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Journal articles on the topic "ZNF318"
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Nizhnichenko, Vladimir A., Alexey V. Boyko, Talia T. Ginanova, and Igor Yu Dolmatov. "Muscle Regeneration in Holothurians without the Upregulation of Muscle Genes." International Journal of Molecular Sciences 23, no. 24 (December 16, 2022): 16037. http://dx.doi.org/10.3390/ijms232416037.
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The holothurian Eupentacta fraudatrix is capable of fully restoring its muscles after transverse dissection. Although the regeneration of these structures is well studied at the cellular level, the molecular basis of the process remains poorly understood. To identify genes that may be involved in the regulation of muscle regeneration, the transcriptome of the longitudinal muscle band of E. fraudatrix has been sequenced at different time periods post-injury. An analysis of the map of biological processes and pathways has shown that most genes associated with myogenesis decrease their expression during the regeneration. The only exception is the genes united by the GO term “heart valve development”. This may indicate the antiquity of mechanisms of mesodermal structure transformation, which was co-opted into various morphogeneses in deuterostomes. Two groups of genes that play a key role in the regeneration have been analyzed: transcription factors and matrix metalloproteinases. A total of six transcription factor genes (Ef-HOX5, Ef-ZEB2, Ef-RARB, Ef-RUNX1, Ef-SOX17, and Ef-ZNF318) and seven matrix metalloproteinase genes (Ef-MMP11, Ef-MMP13, Ef-MMP13-1, Ef-MMP16-2, Ef-MMP16-3, Ef-MMP24, and Ef-MMP24-1) showing differential expression during myogenesis have been revealed. The identified genes are assumed to be involved in the muscle regeneration in holothurians.
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Mitchell, Emily, Michael Spencer Chapman, Nicholas Williams, Kevin J. Dawson, Nicole Mende, Emily Calderbank, Hyunchul Jung, et al. "Clonal Dynamics of Normal Haematopoiesis with Human Ageing." Blood 138, Supplement 1 (November 5, 2021): 598. http://dx.doi.org/10.1182/blood-2021-150152.
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Abstract The haematopoietic system manifests several age-associated phenotypes including anaemia; loss of regenerative capacity, especially in the face of insults such as infection, chemotherapy or blood loss; and increased risk of clonal haematopoiesis and blood cancers. The cellular alterations that underpin these age-related phenotypes, which typically manifest in individuals aged over 70, remain elusive. We aimed to investigate whether changes in HSC population structure with age might underlie any aspects of haematopoietic system ageing. We sequenced 3579 genomes from single-cell-derived colonies of haematopoietic stem cell/multipotent progenitors (HSC/MPPs) from 10 haematologically normal subjects aged 0-81 years. HSC/MPPs accumulated 17 somatic mutations/year after birth with no increased rate of mutation accumulation in the elderly. HSC/MPP telomere length declined by 30 bp/yr. In cord blood and adults aged <65, a small proportion of HSC/MPPs had unexpectedly long telomeres, as assessed using several criteria for outliers. The proportion of cells with unexpectedly long telomeres reduced in frequency with age. Given that telomeres shorten at cell division, these outlier cells have presumably undergone fewer historic cell divisions, supporting the existence of a rare population of dormant HSCs in humans that declines in frequency with age. To interrogate changes in HSC population structure with age, we used the pattern of unique and shared mutations between the sampled cells from each individual to reconstruct their phylogenetic relationships. The frequency of branch-points (known as coalescences) in phylogenetic trees in a neutrally evolving, well-mixed population of somatic cells is primarily determined by the product of population size and time between symmetric self-renewal cell divisions (Nt). Smaller populations and more frequent symmetric divisions both increase the density of coalescences. Specific clones can come to dominate either through neutral drift or positive selection. We found that haematopoiesis in adults aged <65 was polyclonal, with high indices of clonal diversity. The number and pattern of coalescent events in the phylogenies showed that a stable population of 20,000 to 200,000 HSC/MPPs was contributing evenly to blood production in young adult life. In contrast, haematopoiesis in individuals aged >75 showed profoundly decreased clonal diversity. In each elderly subject, 30-60% of haematopoiesis was accounted for by 12-18 independent clones, each contributing 1-34% of blood production. Most clones had begun their expansion before age 40, but only 22% had known driver mutations. We used the ratio of non-synonymous to synonymous mutations (dN/dS) to identify any excess of non-synonymous (driver) mutations in the dataset. This genome-wide selection analysis estimated that 1/34 to 1/12 non-synonymous mutations were drivers, occurring at a constant rate throughout life, such that the set of 300 - 400 HSC/MPPs sampled from each adult individual harboured around 100 driver mutations, over 10-fold higher than the number of known drivers we could identify. Novel drivers affected a wider pool of genes than identified in blood cancers. The genes DNMT3A, ZNF318 and HIST2H3D were identified as being under significant positive selection in HSC/MPPs, despite ZNF318 and HIST2H3D not being enriched in the setting of myeloid malignancies. Loss of Y chromosome conferred selective benefits on HSC/MPPs in males. Simulations from a simple model of haematopoiesis, with constant HSC population size and constant acquisition of driver mutations conferring moderate fitness benefits, entirely explained the abrupt change in clonal structure observed in the elderly, which could not be explained by neutral models incorporating drift alone. Our data supports the view that dramatically decreased clonal diversity is a universal feature of haematopoiesis in aged humans, underpinned by pervasive positive selection acting on many more genes than currently known. By old age the majority of HSCs harbour at least one driver mutation. With such ubiquity of driver mutations, selected purely for their competitive advantage within the stem cell compartment, and with the wholesale rewiring of cellular pathways they induce, it is feasible that they may contribute to age-related phenotypes beyond the increased risk of blood cancer. Disclosures Spencer: Wugen, Inc.: Consultancy, Other: Stock Options. Vassiliou: Kymab Ltd: Divested equity in a private or publicly-traded company in the past 24 months; STRM.BIO: Consultancy; Astrazeneca: Consultancy. Kent: STRM.bio: Research Funding. Campbell: Mu Genomics: Current holder of individual stocks in a privately-held company, Membership on an entity's Board of Directors or advisory committees.
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Sobocińska, Joanna, Joanna Nowakowska, Sara Molenda, Anna Olechnowicz, Kacper Guglas, Joanna Kozłowska-Masłoń, Urszula Kazimierczak, et al. "Zinc Finger Proteins in Head and Neck Squamous Cell Carcinomas: ZNF540 May Serve as a Biomarker." Current Oncology 29, no. 12 (December 16, 2022): 9896–915. http://dx.doi.org/10.3390/curroncol29120779.
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Head and neck squamous cell carcinoma (HNSCC) is one of the ten most common cancers. Most cancer cases originate from alcohol and tobacco consumption. However, studies have demonstrated that human papillomavirus (HPV) infection, particularly HPV-16, may also significantly influence disease progression. The KRAB-ZNF family of genes is involved in epigenetic suppression, and its involvement in carcinogenesis is the subject of extensive studies. The available literature data demonstrate that they may play different roles, both as tumor suppressors and oncogenes. In this study, six ZNF genes, ZFP28, ZNF132, ZNF418, ZNF426, ZNF540, and ZNF880, were tested using several in silico approaches based on the TCGA and GEO datasets. Our analyses indicate that the expression of the analyzed ZNFs was significantly downregulated in tumor tissues and depended on tumor localization. The expression levels of ZNFs differed between HPV-positive vs. HPV-negative patients depending on the clinical-pathological parameters. More specifically, the patients with higher levels of ZNF418 and ZNF540 showed better survival rates than those with a lower expression. In addition, the level of ZNF540 expression in HPV-positive (HPV(+)) patients was higher than in HPV-negative (HPV(−)) patients (p < 0.0001) and was associated with better overall survival (OS). In conclusion, we demonstrate that ZNF540 expression highly correlates with HPV infection, which renders ZNF540 a potential biomarker for HNSCC prognosis and treatment.
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Dougherty, Michael P., Lynn P. Chorich, and Lawrence Clarke Layman. "Evaluation of Mayer-Rokitansky-Kuster-Hauser (MRKH) Patient Families by Whole Genome Sequencing." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A501—A502. http://dx.doi.org/10.1210/jendso/bvab048.1025.
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Abstract Introduction: MRKH is a characterized by the congenital absence of the uterus and vagina in 46,XX individuals. A subset of these patients also has associated renal, skeletal, cardiac and/or auditory defects. Familial cases suggest a genetic component, but to date only pathogenic variants in WNT4 and HNF1B have been confirmed. We hypothesize that de novo heterozygous variants in candidate genes will be present in some patients with MRKH. Methods: DNAs from 30 quads (an MRKH proband and three relatives) were subjected to whole genome sequencing (WGS), and heterozygous variants in coding regions with < 0.02 frequency were filtered by two different methods. In the first approach, variants were filtered by 1) top consequence variant (splice site, stop-gain, frameshift, and missense, respectively); 2) impact score; 3) mapping quality; 4) cytobands; 5) intolerance; 6) de novo variants; and 7) plausibility based on familial genotype. The second approach considered only heterozygous variants found in the proband and absent in all other family members, which were then filtered by top consequence (splice donor and acceptor sites, stop-gain, frameshift). Results: Five pedigrees were excluded for inadequate sequence in one or more individuals. 55,033 variants in coding regions with < 2% frequency were identified in the 25 remaining quads for analysis. Using the first approach, 42 candidate gene variants in 32 genes were identified - 12 splice variants, 10 stop-gains, 15 frameshift variants and 5 missense variants. Of these, MUC22 contained 2 missense variants from different families. Additionally, DICER1 had multiple splice variants and is essential for mouse urogenital tract development. In the second approach, 39 candidate genes were identified—6 splice variants in 6 genes, 18 stop-gains in 17 genes, and 17 frameshift variants in 16 genes. Zinc finger genes (ZNF418, ZNF646, ZNF135, and ZNF772) comprised the most frequent class of the 39 genes. Two genes (MIR4436A and ZNF418) contained attractive variants in two different families. Conclusion: WGS has been shown to improve detection of gene variants in coding regions, more so than whole exome sequencing (WES). We previously performed WES on 111 MRKH probands without family members and analyzed variants in candidate genes suggested by mouse and preliminary human studies. Interestingly, in this study, only three genes overlapped with previously suspected candidate genes. Here, we identified new candidates based upon potential deleteriousness. These candidate genes will be studied further in our families to determine their role in Mullerian development.
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Ishikawa, S., M. Kai, Y. Takei, K. Okui, T. Takahashi, M. Suzuki, M. Ogawa, and Y. Nakamura. "Isolation and mapping of a human zinc finger gene (ZNF188) homologous to ZNF187, a serum-response-element binding protein." Cytogenetic and Genome Research 77, no. 3-4 (1997): 185–89. http://dx.doi.org/10.1159/000134572.
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Yan, Feng-Juan, Yong-Jian Wang, Shi-Ran Yan, Jun Lu, and Yuan-Lin Zheng. "ZNF300 stimulates fatty acid oxidation and alleviates hepatosteatosis through regulating PPARα." Biochemical Journal 476, no. 2 (January 31, 2019): 385–404. http://dx.doi.org/10.1042/bcj20180517.
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Abstract ZNF300 plays an important role in the regulation of HBV-related hepatocellular carcinoma. However, little is known about the role of ZNF300 in lipid metabolism and NAFLD. In the present study, we observed that ZNF300 expression was markedly decreased in free fatty acid (FFA)-induced fatty liver. Overexpressed ZNF300 alleviated hepatic lipid accumulation, whereas knockdown of ZNF300 enhanced the FFA-induced lipid accumulation. Investigations of the underlying mechanisms revealed that ZNF300 directly binds to and regulates the PPARα expression, thus promoting fatty acid oxidation. Furthermore, bisulfite pyrosequencing PCR (BSP) analysis identified the hypermethylation status of ZNF300 gene in FFA-treated hepatocytes. Importantly, the suppression of ZNF300 could be blocked by DNA methyltransferase inhibitor (5-azadC) or DNMT3a-siRNA. These results suggested that ZNF300 plays an important role in hepatic lipid metabolism via PPARα promoting fatty acid oxidation and this effect might be blocked by DNMT3a-mediated methylation of ZNF300. Therefore, in addition to ZNF300 expression levels, the methylation status of this gene also has a potential as a prognostic biomarker.
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Pieraccioli, Marco, Sara Nicolai, Consuelo Pitolli, Massimiliano Agostini, Alexey Antonov, Michal Malewicz, Richard A. Knight, Giuseppe Raschellà, and Gerry Melino. "ZNF281 inhibits neuronal differentiation and is a prognostic marker for neuroblastoma." Proceedings of the National Academy of Sciences 115, no. 28 (June 25, 2018): 7356–61. http://dx.doi.org/10.1073/pnas.1801435115.
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Derangement of cellular differentiation because of mutation or inappropriate expression of specific genes is a common feature in tumors. Here, we show that the expression of ZNF281, a zinc finger factor involved in several cellular processes, decreases during terminal differentiation of murine cortical neurons and in retinoic acid-induced differentiation of neuroblastoma (NB) cells. The ectopic expression of ZNF281 inhibits the neuronal differentiation of murine cortical neurons and NB cells, whereas its silencing causes the opposite effect. Furthermore, TAp73 inhibits the expression of ZNF281 through miR34a. Conversely, MYCN promotes the expression of ZNF281 at least in part by inhibiting miR34a. These findings imply a functional network that includes p73, MYCN, and ZNF281 in NB cells, where ZNF281 acts by negatively affecting neuronal differentiation. Array analysis of NB cells silenced for ZNF281 expression identified GDNF and NRP2 as two transcriptional targets inhibited by ZNF281. Binding of ZNF281 to the promoters of these genes suggests a direct mechanism of repression. Bioinformatic analysis of NB datasets indicates that ZNF281 expression is higher in aggressive, undifferentiated stage 4 than in localized stage 1 tumors supporting a central role of ZNF281 in affecting the differentiation of NB. Furthermore, patients with NB with high expression of ZNF281 have a poor clinical outcome compared with low-expressors. These observations suggest that ZNF281 is a controller of neuronal differentiation that should be evaluated as a prognostic marker in NB.
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Deng, Yu-Qin, Gang-Yong Kong, Song Li, Fen Li, and Si-Lu Wen. "Upregulation of lnc-ZNF281 Inhibits the Progression of Glioma via the AKT/GSK-3β/β-Catenin Signaling Pathway." Journal of Immunology Research 2021 (May 11, 2021): 1–9. http://dx.doi.org/10.1155/2021/5573071.
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The purpose of this study is to elucidate the roles and potential underlying mechanisms of long noncoding RNA lnc-ZNF281 in glioma. We performed qRT-PCR to detect the expression levels of lnc-ZNF281 in glioma tissues. The effects of lnc-ZNF281 on the proliferative and migrative abilities of T98G and HS683 glioma cells were examined by cell proliferation assay, colony formation assay, wound-healing assay, and transwell assay. Also, the effects of lnc-ZNF281 on AKT/GSK-3β/β-catenin pathway were analyzed. The results showed that the expression of lnc-ZNF281 in glioma tissues was decreased compared with normal tissues. lnc-ZNF281 overexpression inhibited the proliferative and migrative abilities of glioma cells, while lnc-ZNF281 knockdown obtained the opposite findings. Besides, overexpression of lnc-ZNF281 in glioma cells inactivated the AKT/GSK-3β/β-catenin signaling pathway. Furthermore, β-catenin activation reversed the suppressive effects of lnc-ZNF281 on glioma cells. Taken together, lnc-ZNF281 inhibits glioma cell proliferation and migration via AKT/GSK-3β/β-catenin pathway and may serve as a potential target for glioma treatment.
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Fahmé, Pia, Farah Ramadan, Diep Tien Le, Kieu-Oanh Nguyen Thi, Sandra E. Ghayad, Nader Hussein, Chantal Diaz, Martine Croset, Philippe Clézardin, and Pascale A. Cohen. "The Intricate Interplay between the ZNF217 Oncogene and Epigenetic Processes Shapes Tumor Progression." Cancers 14, no. 24 (December 8, 2022): 6043. http://dx.doi.org/10.3390/cancers14246043.
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The oncogenic transcription factor ZNF217 orchestrates several molecular signaling networks to reprogram integrated circuits governing hallmark capabilities within cancer cells. High levels of ZNF217 expression provide advantages to a specific subset of cancer cells to reprogram tumor progression, drug resistance and cancer cell plasticity. ZNF217 expression level, thus, provides a powerful biomarker of poor prognosis and a predictive biomarker for anticancer therapies. Cancer epigenetic mechanisms are well known to support the acquisition of hallmark characteristics during oncogenesis. However, the complex interactions between ZNF217 and epigenetic processes have been poorly appreciated. Deregulated DNA methylation status at ZNF217 locus or an intricate cross-talk between ZNF217 and noncoding RNA networks could explain aberrant ZNF217 expression levels in a cancer cell context. On the other hand, the ZNF217 protein controls gene expression signatures and molecular signaling for tumor progression by tuning DNA methylation status at key promoters by interfering with noncoding RNAs or by refining the epitranscriptome. Altogether, this review focuses on the recent advances in the understanding of ZNF217 collaboration with epigenetics processes to orchestrate oncogenesis. We also discuss the exciting burgeoning translational medicine and candidate therapeutic strategies emerging from those recent findings connecting ZNF217 to epigenetic deregulation in cancer.
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Kubanov, A. A., A. A. Kubanova, A. E. Karamova, and A. A. Mineyeva. "Prevalence of genetic risk factors of psoriasis among the population of the Russian Federation." Vestnik dermatologii i venerologii 90, no. 6 (December 24, 2014): 69–76. http://dx.doi.org/10.25208/0042-4609-2014-90-6-69-76.
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Goal. To assess the prevalence of polymorphisms of genes of the predisposition to psoriasis among the population of the Russian Federation. Materials and methods. The authors examined 546 psoriasis patients and 206 healthy people. The polymorphism of the following genes was assessed: genes encoding proteins of the signaling pathway of the nuclear transcription factor kappa-B - NF-κΒ (NFKBI, TRAF3IP2, TNFAIP3, REL, TYK2, TNIP1, IL-28RA) responsible for congenital immunity; genes participating in the IL-23 signaling pathway responsible for adaptive immunity (IL-23R, IL-12B); genes participating in the presentation of the antigen (ERAP1); genes responsible for skin barrier dysfunction (SERPINB8 ZNF313, ZNF816A). Peripheral blood leucocytes served as the DNA source. Polymorphisms of IL-23R, IL-28RA, SERPINB8, TRAF3IP2, TNFAIP3, REL, ZNF313, IL-12B, TNIP1, ZNF816A, ERAP1 genes were determined by the real-time PCR method; polymorphisms of NFKBI, TYK2 genes were determined by the RFLP assay (Restriction Fragment Length Polymorphism). Results. In psoriasis patients in the Russian Federation, statistically significant differences in the distribution of allele frequencies were determined for IL-23R-G/G, IL-23R-A/A, TRAF3IP2-A/A, TRAF3IP2-G/G, TNFAIP3-A/C, TNFAIP3-A/A, ZNF313-C/C, TYK2-T/T, TYK2-T/G, TNIP1-G/G, TNIP1-A/G, REL-A/A, ERAP1-G/G genotypes.
Dissertations / Theses on the topic "ZNF318"
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Ke, Qi. "Negative Regulation of Host Innate Immune Signaling and Response Pathways by Viral and Host Regulatory Factors." University of Toledo / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1470185159.
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Strachan, Joanna. "Expression and interactions of the ubiquitin receptor ZNF216." Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12707/.
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Muscle atrophy is a feature of many chronic diseases and contributes to both morbidity and mortality, emphasising the importance of understanding the molecular pathways involved. Zinc finger protein 216 (ZNF216) is an atrogene, a gene which is up-regulated during and directly mediates skeletal muscle atrophy, and encodes the ubiquitin (Ub) receptor protein ZNF216. Herein it is demonstrated that ZNF216 mRNA levels increase in the extensor digitorum longus (EDL) in a lipopolysaccharide (LPS)-infusion rat model of muscle atrophy, relative to saline control. However, combined administration of low level dexamethasone (Dex) with LPS, although sparing muscles from atrophy, did not blunt ZNF216 expression which parallels previous observations for the atrogenes muscle atrophy F-box protein (MAFbx) and muscle RING-finger 1 (MuRF1). ZNF216 expression levels were further elevated in biceps femoris muscle in rats dosed with the statin drug simvastatin (in which severe muscle damage and atrophy occurs), relative to control rats. The ZNF216 protein’s Ub-binding ability and its reported association with the 26S proteasome indicates it may shuttle proteins targeted for degradation to the proteasome as part of the atrophy programme. We utilised immobilised recombinant ZNF216 protein and its Ub-binding Znf_A20 domain alone to capture Ub-modified proteins from rat skeletal muscle that may represent ZNF216’s substrates. Bound proteins specifically eluted by deubiquitination were identified via liquid chromatography tandem mass spectrometry (LC-MS/MS) and included adenylate kinase 1 (AK1) and actin, both previously proposed as substrates of MuRF1. However, ion scores for all candidates were below the accepted threshold of significance and immunoblotting failed to validate LC-MS/MS data. This approach also revealed an increase in a low molecular weight Ub-positive protein from EDL muscle after 24hrs of LPS infusion. Retrospective analysis revealed this Ub-positive protein was consistently captured in other experiments and confirmed by protein MS and immunoblotting to represent an unmodified and unanchored (i.e. not attached to a substrate) K48-linked Ub dimer. Subsequent capture of the Ub dimer using the Znf_UBP domain of isopeptidase T (isoT), a Ub-binding domain selective for the free C-terminus of Ub, confirmed the dimer was unanchored and also revealed a ladder of longer endogenous unanchored poly-Ub chains. Optimised affinity capture conditions has afforded the first opportunity to purify longer free poly-Ub chains and perform the initial molecular analyses of endogenous unanchored poly-Ub purified from in vivo sources.
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Hahn, Stefanie. "Characterization of ZNF281 and its role in colorectal carcinogenesis." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-177446.
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The vast majority of colorectal cancer (CRC)-related deaths is caused by the metastatic spread of tumor cells to distant organs rather than by the growth of the primary tumor. However, until today the mechanisms involved in CRC metastasis are not completely understood. For cancer cells the epithelial-mesenchymal transition (EMT) is thought to represent a prerequisite to invade adjacent tissue and form metastases at distant sites. Transcription factors, cytokines or oncogenic signaling pathways play an important role in the regulation of the EMT program. Recently, the oncoprotein c-MYC was shown to induce EMT, e.g. by enhancing SNAIL expression. Previously an interaction between c-MYC and the transcription factor ZNF281/ZBP-99 has been described. However, so far it remained elusive which upstream signals regulate ZNF281 levels or activity and furthermore, what functions are mediated by ZNF281, which may contribute to the c-MYC-mediated tumor progression. Here, it could be shown that SNAIL and miR-34a/b/c control the expression of ZNF281 in a coherent feed-forward-loop: the EMT-transcription factor SNAIL directly induced ZNF281 transcription and repressed miR-34a/b/c, thereby alleviating ZNF281 from direct down-regulation by miR-34. Moreover, p53 activation led to a miR-34a-dependent down-regulation of ZNF281 expression. Additionally, in CRC cells it could be demonstrated, that ectopic ZNF281 expression induces EMT. This process was mediated by and dependent on the direct induction of SNAIL. Furthermore, ectopic ZNF281 increased migration/invasion, and enhanced β-catenin activity. Expression of the stemness markers LGR5 was directly and CD133 indirectly induced by ectopic ZNF281 expression, which also increased sphere formation. Conversely, in CRC cells the experimental down-regulation of ZNF281 resulted in a mesenchymal-epithelial transition (MET), inhibited migration/invasion and decreased sphere formation. Additionally, repression of ZNF281 led to decreased formation of lung metastases by CRC cells in a xenograft mouse tumor model. Furthermore, ZNF281 protein expression was indirectly elevated by ectopic c-MYC expression. Inactivation of ZNF281 prevented the induction of EMT by c-MYC or SNAIL. The analysis of tumor samples revealed that ZNF281 expression increases during CRC progression and correlates with tumor recurrence.
Taken together, the results identify ZNF281 as a new EMT-promoting transcription factor, which contributes to metastasis formation in CRC. In the future, this knowledge may be exploited for therapeutic and diagnostic purposes in cancer therapy.
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Nguyen, Thanh Nhan. "Deeper insights into the deleterious roles of ZNF217 in tumorigenesis and the identification of a novel and functional interplay between ZNF217 and ERalpha in breast cancer." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10331.
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ZNF217 est un oncogène potentiel codant pour un facteur de transcription Krüppel-like. Cette étude vise à explorer le rôle délétère et la valeur pronostique de ZNF217 dans le cancer du sein. Nos résultats ont montré que : (i) des niveaux d'expression élevés de ZNF217 (tant au niveau de l'ARNm qu'au niveau protéique) sont associés à un mauvais pronostic chez les patientes atteintes d'un cancer du sein, et plus particulièrement dans les cancers du sein de type ER+/Luminaux/Luminaux A ; (ii) ZNF217 induit la transition épithélio mésenchymateuse (EMT) dans les cellules épithéliales mammaires humaines via la voie de signalisation du TGF-beta ; (iii) ZNF217 induit un phénotype agressif dans les cellules cancéreuses mammaires se traduisant in vitro par la stimulation de la croissance indépendante de l'ancrage, de la migration et de l'invasion cellulaire ; (iv) ZNF217 stimule la croissance tumorale et le développement spontané de métastases chez la souris ; (v) ZNF217 se lie à ERalpha et augmente l'activité transcriptionnelle ligand-dépendante de ce dernier en favorisant le recrutement d'ERalpha sur les éléments de réponse aux oestrogènes (EREs) ; (vi) ZNF217 stimule la formation de mammosphères dans des lignées cellulaires de cancer du sein ER– ou ER+ ; (vii) ZNF217 induit la résistance à l'hormonothérapie (tamoxifène) dans des cellules cancéreuses mammaires ER+ ; (viii) des niveaux élevés d'expression de ZNF217 sont associés à un mauvais pronostic en terme de survie sans récidive chez les patientes atteintes d'un cancer du sein et traitées par hormonothérapie uniquement. Nos résultats suggèrent que l'expression de ZNF217 représente un nouveau et puissant biomarqueur pronostique dans le cancer du sein ER+/Luminal/Luminal A, permettant la re-stratification de ces cancers du sein dits « de bon pronostic », pour lesquels il n'existe pas à l'heure actuelle de biomarqueurs permettant de les identifier. En conclusion, ZNF217 représente une nouvelle cible thérapeutique pour le traitement personnalisé des patientes atteintes d'un cancer du sein et exprimant de forts niveaux d'expression de ZNF217, en particulier les patientes ER+/ZNF217+ZNF217 is a candidate oncogene encoding for a Krüppel-like transcription factor. This study aims at exploring deeper insights on deleterious roles of ZNF217 and the prognostic significance of ZNF217 expression in breast cancers. We found that: (i) high levels of ZNF217 expression (at both mRNA and protein levels) are associated with poor prognosis in breast cancer patients, more particularly in ER+/Luminal/Luminal A breast cancers; (ii) ZNF217 induces epithelial-mesenchymal transition (EMT) in human mammary epithelial cells via the TGF-beta-activated Smad signaling pathway; (iii) in vitro ZNF217 stimulates several aggressive phenotypes in breast cancer cells, including anchorage-independent growth, cell migration and invasion; (iv) ZNF217 stimulates tumor growth and promotes the development of metastases in vivo; (v) ZNF217 binds with ERalpha and enhances 17beta- estradiol (E2)-induced ERalpha transactivation by increasing the recruitment of ERalpha to estrogen-responsive elements (EREs); (vi) ZNF217 increases mammosphere formation in ER– or ER+ breast cancer cell lines; (vii) ZNF217 confers resistance to endocrine therapy (tamoxifen) in ER+ breast cancer cells, and (viii) high levels of ZNF217 expression are associated with shorter relapse-free survival (RFS) in breast cancer patients treated with endocrine therapy only. Our findings suggest that ZNF217 expression represents a novel and powerful prognostic biomarker in ER+/Luminal/Luminal A breast cancers, allowing the re-stratification of these “good prognosis” breast cancers, which are currently not further classified by any other biomarkers available. In conclusion, ZNF217 could be a potential therapeutic target for a personalized treatment strategy in patients overexpressing ZNF217, in particular in ER+/ZNF217+ patients
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Mallin, Lucy Janet. "Understanding the relationship between IRF-1 and the transcriptional repressor ZNF350." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15893.
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Interferon regulatory factor-1 (IRF-1) is a transcription factor and tumour suppressor, involved in many diverse cellular processes including immune responses and growth regulation. An interesting feature of IRF-1 is that it can both activate and repress gene expression, possibly by acting with co-activator or co-repressor proteins. In a previous phage display assay, a homologous peptide to the known repressor protein, zinc finger 350 (ZNF350), was found to bind to the C-terminus of IRF-1. ZNF350, also known as ZBRK1 (Zinc finger and BRCA1-interacting protein with KRAB domain-1), is a member of the Krüppel-associated box (KRAB)-containing zinc finger (KZF) proteins, which is a group of the widely distributed transcriptional repression proteins in mammals. ZNF350 has previously been shown to repress the expression of a number of genes including ANG1 and GADD45A, often in complex with other proteins. This study confirms the direct interaction between IRF-1 and ZNF350 and identifies key residues, including the LXXLL repression motif within the C-terminus of IRF-1, necessary for the binding interface. The two proteins have additionally been shown to interact within a cellular environment, shown by using techniques including immunoprecipitation and a proximity ligation assay. In addition, the ZNF350/IRF-1 complex formation appears to occur in the basal state of the cell, as opposed to in response to cellular stress such as viral infection or DNA damage. On the basis of ZNF350 being a negative regulator of transcription, a novel technique was developed to identify putative targets of both ZNF350 and IRF-1. This involved an initial bioinformatics screen using candidate IRF-1 binding site data obtained from CENTIPEDE, an algorithm that combines genome sequence information, with cell-specific experimental data to map bound TF binding sites. This allowed for the identification of novel target genes that contained the ZNF350 consensus binding site, GGGxxCAGxxxTTT, within close proximity to an IRF-1 consensus site, such as the immune response gene IL-12A. Lastly, a peptide phage display screen was combined with high-throughput sequencing to identify other potential binding partners of ZNF350 and perhaps help to understand the mechanism by which transcriptional repression is controlled by complex formation.
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Bellanger, Aurélie. "ZNF217, un rôle majeur dans le cancer du sein : un nouvel instigateur du développement de métastases ostéolytiques : isoforme ZNF217-ΔE4 : implication en cancérogénèse mammaire et valeur pronostique." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1007.
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ZNF217 est un oncogène codant pour un facteur de transcription de la famille Krüppel-like. Nos objectifs sont d'explorer le rôle de l'oncogène ZNF217 dans le développement de métastases du cancer du sein à tropisme osseux et la valeur pronostique ainsi que les fonctions d'une nouvelle isoforme de ZNF217. Nous avons identifié que de forts niveaux d'expression de l'ARNm de ZNF217 dans les tumeurs primitives du sein pourrait être un indicateur d'un développement ultérieur de métastases osseuses. Nous avons montré que ZNF217 est un nouvel activateur de la voie BMP et que l'inhibition de cette voie permet de reverser les propriétés métastatiques des cellules ZNF217 positives in vitro (migration, invasion et chimiotactisme vers des cellules osseuses). In vivo chez la souris, les cellules ZNF217-positives de cancer du sein développent très rapidement des métastases ostéolytiques. Dans notre deuxième axe de travail, nous avons prouvé l'existence de l'isoforme ZNF217-?E4 et montré qu'elle possède une valeur de mauvais pronostic dans le cancer du sein ER-a+. Les cellules surexprimant ZNF217-?E4 développent un phénotype encore plus agressif que les cellules possédant la forme WT (prolifération, résistance au paclitaxel), et de manière intéressante, ZNF217-?E4 semble jouer un rôle de régulateur de l'expression de ZNF217-WT. En conclusion, ZNF217 et/ou la voie BMP pourraient représenter des cibles thérapeutiques dans le traitement des cancers du sein ZNF217-positifZNF217 is an oncogene encoding for a Krüppel-like transcription factor. Our aims were to explore the roles of the ZNF217 oncogene in the development of breast cancer metastases to the bone and to decipher the prognostic value and the functions of a new ZNF217 isoform. Our work identified that high ZNF217 mRNA expression levels within the primitive breast tumor could represent an indicator for future recurrence to the bone. Further in vitro experiment demonstrated that ZNF217 is a new activator of the BMP pathway and that the inhibition of this pathway could inhibit the metastatic properties of ZNF217-positive breast cancer cells in vitro (migration, invasion, chemotaxis to bone cells). In vivo in mice, ZNF217-positive breast cancer cells developed osteolytic metastases very faster. In our second axis, we have proven the existence of the ZNF217-?E4 isoform and we found that this isoform possesses a prognostic significance associated with a poor prognosis in ER-a+ breast cancer. Furthermore, cells overexpressing ZNF217-?E4 developed a more aggressive phenotype than cells overexpressing ZNF217-WT (proliferation, paclitaxel resistance). Interestingly, ZNF217-?E4 seems to play a regulatory role regarding ZNF217-WT expression. In conclusion, ZNF217 and/or the BMP pathway could represent potential therapeutical targets in the management of ZNF217 positive breast cancer
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PIERACCIOLI, MARCO. "Functional role of the zinc finger factor ZNF281 in DNA damage response." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2015. http://hdl.handle.net/2108/203092.
Full textAbstract:
La sopravvivenza degli organismi dipende dall'accurata trasmissione dell'informazione genetica durante i processi che portano alla divisione cellulare. Questa fedele trasmissione richiede non soloun'elevata precisione nella replicazione del DNA e nella perfetta segregazione cromosomica, ma anche la capacità di sopravvivere ai danni al DNA spontanei o indotti minimizzando il numero di mutazioni ereditabili dalle cellule figlie. Le cellule sono constantemente soggette agli effetti citotossici e mutageni degli agenti in grado di causare danno al DNA. Per rispondere e difendersi da questa minaccia, le cellule eucariotiche hanno evoluto dei processi che sono collettivamente catalogati come risposta al danno al DNA (DDR). La DDR è una complessa via di trasduzione del segnale che ha la capacità di riconoscere la presenza di danni al DNA e trasdurre questa informazione nella cellula al fine di attivare i processi di riparo. Infatti, le cellule possiedono diversi enzimi capaci di rimodellare e riparare il DNA, comunque la loro attività deve essere spazialmente e temporalmente regolata per ottimizzare il riparo del DNA e prevenire potenziali e deleterie alterazioni nella struttura del DNA. In questi ultimi anni considerevoli progressi sono stati fatti per delucidare le componenti e i processi che caratterizzano la DDR eucariotica. Nonostante questo, un punto centrale in questo campo di studio rimane l'identificazione dei geni e delle proteine che controllano l'espressione delle proteine coinvolte nella DDR. Di interesse è la recente scoperta di un numero crescente di fattori di trascrizione che in grado di regolare direttamente la riparazione del DNA e che fanno parte come componenti integrali del macchinario di riparo stesso con meccanismi indipendenti dalla loro abilità di promuovere e/o reprimere la trascrizione. Infatti, gli agenti di danno al DNA (radiazioni, chemioterapia, agenti genotossici) sono in grado di promuovere la traslocazione di alcuni fattori di trascrizione direttamente sulle lesioni al DNA, dove partecipano all'attivazione del riparo al DNA. ZNF281 è un fattore di trascrizione appartenente alla tipologia degli "zinc finger" coinvolto nel mantenimento della staminalità cellulare e nei processi di transizione epiteliale-mesenchimale (EMT). In questo studio vengono analizzati i ruoli di ZNF281 durante la DDR. Infatti, riportiamo che l'espressione di ZNF281 aumenta sia a livello di mRNA, che di proteina dopo stress genotossico indotto da agenti chimici che causano danno al DNA (etoposide, doxorubicina, camptotecina) in diversi sistemi quali le cellule tumorali, cellule di cheratinociti primari e nell’epidermide del Mus musculus. Il comet assay dimostra che il riparo al DNA è ritardato nelle cellule silenziate per l'espressione di ZNF281 e trattate con etoposide. Inoltre, l'analisi con RT profiler array ha dimostrato che l'espressione di dieci geni coinvolti nella risposta al danno al DNA è diminuita nelle cellule trattate con etoposide e silenziate per l'espressione di ZNF281. In linea con questa scoperta, XRCC2 e XRCC2, due geni che prendono parte rispettivamente ai processi di ricombinazione omologa (HR) e Non Homologous End Joining (NHEJ), sono trascrizionalmente attivati da ZNF281 attraverso un meccanismo dipendente dal legame al DNA come dimostrato da esperimenti di saggio della luciferasi e di immunoprecipitazione della cromatina (ChIP). Inoltre, ZNF281 è un co-fattore della proteina c-Myc per l'attivazione dell'espressione della nucleolina e della ciclina B1; mentre c-Myc, anche se in grado di legare promotori di XRCC2 e XRCC4, non è capace di promuovere la trascrizione o di modificare l'attività di ZNF281 sui promotori di questi due geni. L'analisi bioinformatica di una coorte di 1971 pazienti affetti da cancro alla mammella rivela una correlazione statisticamente significativa tra l'espressione di ZNF281 e di XRCC2. Inoltre l'analisi proteomica e il proximity ligation assay (PLA) dimostrano che ZNF281 interagisce con DNA-PK, un'importante proteina del processo di DDR, suggerendo per ZNF281, un ruolo indipendente dalla trascrizione. In sintesi, i risultati discussi in questo lavoro, evidenziano per la prima volta il coinvolgimento di ZNF281 nella risposta cellulare a stress genotossici attraverso un controllo esercitato sull'espressione di geni che agiscono in differenti meccanismi di riparo al danno e attraverso la sua interazione con DNA-PK.The survival of organisms depends on the accurate transmission of genetic information from one cell to its daughters. Such faithful transmission requires not only extreme accuracy in replication of DNA and precision in chromosome distribution, but also the ability to survive spontaneous and induced DNA damage while minimizing the number of heritable mutations. Therefore, cells are constantly under threat from the cytotoxic and mutagenic effects of DNA damaging agents. To respond to these threats, eukaryotes have evolved the DNA damage response (DDR). The DDR is a complex array of different mechanisms that have the ability to sense DNA damage and transduce this information to the cell in order to modulate cellular responses to DNA damage. Cells possess several enzymatic tools capable of remodeling and repairing DNA; however, their activities must be tightly regulated in a temporal, spatial, and DNA lesion-appropriate fashion to optimize repair and prevent unnecessary and potentially deleterious alterations in the structure of DNA during normal cellular processes. During the past several years, considerable progress has been made in elucidating the components and the processes of the eukaryotic DDR. A central issue in this field, which remains to be understood in greater detail, is the identification of the controllers of the expression of DDR proteins. Interestingly, in recent years an increasing number of studies have revealed that several TFs regulate DNA repair directly and can function as integral components of the repair machinery itself in a transcription independent fashion. In fact, DNA damage-inducing insults (irradiation, chemotherapy drugs) promote translocation of some TFs directly to DNA lesions, where they actively facilitate DNA repair. ZNF281 is a zinc finger transcription factor involved in the control of cellular stemness and Epithelial Mesenchymal Transition (EMT). In this study we analyze the roles of ZNF281 during DDR. We report that ZNF281 expression increased after genotoxic stress caused by DNA damaging drugs (Etoposide, Doxorubicin, Camptothecin) in cancer cell lines, normal keratinocytes and in mouse skin in vivo. Comet assays demonstrated that DNA repair was delayed in cells silenced for the expression of ZNF281 and treated with Etoposide. Furthermore, RT profiler array analysis demonstrated that the expression of ten DDR genes was down-regulated in cells treated with Etoposide and silenced for ZNF281. In line with these findings, XRCC2 and XRCC4, two genes that take part in Homologous Recombination (HR) and Non Homologous End Joining (NHEJ) respectively, were transcriptionally activated by ZNF281 through a DNA binding-dependent mechanism as demonstrated by luciferase assays and Chromatin crosslinking ImmunoPrecipitation (ChIP) experiments. In addition, ZNF281 works as a c-Myc co-factor to stimulate the expression of nucleolin and cyclin B1; instead c-Myc, which also binds to the promoters of XRCC2 and XRCC4, was unable to promote their transcription or to modify ZNF281 activity. Bioinformatic analysis of 1971 breast cancer patients disclosed a significant correlation between the expression of ZNF281 and XRCC2. Moreover proteomic analysis and Proximity Ligation Assay (PLA) demonstrated that ZNF281 interacts with DNA-PK, an important protein of DDR, suggesting a transcription-independent role of ZNF281 in DDR. Our data highlight, for the first time, the involvement of ZNF281 in the cellular response to genotoxic stress through the control exercised on the expression of genes that act in different repair mechanisms and through interaction with with corecomponents of DNA repair pathways.
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Ogo, Ogo Agbor. "Cellular responses to zinc involving the transcription factor ZNF658 and its target genes." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2752.
Full textAbstract:
Zinc is an essential trace element that plays a crucial role in catalytic, structural and regulatory functions of many proteins including enzymes and transcription factors; thus maintenance of zinc balance is critical for normal cellular function. Cellular mechanisms that maintain zinc balance include the regulation of genes coding for proteins that play vital roles in zinc homeostasis. These proteins include zinc transporters belonging to the ZIP (SLC39A) and ZnT (SLC30A) families as well as the zinc-binding metallothionein proteins. In contrast to bacterial and yeast systems, a transcription factor responsible for mediating transcriptional repression of a suite of genes in response to elevated zinc levels in mammals has hitherto not been identified. Using Caco-2 cells as a model of human intestinal epithelial cells and detection of protein binding by electrophoretic mobility shift analysis, we show that zinc finger protein ZNF658 binds specifically to the zinc transcriptional regulatory element (ZTRE), previously demonstrated to mediate this response in a panel of three genes: SLC30A5 (ZnT5 zinc transporter), SLC30A10 (ZnT10 zinc transporter) and CBWD (whose prokaryotic homologs are emerging players in metal biology). We also demonstrate that siRNA-driven reduction of ZNF658 attenuated or abrogated transcriptional repression in response to elevated zinc levels of these same genes by measuring transcript abundance using RT-qPCR and using promoter-reporter gene constructs. In addition, the region of ZNF658 responsible for binding to the ZTRE was identified (the C-terminal zinc finger domain) and the requirement for both sides of the palindromic ZTRE sequence for function was demonstrated. This study therefore identifies the first metazoan transcription factor that plays a pivotal role in the orchestrated cellular response to increased zinc levels to restore cellular zinc balance necessary to achieve a broad spectrum of zinc-dependent functions and begins to probe its molecular action. We also report an important role for the mammalian CBWD gene product in protection of cells from either depleted or excess zinc by virtue of the fact that overexpression of recombinant CBWD protein altered cellular tolerance to both elevated and depleted levels of zinc consistent with a homeostatic function. In addition, we present preliminary evidence that changes in the expression of ZNF658 and its target genes, in particular SLC30A10 (ZnT10), may be related to cell senescence, suggesting that changes in zinc homeostasis are components of this process. Overall, the work presented contributes to understanding zinc regulated gene expression and cellular zinc homeostasis.
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Hahn, Stefanie [Verfasser], and Heiko [Akademischer Betreuer] Hermeking. "Characterization of ZNF281 and its role in colorectal carcinogenesis / Stefanie Hahn. Betreuer: Heiko Hermeking." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1065610114/34.
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Jordanovski, Darko [Verfasser], Thorsten [Akademischer Betreuer] Hoppe, and Herbert [Akademischer Betreuer] Pfister. "Posttranslationale Kontrolle des zellulären Transkriptionsfaktors PBF/ZNF395 / Darko Jordanovski. Gutachter: Thorsten Hoppe ; Herbert Pfister." Köln : Universitäts- und Stadtbibliothek Köln, 2012. http://d-nb.info/1038224853/34.
Full textBook chapters on the topic "ZNF318"
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Jordanovski, Darko, Christine Herwartz, and Gertrud Steger. "ZNF395 (HDBP2 /PBF) is a Target Gene of Hif-1α." In Huntington's Disease - Core Concepts and Current Advances. InTech, 2012. http://dx.doi.org/10.5772/30659.
Full textConference papers on the topic "ZNF318"
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Pérez Huacuja Urista, J. M., M. Maldonado, J. Calyeca, R. Ramirez, C. Becerril, M. Selman, and A. Pardo. "Role of ZNF365 in Pulmonary Fibrosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5238.
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Pérez Huacuja Urista, J. M., M. Maldonado, F. Toscano-Marquez, R. Ramírez, C. Becerril, Y. Romero, M. Selman, and A. Pardo. "ZNF365 Downregulation Induces Senescence in Lung Fibroblasts and Epithelial Cells." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1951.
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Messana, Matthew J., Chao Yang, and Laurie E. Littlepage. "Abstract 4252: Regulation of the oncogene ZNF217 by localization in breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4252.
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Messana, Matthew J., and Laurie E. Littlepage. "Abstract 1979: Regulation of the oncogene ZNF217 by localization in breast cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1979.
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Furukawa, Daisuke, Tsuyoshi Chijiwa, Masahiro Matsuyama, Masaya Mukai, Ei-ichi Matsuo, Osamu Nishimura, Kenji Kawai, et al. "Abstract 1543: Clinical significance of ZNF185 intracellular localization in pancreatic ductal carcinoma." 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.am2016-1543.
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Nolte, Elke, Jaroslaw Szczyrba, Martin Hart, Celina Döll, Sven Wach, Helge Taubert, Bastian Keck, et al. "Abstract 3090: miR-24 influences proliferation of prostate cancer cellsin vitrovia targeting ZNF217." 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.am2013-3090.
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Suarez, Christopher, Sunil S. Badve, and Laurie E. Littlepage. "Abstract B47: The role of ZNF217 in the development of breast cancer chemoresistance." In Abstracts: AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; June 18-21, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.pms14-b47.
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Brown, Kevin M., Jun Fang, Jinping Jia, Zhaoming Wang, Matthew Makowski, Tongwu Zhang, Jason Hoskins, et al. "Abstract 4610: Functional characterization of a multicancer risk locus on chr5p15.33 reveals regulation ofTERTby ZNF148." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4610.
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Facchine, Beth, Junmin Wu, Megan Fabry, Matt Messana, William Kaliney, and Laurie Littlepage. "Abstract 3341: Inhibiting the destruction of the oncogene ZNF217 promotes breast cancer metastasis to lung." 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.am2018-3341.
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Martínez, Alejandra Rodríguez, Elisa M. Vuorinen, Anastasia Shcherban, Nina K. Rajala, Matti Nykter, and Anne Kallioniemi. "Abstract 3353: ZNF414 as a functionally relevant transcription factor in pancreatic and breast cancer cells." 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.am2018-3353.
Full textReports on the topic "ZNF318"
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Gregg, Jeffrey P., and Sheryl R. Krig. The ZNF217 Breast Cancer Oncogene Amplified at 20q13: A Potential Marker for Invasiveness. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada564327.
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