Relevant bibliographies by topics / Zc3h10

Academic literature on the topic 'Zc3h10'

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Published: 9 March 2023

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Journal articles on the topic "Zc3h10"

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Wang, Luyu, Yaping Gao, Jinpeng Wang, Ning Huang, Qiang Jiang, Zhihua Ju, Chunhong Yang, et al. "Selection Signature and CRISPR/Cas9-Mediated Gene Knockout Analyses Reveal ZC3H10 Involved in Cold Adaptation in Chinese Native Cattle." Genes 13, no. 10 (October 20, 2022): 1910. http://dx.doi.org/10.3390/genes13101910.

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Cold stress is an important factor affecting cattle health, production performance, and reproductive efficiency. Understanding of the potential mechanism underlying genetic adaptation to local environments, particularly extreme cold environment, is limited. Here, by using FLK and hapFLK methods, we found that the Zinc finger CCCH-type containing 10 (ZC3H10) gene underwent positive selection in the Menggu, Fuzhou, Anxi, and Shigatse humped cattle breeds that are distributed in the cold areas of China. Furthermore, ZC3H10 expression significantly increased in bovine fetal fibroblast (BFF) cells at 28 °C for 4 h. ZC3H10 knockout BFFs were generated using CRISPR/Cas9. Wild and ZC3H10-deleted BFFs were treated at two temperatures and were divided into four groups (WT, wild and cultured at 38 °C; KO, ZC3H10−/− and 38 °C; WT_LT, wild, and 28 °C for 4 h; and KO_LT, ZC3H10−/− and 28 °C for 4 h. A total of 466, 598, 519, and 650 differently expressed genes (two-fold or more than two-fold changes) were identified by determining transcriptomic difference (KO_LT vs. KO, WT_LT vs. WT, KO vs. WT, and KO_LT vs. WT_LT, respectively). Loss of ZC3H10 dysregulated pathways involved in thermogenesis and immunity, and ZC3H10 participated in immunity-related pathways induced by cold stress and regulated genes involved in glucose and lipid metabolism and lipid transport (PLTP and APOA1), thereby facilitating adaptability to cold stress. Our findings provide a foundation for further studies on the function of ZC3H10 in cold stress and development of bovine breeding strategies for combatting the influences of cold climate.
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Garg, Ankur, Yvette Roske, Shinnosuke Yamada, Takuya Uehata, Osamu Takeuchi, and Udo Heinemann. "PIN and CCCH Zn-finger domains coordinate RNA targeting in ZC3H12 family endoribonucleases." Nucleic Acids Research 49, no. 9 (May 5, 2021): 5369–81. http://dx.doi.org/10.1093/nar/gkab316.

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Abstract The CCCH-type zinc finger (ZnF) containing ZC3H12 ribonucleases are crucial in post-transcriptional immune homoeostasis with ZC3H12A being the only structurally studied member of the family. In this study, we present a structural-biochemical characterization of ZC3H12C, which is linked with chronic immune disorders like psoriasis. We established that the RNA substrate is cooperatively recognized by the PIN and ZnF domains of ZC3H12C and analyzed the crystal structure of ZC3H12C bound to a single-stranded RNA substrate. The RNA engages in hydrogen-bonded contacts and stacking interactions with the PIN and ZnF domains simultaneously. The ZC3H12 ZnF shows unprecedented structural features not previously observed in any member of the CCCH-ZnF family and utilizes stacking interactions via a unique combination of spatially conserved aromatic residues to align the target transcript in a bent conformation onto the ZnF scaffold. Further comparative structural analysis of ZC3H12 CCCH-ZnF suggests that a trinucleotide sequence is recognized by ZC3H12 ZnF in target RNA. Our work not only describes the initial structure-biochemical study on ZC3H12C, but also provides the first molecular insight into RNA recognition by a ZC3H12 family member. Finally, our work points to an evolutionary code for RNA recognition adopted by CCCH-type ZnF proteins.
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Yi, Danielle, Jon M. Dempersmier, Hai P. Nguyen, Jose A. Viscarra, Jennie Dinh, Chihiro Tabuchi, Yuhui Wang, and Hei Sook Sul. "Zc3h10 Acts as a Transcription Factor and Is Phosphorylated to Activate the Thermogenic Program." Cell Reports 29, no. 9 (November 2019): 2621–33. http://dx.doi.org/10.1016/j.celrep.2019.10.099.

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Erben, Esteban, Kevin Leiss, Bin Liu, Diana Inchaustegui Gil, Claudia Helbig, and Christine Clayton. "Insights into the functions and RNA binding of Trypanosoma brucei ZC3H22, RBP9 and DRBD7." Parasitology 148, no. 10 (February 4, 2021): 1186–95. http://dx.doi.org/10.1017/s0031182021000123.

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AbstractTrypanosoma brucei is unusually reliant on mRNA-binding proteins to control mRNA fate, because its protein-coding genes lack individual promoters. We here focus on three trypanosome RNA-binding proteins. ZC3H22 is specific to Tsetse fly forms, RBP9 is preferentially expressed in bloodstream forms; and DRBD7 is constitutively expressed. Depletion of RBP9 or DRBD7 did not affect bloodstream-form trypanosome growth. ZC3H22 depletion from procyclic forms caused cell clumping, decreased expression of genes required for cell growth and proliferation, and increased expression of some epimastigote markers. Apart from decreases in mRNAs encoding enzymes of glucose metabolism, levels of most ZC3H22-bound transcripts were unaffected by ZC3H22 depletion. We compared ZC3H22, RBP9 and DRBD7 RNA binding with that of 16 other RNA-binding proteins. ZC3H22, PUF3 and ERBP1 show a preference for ribosomal protein mRNAs. RBP9 preferentially binds mRNAs that are more abundant in bloodstream forms than in procyclic forms. RBP9, ZC3H5, ZC3H30 and DRBD7 prefer mRNAs with long coding regions; UBP1-associated mRNAs have long 3′-untranslated regions; and RRM1 prefers mRNAs with long 3′or 5′-untranslated regions. We suggest that proteins that prefer long mRNAs may have relatively short or degenerate binding sites, and that preferences for A or U increase binding in untranslated regions.
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Ouna, Benard Aswani, Mhairi Stewart, Claudia Helbig, and Christine Clayton. "The Trypanosoma brucei CCCH zinc finger proteins ZC3H12 and ZC3H13." Molecular and Biochemical Parasitology 183, no. 2 (June 2012): 184–88. http://dx.doi.org/10.1016/j.molbiopara.2012.02.006.

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Yi, Danielle, Hai P. Nguyen, and Hei Sook Sul. "Epigenetic dynamics of the thermogenic gene program of adipocytes." Biochemical Journal 477, no. 6 (March 27, 2020): 1137–48. http://dx.doi.org/10.1042/bcj20190599.

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Brown adipose tissue (BAT) is a metabolically beneficial organ capable of burning fat by dissipating chemical energy into heat, thereby increasing energy expenditure. Moreover, subcutaneous white adipose tissue can undergo so-called browning/beiging. The recent recognition of the presence of brown or beige adipocytes in human adults has attracted much attention to elucidate the molecular mechanism underlying the thermogenic adipose program. Many key transcriptional regulators critical for the thermogenic gene program centering on activating the UCP1 promoter, have been discovered. Thermogenic gene expression in brown adipocytes rely on co-ordinated actions of a multitude of transcription factors, including EBF2, PPARγ, Zfp516 and Zc3h10. These transcription factors probably integrate into a cohesive network for BAT gene program. Moreover, these transcription factors recruit epigenetic factors, such as LSD1 and MLL3/4, for specific histone signatures to establish the favorable chromatin landscape. In this review, we discuss advances made in understanding the molecular mechanism underlying the thermogenic gene program, particularly epigenetic regulation.
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Wawro, Mateusz, Karolina Wawro, Jakub Kochan, Aleksandra Solecka, Weronika Sowinska, Agata Lichawska-Cieslar, Jolanta Jura, and Aneta Kasza. "ZC3H12B/MCPIP2, a new active member of the ZC3H12 family." RNA 25, no. 7 (April 15, 2019): 840–56. http://dx.doi.org/10.1261/rna.071381.119.

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Wawro, Mateusz, Karolina Wawro, Jakub Kochan, Aleksandra Solecka, Weronika Sowinska, Agata Lichawska-Cieslar, Jolanta Jura, and Aneta Kasza. "Corrigendum: ZC3H12B/MCPIP2, a new active member of the ZC3H12 family." RNA 25, no. 9 (August 16, 2019): 1226_2. http://dx.doi.org/10.1261/rna.072421.119.

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Chakraborty, Chaitali, Abeer Fadda, Esteban Erben, Smiths Lueong, Jörg Hoheisel, Elisha Mugo, and Christine Clayton. "Interactions of CAF1-NOT complex components from Trypanosoma brucei." F1000Research 6 (June 9, 2017): 858. http://dx.doi.org/10.12688/f1000research.11750.1.

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The CAF1-NOT complex of Trypanosoma brucei, like that of other eukaryotes, contains several NOT proteins (NOT1, NOT3, NOT3/5, NOT10, and NOT11), NOT9/CAF40, and the CAF1 deadenylase, which targets 3' poly(A) tails. Again like other eukaryotes, deadenylation is the first step in the degradation of most trypanosome mRNAs. In animal cells, destruction of unstable mRNAs is accelerated by proteins that bind the RNA in a sequence-specific fashion, and also recruit the CAF1-NOT complex. However, this has not yet been demonstrated for T. brucei. To find interaction partners for the trypanosome NOT complex, we did a genome-wide yeast two-hybrid screen, using a random shotgun protein fragment library, with the subunits CAF40, NOT2, NOT10 and NOT11 as baits. To assess interaction specificity, we compared the results with those from other trypanosome proteins, including the cyclin-F-box protein CFB1. The yeast 2-hybrid screen yielded four putatively interacting proteins for NOT2, eleven for NOT11, but only one for NOT9/CAF40. Both CFB1 and NOT10 had over a hundred potential interactions, indicating a lack of specificity. Nevertheless, a detected interaction between NOT10 and NOT11 is likely to be genuine. We also identified proteins that co-purify with affinity tagged NOT9/CAF40 by mass spectrometry. The co-purifying proteins did not include the 2-hybrid partner, but the results confirmed NOT9/CAF40 association with the CAF1-NOT complex, and suggested interactions with expression-repressing RNA-binding proteins (ZC3H8, ZC3H30, and ZC3H46) and the deadenylase PARN3.
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Trenaman, Anna, Lucy Glover, Sebastian Hutchinson, and David Horn. "A post-transcriptional respiratome regulon in trypanosomes." Nucleic Acids Research 47, no. 13 (May 25, 2019): 7063–77. http://dx.doi.org/10.1093/nar/gkz455.

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Abstract Post-transcriptional regulons coordinate the expression of groups of genes in eukaryotic cells, yet relatively few have been characterized. Parasitic trypanosomatids are particularly good models for studies on such mechanisms because they exhibit almost exclusive polycistronic, and unregulated, transcription. Here, we identify the Trypanosoma brucei ZC3H39/40 RNA-binding proteins as regulators of the respiratome; the mitochondrial electron transport chain (complexes I–IV) and the FoF1-ATP synthase (complex V). A high-throughput RNAi screen initially implicated both ZC3H proteins in variant surface glycoprotein (VSG) gene silencing. This link was confirmed and both proteins were shown to form a cytoplasmic ZC3H39/40 complex. Transcriptome and mRNA-interactome analyses indicated that the impact on VSG silencing was indirect, while the ZC3H39/40 complex specifically bound and stabilized transcripts encoding respiratome-complexes. Quantitative proteomic analyses revealed specific positive control of >20 components from complexes I, II and V. Our findings establish a link between the mitochondrial respiratome and VSG gene silencing in bloodstream form T. brucei. They also reveal a major respiratome regulon controlled by the conserved trypanosomatid ZC3H39/40 RNA-binding proteins.
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Dissertations / Theses on the topic "Zc3h10"

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Audano, M. "THE RNA BINDING PROTEIN ZC3H10 COUPLES MITOCHONDRIAL FUNCTION AND IRON METABOLISM." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/481986.

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Mitochondria play a crucial role in energy metabolism. Mitochondria have their own genome (mtDNA), whose replication and transcription are mainly regulated by the mitochondrial transcription factor A (Tfam). Recent researches demonstrate how mitochondria participate to a large number of cellular processes like cell cycle and differentiation. Our goal is to identify new mitochondrial regulators to light up the molecular mechanisms underlying mitochondrial function biology. We used a high throughput screening in 293 cells in order to identify positive mitochondrial regulators. By these means, we identified Zinc Finger CCCH-type containing 10 (Zc3h10) as the best hit. Following experiments demonstrated that Zc3h10 knockdown decreased mitochondrial function and differentiation in myotubes. RNA immunoprecipitation assay indicates that Zc3h10 is able to bind 410 transcripts. Several target genes are involved in energy metabolism and iron balance. Notably, Zc3h10 downregulation in C2C12 leads to iron overload while its overexpression restores ferric ion content to control levels. Collectively, our findings annotate Zc3h10 as a new mitochondrial regulator in skeletal muscle.
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PEDRETTI, SILVIA. "THE NOVEL MITOCHONDRIAL REGULATOR ZC3H10 CONTROLS THE WHITE ADIPOCYTE DIFFERENTIATION PROGRAM." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/796662.

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Mitochondria play a crucial role in many cellular processes, and they are essential organelles for the cell’s health. Beside their contribution to energy production, they are key regulators of tissue development and cell differentiation. In this context, a new mitochondrial regulator, zinc finger CCCH-type containing 10 (Zc3h10) protein has been recently discovered, and we validated its role during white adipocytes differentiation. The commitment of mesenchymal stem cells to pre-adipocytes is stimulated by hormonal induction. During adipocytes differentiation, pre-adipocytes undergo blunted protein synthesis, cytoskeleton remodeling and increased mitochondrial function to support anabolic pathways. All these molecular changes enable differentiation into mature adipocytes. We found that Zc3h10 is a critical regulator of the early stages of adipogenesis. Indeed, Zc3h10 depletion in pre-adipocytes resulted in increased protein translation and impaired filamentous (F)-actin remodeling, thus resulting in mitochondrial and metabolic dysfunction, incorrect mitotic clonal expansion (MCE), impaired lipid accumulation and terminal differentiation. In contrast, Zc3h10 overexpression yielded mature adipocytes with remarkably increased lipid droplet size. Overall, our results establish Zc3h10 as a fundamental pro-adipogenic transcription factor that represses protein synthesis and promotes F-actin/mitochondria dynamics to ensure proper energy metabolism, MCE and favor lipid accumulation to allow final adipocytes differentiation.
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Inchaustegui, Gil Diana Patricia [Verfasser], and Christine [Akademischer Betreuer] Clayton. "Purification of specific mRNP via the nascent polypeptide The RNA Binding Proteins ZC3H22 and ZC3H38 / Diana Patricia Inchaustegui Gil ; Betreuer: Christine Clayton." Heidelberg : Universitätsbibliothek Heidelberg, 2015. http://d-nb.info/1180499891/34.

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Benbahouche, Nour el Houda. "Investigating the role of extended CBC complexes in RNA metabolism." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTS002.

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Le CBC intervient dans de nombreuses étapes du métabolisme des ARN, telle que l’épissage, la maturation de l’extrémité 3’, la dégradation, l’export et la traduction. Ainsi, le CBC constitue un complexe majeur qui peut orchestrer les différentes étapes de maturation des ARN. Récemment, nous avons identifié le complexe CBCAP, composé de CBC, ARS2 et PHAX. Nous avons montré que la protéine ARS2 stimule la formation des extrémités 3’ de plusieurs familles d’ARN dont les snARN. De plus, ARS2 stimule le recrutement de PHAX sur le CBC. Ainsi, nous proposons un modèle où CBC-ARS2 stimule la formation de l’extrémité 3’ des pré-snARN et recrute PHAX pour favoriser leur export. Une autre étude a identifié un autre complexe le CBCN, constitué de CBC, Ars2, et de ZC3H18-NEXT au lieu de PHAX. CBCN recrute l’exosome et stimule la dégradation de certains ARN, comme les PROMPTS et les transcrits «read-through » des snARN et des ARNm d’histone. Ainsi, PHAX et ZC3H18 destinent leur ARN cibles vers l’export ou la dégradation. Il a été montré que PHAX reconnait et lie spécialement les ARN de petite taille. D’une manière remarquable, nos données de CLIP-Seq et de RIP suivie par des analyses avec des puces « All genes » montrent que PHAX lie aussi d’autres familles d’ARN. En effet, PHAX lie les ARNm ainsi que des ARN non-codant avec une légère préférence pour les snARN (en comparaison avec ZC3H18). Afin de mieux comprendre le rôle de PHAX et ZC3H18, j’ai tout d’abord démontré si les deux protéines se lient simultanément au CBC. Pour ce faire, J’ai réalisé des tests de compétitions entre PHAX et ZC3H18, in vivo, et j’ai montré que la surexpression de ZC3H18 déplace PHAX du CBC et vice versa. Puis en utilisant la technique de « Tethering Assays » j’ai pu montrer que PHAX et ZC3H18 ont des effets opposés sur la biogénèse des ARNm. De plus PHAX semble avoir un effet positif sur la maturation des ARNm et ce, en empêchant ZC3H18 et l’exosome d’être recruter. Nous avons aussi montré que la déplétion de PHAX et ZC3H18 a des conséquences fonctionnelles sur le taux des formes matures des snARN. Dans le but de caractériser la protéine ZC3H18, j’ai réalisé un crible double-hybride et j’ai montré que ZC3H18 interagit avec plusieurs facteurs d’épissage. J’ai aussi identifié les domaines de ZC3H18 impliqués dans ses différentes interactions. D’une manière intéressante, l’interaction de ZC3H18 avec certains facteurs d’épissage peut être exclusive à son interaction avec NEXT. De plus, des expériences de protéomique réalisés sur un des facteurs d’épissage trouvé dans le crible, montrent qu’il co-purifie au sein d’un complexe qui pourrait faire le lien entre la coiffe et la machinerie d’épissage. En accord avec ces résultats, nos données de RNA-seq montrent que la déplétion de ZC3H18 engendre un défaut d’épissage pour des introns qui sont proches de la coiffe et ceci pour un nombre restreint de gènes. Ainsi, notre travail décode davantage le rôle de la coiffe dans les différentes étapes de maturation des ARN et suggère un modèle où la séquence des transcrits naissant stimule la formation d’un complexe spécifique à cet ARN parmi plusieurs autres
The cap binding complex (CBC) plays a key role in a number of gene expression pathways and has been proposed to participate in the discrimination of RNA families. It also enhances many RNA processing steps, including transcription, splicing, 3’end formation, degradation, export and translation.Recently, we identified the CBCAP complex, composed of CBC, Ars2 and PHAX. We showed that Ars2 stimulates snRNA 3'-end processing as well as PHAX binding to the CBC, hence coupling snRNA maturation with their export. Other studies showed that the CBC and ARS2 can form another complex that contains ZC3H18-NEXT instead of PHAX. This complex, named CBCN, is a cofactor of the RNA exosome and is involved in the degradation of cryptic RNAs such as PROMPTs and read-through transcripts at histone and snRNA genes. Thus, PHAX and ZC3H18 target specific families of capped RNA toward either export or degradation. Previous studies proposed that PHAX binds specifically to small RNAs and discriminates them over other RNA species. Surprisingly, our CLIP-Seq and RIP-microarrays data showed that in contrast to expectations, PHAX was not specific for snRNAs. It also binds mRNAs as well as other non-coding RNAs and has a weak preference for snRNAs comparing to ZC3H18. To better understand the role of PHAX and ZC3H18, Ifirst determined whether PHAX and ZC3H18 can bind simultaneously to the CBC. Competitive LUMIER IPs indicated that binding of these proteins is mutually exclusive. I then used tethering assays and could show that PHAX and ZC3H18 have opposite effect on mRNA biogenesis. These data go against a model where binding of PHAX or ZC3H18 discriminate RNA families, and instead suggest promiscuous binding for these proteins. In addition, PHAX may exert a positive effect on mRNA processing by preventing binding of ZC3H18 and recruitment of the RNA exosome. Last but not least, our RT-QPCR data show that PHAX and ZC3H18 depletions have functional consequences on the level of mature snRNA, and this is due to a competition between both proteins which occur on those snRNA read-through transcripts.To further explore the role of ZC3H18, I performed a two-hybrid screen and identified several splicing factors. I could validate these interactions, identify the domains involved and show that binding of some of these factors is exclusive with that of NEXT. Importantly, proteomic experiments with one of these factors identified a complex that makes the link between the cap and the splicing machinery. In agreement, RNA-Seq analysis of ZC3H18 knock-down cells showed alterations in splicing of cap-proximal introns, for a small set of genes.Altogether, this work reveals how the multiple roles of the RNA cap are achieved at the biochemical level, and suggests that the nascent RNA sequence triggers formation of one among several mutually exclusive complexes
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Al-Hasani, Jafaar [Verfasser]. "Functional analysis of the CAD-risk gene Zc3hc1 / Jafaar Al-Hasani." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2018. http://d-nb.info/1153438062/34.

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Klein, Cornelia Andrea [Verfasser], and Christine [Akademischer Betreuer] Clayton. "The role of ZC3H32 in Trypanosoma brucei / Cornelia Andrea Klein ; Betreuer: Christine Clayton." Heidelberg : Universitätsbibliothek Heidelberg, 2014. http://d-nb.info/1179925262/34.

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Chakraborty, Chaitali [Verfasser], and Christine [Akademischer Betreuer] Clayton. "Interactions of the CAF1-NOT complex and the role of ZC3H30 in combating stress in Trypanosoma brucei / Chaitali Chakraborty ; Betreuer: Christine Clayton." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/117714896X/34.

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Younis, Shady. "Functional characterization of the biological significance of the ZBED6/ZC3H11A locus in placental mammals." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-329190.

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The recent advances in molecular and computational biology have made possible the study of complicated transcriptional regulatory networks that control a wide range of biological processes and phenotypic traits. In this thesis, several approaches were combined including next generation sequencing, gene expression profiling, chromatin and RNA immunoprecipitation, bioinformatics and genome editing methods in order to characterize the biological significance of the ZBED6 and ZC3H11A genes. A mutation in the binding site of ZBED6, located in an intron of IGF2, disrupts the binding and leads to 3-fold upregulation of IGF2 mRNA in pig muscle tissues. The first part of the thesis presents a detailed functional characterization of ZBED6. Transient silencing of ZBED6 expression in mouse myoblasts led to increased Igf2 expression (~2-fold). ChIP-seq analysis of ZBED6 and histone modifications showed that ZBED6 preferentially binds active promoters and modulates their transcriptional activities (paper I). In the follow-up studies using CRISPR/Cas9 we showed that either the deletion of ZBED6 or its binding site in Igf2 (Igf2ΔGGCT) led to more than 30-fold up-regulation of Igf2 expression in myoblasts. Differentiation of these genetically engineered cells resulted in hypertrophic myotubes. Transcriptome analysis revealed ~30% overlap between the differentially expressed genes in Zbed6-/- and Igf2ΔGGCT myotubes, with significant enrichment of muscle-specific genes. ZBED6-overexpression in myoblasts led to cell cycle arrest, reduced cell viability, reduced mitochondrial activities and impaired the differentiation of myoblasts (paper II). Further studies on cancer cells showed that ZBED6 influences the growth of colorectal cancer cells with dramatic changes in the transcription of hundreds of cancer-related genes (paper III). The phenotypic characterization of Zbed6-/- and Igf2pA/mG mouse models showed that the ZBED6-Igf2 axis has a major effect on regulating muscle growth and the growth of internal organs. Transcriptome analysis demonstrated a massive up-regulation of Igf2 expression (~30-fold) in adult tissues, but not in fetal tissues, of transgenic mice (paper IV). In the second part of the thesis we investigated the cellular function of Zc3h11a, the gene harboring ZBED6 in one of its first introns. The function of the ZC3H11A protein is so far poorly characterized. We show that ZC3H11A is a novel stress-induced protein that is required for efficient mRNA export from the nucleus. The inactivation of ZC3H11A inhibited the growth of multiple viruses including HIV, influenza, HSV and adenoviruses (paper V).
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Zhou, Tianwei. "The role of ZC3H12A in «Pseudomonas aeruginosa» infection of airway epithelial cells and implication in Cystic Fibrosis." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104662.

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Cystic fibrosis (CF) is the most common fatal genetic disease affecting Canadian Caucasians. The majority of CF patients suffered from perpetual inflammation caused by Pseudomonas aeruginosa (P. aeruginosa). Previous, we found cells lacking functionalCFTR exhibit IL6 hypersecretion phenotype and a concomitant hyperactivity of p38 MAPK in response to P. aeruginosa. Therefore, I dedicated my master's thesis to investigate the link between increased IL6 production and p38 MAPK. ZC3H12A, an IL6-specific ribonuclease, was found to be a novel substrate of p38 MAPK and negatively regulated IL6 production from P. aeruginosa-stimulated airway epithelial cells. Together, these discoveries demonstrated a direct link between a specific signal transduction pathway and am RNA stability modulator, both of which contribute to the regulation of IL6 gene expression at a post-transcriptional level.
La fibrose kystique (FK) est la maladie génétique mortelle la plus fréquente parmi les canadiens d'origine caucasienne. La majorité des personnes atteintes souffrent d'une inflammation chronique causée par la bactérie Pseudomonas aeruginosa (P. aeruginosa). Précédemment, nous avons découvert que des cellules dépourvues de protéine CFTR fonctionnelle présentent un phénotype d'hypersécrétion d'interleukin-6 et d'hyperactivité concomitante de la MAPK p38 en réponse à la bactérie. J'ai donc consacré ma maîtrise à étudier le lien potentiel entre la MAPK p38 et la production élevée d'IL6. La ribonuclease ZC3H12A, spécifique envers IL6, fut découverte comme un nouveau substrat de la MAPK p38. Ces découvertes ont démontré un lien direct entre une voie spécifique de transduction du signal et un modulateur de stabilité de l'ARNm, les deux contribuant à la régulation post-transcriptionnelle de l'expression d'IL6.
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Linseman, Tara. "Functional Analysis of a Coding Variant In ZC3HC1 at 7q32.2 Associated with Protection Against Coronary Artery Disease (CAD)." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34329.

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Coronary artery disease (CAD), characterized by the narrowing of coronary arteries through the complex manifestation and development of atherosclerosis, is a complex disease and one of the leading causes of death worldwide. Both genetic and environmental factors are believed to contribute equally to the risk of CAD. Recently, a study identified a non-synonymous coding variant, rs11556924, (MAF, 0.38) in ZC3HC1 associated with protection against CAD (p= 9.8x10-18; OR= 0.90). NIPA, encoded by ZC3HC1, is a characterized F-Box protein and regulator of cell cycle. Since the amino acid change (Arg363His) is in a conserved region of NIPA and is predicted to have functional effects (Polyphen-2), this study aimed at understanding the functional implications of this amino acid change on NIPA and cell cycle regulation. Here we are able to effectively show a) allele specific differences in mRNA expression in whole blood, b) a slight structural difference between NIPA363Arg and NIPA363His variants, c) proliferation rates of NIPA363Arg expressing cells were significantly increased, and d) phosphorylation of a critical serine residue in close proximity to aa.363 is not statistically different between the two variants. These results suggest that rs11556924 plays a direct role in development of CAD through its disruption of cell cycle regulation and NIPA mRNA availability. This study is the first to identify a molecular basis for the association of rs11556924 to CAD development.
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Books on the topic "Zc3h10"

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Books, La Rontisse. Livre de Caisse: Cahier de Comptabilité des Recettes et des Achats , Carnet de Compte des Recettes et des dépenses★ Conforme Aux Obligations Comptables ★ZC30. Independently Published, 2021.

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Book chapters on the topic "Zc3h10"

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Rha, Jennifer, Stephanie K. Jones, and Anita H. Corbett. "ZC3H14." In Encyclopedia of Signaling Molecules, 6024–30. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101743.

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Rha, Jennifer, Stephanie K. Jones, and Anita H. Corbett. "ZC3H14." In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101743-1.

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Conference papers on the topic "Zc3h10"

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Huang, J., and J. Chao. "ZC3H4-Mediated Macrophage Activation in Silica-Induced Pulmonary Fibrosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2641.

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Kanakkanthara, Arun, Catherine J. Huntoon, Xiaonan Hou, Minzhi Zhang, Ethan P. Heinzen, Ann L. Oberg, John S. Weroha, Scott H. Kaufmann, and Larry M. Karnitz. "Abstract A33: Loss of ZC3H18 disrupts homologous recombination repair and sensitizes ovarian cancer cells to PARP inhibitors and DNA cross-linking agents." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-a33.

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Schmidt, John A., Emily Duffner, Gerard Walker, Keith G. Danielson, and Janice E. Knepper. "Abstract 2555: ZC3H8 associates with PML bodies and influences aggressive tumor cell behavior." 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.am2017-2555.

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Schmidt, John A., Tyler Doan, Emanuel Irizarry, Emily Harris, Keith G. Danielson, and Janice E. Knepper. "Abstract 1713: Molecular dissection of Zc3h8 functional domains and the implications for the oncogenic phenotype." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1713.

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Schmidt, John A., Tyler Doan, Emanuel Irizarry, Emily Harris, Keith G. Danielson, and Janice E. Knepper. "Abstract 1713: Molecular dissection of Zc3h8 functional domains and the implications for the oncogenic phenotype." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1713.

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Schmidt, John A., Keith G. Danielson, Jani L. Swiatek, Emily R. Duffner, and Janice E. Knepper. "Abstract 1134: Association of ZC3H8 with nuclear bodies and its role in promoting tumor cell behaviorin vitroandin vivo." 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.am2016-1134.

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Li, Spencer, John A. Schmidt, and Janice E. Knepper. "Abstract 1757: The effect of Zc3h8 expression levels on sensitivity to DNA damage and repair in mouse mammary cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1757.

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Li, Spencer, John A. Schmidt, and Janice E. Knepper. "Abstract 1757: The effect of Zc3h8 expression levels on sensitivity to DNA damage and repair in mouse mammary cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1757.

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Schmidt, John A., Emily R. Duffner, Emily M. Harris, Tyler Doan, Emanuel Irizarry, Keith G. Danielson, and Janice E. Knepper. "Abstract 2484: Structural analysis of features contributing to the oncogenic phenotype conferred by the zinc finger nuclear body protein Zc3h8." 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.am2018-2484.

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