing their efficacy presents an avenue to increase profit. Pesticides containing both insecticidal and growth enhancing properties may be a viable option to increased profitability. In cotton (Gossypium hirsutum L.), early season applications of some insecticides have shown effects similar to those of plant growth regulators (PGRs). TRIMAX?? (imidacloprid) is one of these purported PGR insecticides. TRIMAX?? and Centric?? 40WG (thiamethoxam), both nitroguanidine insecticides, have properties that may exhibit PGR activity. A two - year field study was conducted at the Texas A&M Agricultural Experiment Station in Burleson County, Texas to assess the physiological effects of Centric?? 40WG and TRIMAX?? on cotton. The statistical design consisted of a randomized complete block with four replications. Treatments consisted of each insecticide being applied one, two, and three times at the 5- leaf stage, 5- leaf stage plus 10 days after initial treatment (DAIT), and 5-leaf stage plus 10 DAIT plus 20 DAIT. Rates consisted of TRIMAX?? and Centric?? 40WG being applied at 0.020 and 0.017 L/ha, respectively. Data was collected for plant height, total number of nodes, biomass partitioning, photosynthetic rate, midseason plant mapping, end of season box- mapping, yield, and fiber quality analysis. No significant differences in lint yield were observed among any of the insecticide PGR treatments. There was a general trend for numeric decreases in lint yield with each additional insecticide application for both chemistries, with the exception of TRIMAX?? at three applications in 2004. No significant differences were detected in any of the growth parameters that were measured (height, total nodes, biomass partitioning, and leaf area). Numerical differences resulted in trends, but rate responses did not follow any logical pattern. Numerous trends and rate responses were also observed in the Absolute and Relative Growth Rates, and photosynthetic rates, but no significant differences were evident. In general, as more insecticide was applied, the photosynthetic rates decreased along with lint yield. Based on the parameters investigated during the course of this two-year study, there is no conclusive evidence that supports TRIMAX?? or Centric?? 40WG as being growth and or yield enhancers in cotton.

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Книги з теми "TRIM18"

Sodums, Dzintars. Jauni trimdā. Rīgā: "Karogs", 1997.

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Odom, Joe. TRIMIX diver manual. 3rd ed. Topsham, Me.]: Technical Diving International, 1998.

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Ribbons & trims. New York: Potter Craft, 2007.

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Professor Trim's becoming slimmer. St. Leonards, N.S.W: Allen & Unwin, 2003.

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Kont͡s︡ert za trima. Sofii͡a︡: Profizdat, 1986.

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Hennessy, Mark. Trim. Dublin: Royal Irish Academy, 2003.

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David, Cameron-Smith, ed. Professor Trim's ultimate food energy guide. St. Leonards, N.S.W: Allen & Unwin, 2003.

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Rožkalne, Anita. Palma vējā: Literatūrvēsturiskas piezīmes par latviešu trimdu. Rīgā: Pētergailis, 1998.

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Musta, Agim. Kampet e internimit dhe trimat e dëshpërimit. Tiranë: Shtëpia Botuese "Marin Barleti", 2012.

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Cain, Daniel. Un trimis al majestății sale, Nicolae Mișu. București: Editura Anima, 2007.

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Частини книг з теми "TRIM18"

Gooch, Jan W. "Trimer." In Encyclopedic Dictionary of Polymers, 767. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_12131.

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Moss, Joel, and Martha Vaughan. "ARD1/TRIM23." In Encyclopedia of Signaling Molecules, 406–11. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_644.

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Moss, Joel, Michaela U. Gack, and Martha Vaughan. "ARD1/TRIM23." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-6438-9_644-1.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, Takaya Satoh, Joe B. Blumer, Stephen M. Lanier, Ana Kasirer-Friede, et al. "ARD1/TRIM23." In Encyclopedia of Signaling Molecules, 146–50. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_644.

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Templeton, J. L. "Tungsten Trimer Synthesis." In Inorganic Reactions and Methods, 80–81. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2007. http://dx.doi.org/10.1002/9780470145296.ch64.

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Hirota, E., K. Kuchitsu, T. Steimle, J. Vogt, and N. Vogt. "39 C3H6F6 Difluoromethane trimer." In Molecules Containing Three or Four Carbon Atoms and Molecules Containing Five or More Carbon Atoms, 69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41504-3_40.

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Demaison, J. "143 H6O3 Water trimer." In Symmetric Top Molecules, 271–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-47532-3_145.

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Seong, Hongje, Seoung Wug Oh, Brian Price, Euntai Kim, and Joon-Young Lee. "One-Trimap Video Matting." In Lecture Notes in Computer Science, 430–48. Cham: Springer Nature Switzerland, 2022. http://dx.doi.org/10.1007/978-3-031-19818-2_25.

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Demaison, J. "323 C3H6F6 Difluoromethane trimer." In Asymmetric Top Molecules. Part 2, 134. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-10400-8_71.

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Gooch, Jan W. "Trim." In Encyclopedic Dictionary of Polymers, 767. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_12130.

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Duan, Wenyang, Hongsen Zhang, Limin Huang, Jianyu Liu, Wenbo Shao, Guanzhou Cao, and Zhang Shi. "Numerical Simulation of Trim Optimization on Resistance Performance Based on CFD Method." In ASME 2019 38th International Conference on Ocean, Offshore and Arctic Engineering. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/omae2019-96181.

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Abstract In response to the gradually stringent carbon emission requirements of the International Maritime Organization (IMO), the energy-saving methods of the shipping industry have received increasing attention. Today how to reduce fuel consumptions so as to lower carbon emissions to improve the economic and environmental benefits of ships has become a hot topic. As one of the most easily implemented energy-saving methods, trim optimization has caught more and more researchers’ eyes. In this paper, a commercial CFD software STAR-CCM+ was adopted to analyze the influence of trim on the resistance performance of VLCC ship mainly with fixed model method under various typical conditions of the design draft and the ballast draft respectively. The grid convergence was studied at the design draft and the typical numerical simulations were verified by the experimental results before carrying out various numerical simulations of trim optimization. Seven different kinds of trim conditions, which correspond to the changing process of the full scale ship from trimming by stern 4m to bow 4m, were simulated with 3 different speeds of design draft and ballast draft. The changes of total resistance, frictional resistance and residual resistance were analyzed to explore the effect of trims on the ship’s resistance. The variation of ship’s wetted surface area and waterplane area under different trim angles were studied. It was found that under the condition of low Froude number, both the simulation of free trim and sink method and the fixed model method can achieve good accuracy with the method of fixed model reducing the simulation time obviously. Both conditions of the design draft and ballast draft had a certain reduction effect of total resistance for trimming by bow properly, of which the change of frictional resistance is dominant in the decrease of total resistance at design draft while the change of residual resistance is the main cause at ballast draft. The optimum trims were found and the optimal total resistance reduction effects were evaluated. The optimal total resistance reduction effect increased with speed whether at the design or the ballast draft and the reduction effects were more obvious at ballast draft. Meanwhile, it was found that the changes of wetted surface area and the waterplane area with different trims were close to the variation tendency of the frictional resistance.

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Metzler, M., IJ Diets, J. Hoyer, J. Wegert, N. Graf, C. Vokuhl, M. Gessler, RP Kuiper, and MCJ Jongmans. "TRIM28 haploinsufficiency predisposes to Wilms tumor." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687131.

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Fong, Ka-Wing, Jonathan Zhao, Bin Zheng, and Jindan Yu. "Abstract 1521: Role of Trim28 in prostate cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1521.

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Kirkby, David R., and David T. Delpy. "An optoelectronic cross-correlator using a gain modulated avalanche photodiode for measurement of the tissue temporal point spread function." In Advances in Optical Imaging and Photon Migration. Washington, D.C.: Optica Publishing Group, 1996. http://dx.doi.org/10.1364/aoipm.1996.trit108.

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A small and relatively inexpensive optoelectronic cross-correlator, using an avalanche photodiode (APD) detector and without any moving parts has been developed to measure the temporal point spread function (TPSF) of light in tissue. From the TPSF, it is in principle possible to determine the optical properties of the tissue. Currently a temporal response of 275 ps full width half maximum (FWHM) has been achieved. Measurements of the TPSF of a tissue phantom using a synchroscan streak camera and the cross-correlator show excellent agreement, although the achievable signal to noise ratio currently limits the ability of the cross-correlator to detect the low intensity sections of a TPSF.

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Zhang, Changming, Mukherjee Subhas, Tucker-Burden Carol, Monica Chau, Jun Kong, and Daniel Brat. "Abstract 2516: TRIM8 modulates stem-like cells in glioblastoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2516.

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Fel'dman, Edward, and Elena I. Kuznetsova. "Quantum entanglement in trimer clusters." In The International Conference on Micro- and Nano-Electronics 2018, edited by Vladimir F. Lukichev and Konstantin V. Rudenko. SPIE, 2019. http://dx.doi.org/10.1117/12.2520034.

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Pålsson, Lars-Olof, Vidmantas Gulbinas, Tomas Gillbro, Andrei V. Sharkov, Axel Parbel, and Hugo Scheer. "Excited state dynamics of PEC trimer." In The 54th international meeting of physical chemistry: Fast elementary processes in chemical and biological systems. AIP, 1996. http://dx.doi.org/10.1063/1.50200.

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HEŘMAN, PAVEL, and IVAN BARVÍK. "ENERGY RELAXATION AND TRANSFER IN TRIMER." In Proceedings of 2000 International Conference. WORLD SCIENTIFIC, 2001. http://dx.doi.org/10.1142/9789812811387_0049.

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Gupta, Vikas, and Shanmuganathan Raman. "Automatic trimap generation for image matting." In 2016 International Conference on Signal and Information Processing (IConSIP). IEEE, 2016. http://dx.doi.org/10.1109/iconsip.2016.7857477.

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Barclay, A., Nasser Moazzen-Ahmadi, Bob McKellar, and Koorosh Esteki. "INFRARED SPECTRA OF C2H4 DIMER AND TRIMER." In 73rd International Symposium on Molecular Spectroscopy. Urbana, Illinois: University of Illinois at Urbana-Champaign, 2018. http://dx.doi.org/10.15278/isms.2018.te04.

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Звіти організацій з теми "TRIM18"

Strathman, James. Extraboard Management: TriMet Case Study. Portland State University Library, February 2012. http://dx.doi.org/10.15760/trec.4.

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Kalberer, Jennifer L., and Jennifer C. Spanich. Evaluation of the TRIMAX 280 System. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada405546.

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Trumble, E. F. TRIMPWR: A post processor for TRIMHX. Office of Scientific and Technical Information (OSTI), November 1989. http://dx.doi.org/10.2172/6975898.

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Trumble, E. F. Validation and verification summary report for GRIMHX and TRIMHX. Office of Scientific and Technical Information (OSTI), December 1990. http://dx.doi.org/10.2172/10156331.

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Trumble, E. F. Validation and verification summary report for GRIMHX and TRIMHX. Office of Scientific and Technical Information (OSTI), December 1990. http://dx.doi.org/10.2172/5038892.

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Fries, Joseph. Helicopter Trim Analysis. Fort Belvoir, VA: Defense Technical Information Center, June 1996. http://dx.doi.org/10.21236/ada310293.

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Brooks, Stephen. Integrated Fields of Permanent Magnet Dipole Trims. Office of Scientific and Technical Information (OSTI), October 2021. http://dx.doi.org/10.2172/1895098.

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Minden, M. L., and T. R. O'Meara. Range-Doppler, Target-Referencing Imaging Systems (RD-TRIMS). Fort Belvoir, VA: Defense Technical Information Center, January 1990. http://dx.doi.org/10.21236/ada360123.

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Strathman, James, Joseph Broach, and Steve Callas. Evaluation of Short Duration Unscheduled Absences Among Transit Operators: TriMet Case Study. Portland State University Library, September 2009. http://dx.doi.org/10.15760/trec.141.

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Mills, John R. An Introduction To PC-TRIM. Portland, OR: U.S. Department of Agriculture, Forest Service, Pacific Northwest Research Station, 1989. http://dx.doi.org/10.2737/pnw-rn-491.

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