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Journal articles on the topic 'ZNF318'

Author: Grafiati

Published: 1 April 2023

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1

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 (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

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Mitchell, Emily, Michael Spencer Chapman, Nicholas Williams, et al. "Clonal Dynamics of Normal Haematopoiesis with Human Ageing." Blood 138, Supplement 1 (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

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Sobocińska, Joanna, Joanna Nowakowska, Sara Molenda, et al. "Zinc Finger Proteins in Head and Neck Squamous Cell Carcinomas: ZNF540 May Serve as a Biomarker." Current Oncology 29, no. 12 (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, ZFP2

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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 (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

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Ishikawa, S., M. Kai, Y. Takei, et al. "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 та Yuan-Lin Zheng. "ZNF300 stimulates fatty acid oxidation and alleviates hepatosteatosis through regulating PPARα". Biochemical Journal 476, № 2 (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. Furth

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Pieraccioli, Marco, Sara Nicolai, Consuelo Pitolli, et al. "ZNF281 inhibits neuronal differentiation and is a prognostic marker for neuroblastoma." Proceedings of the National Academy of Sciences 115, no. 28 (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

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Deng, Yu-Qin, Gang-Yong Kong, Song Li, Fen Li та 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 (11 травня 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 compare

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9

Fahmé, Pia, Farah Ramadan, Diep Tien Le, et al. "The Intricate Interplay between the ZNF217 Oncogene and Epigenetic Processes Shapes Tumor Progression." Cancers 14, no. 24 (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. Howeve

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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 (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

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11

Quinlan, Kate G. R., Marco Nardini, Alexis Verger, et al. "Specific Recognition of ZNF217 and Other Zinc Finger Proteins at a Surface Groove of C-Terminal Binding Proteins." Molecular and Cellular Biology 26, no. 21 (2006): 8159–72. http://dx.doi.org/10.1128/mcb.00680-06.

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ABSTRACT Numerous transcription factors recruit C-terminal binding protein (CtBP) corepressors. We show that the large zinc finger protein ZNF217 contacts CtBP. ZNF217 is encoded by an oncogene frequently amplified in tumors. ZNF217 contains a typical Pro-X-Asp-Leu-Ser (PXDLS) motif that binds in CtBP's PXDLS-binding cleft. However, ZNF217 also contains a second motif, Arg-Arg-Thr (RRT), that binds a separate surface on CtBP. The crystal structure of CtBP bound to an RRTGAPPAL peptide shows that it contacts a surface crevice distinct from the PXDLS binding cleft. Interestingly, both PXDLS and

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Thillainadesan, Gobi, Majdina Isovic, Esther Loney, Joseph Andrews, Marc Tini, and Joseph Torchia. "Genome Analysis Identifies the p15ink4b Tumor Suppressor as a Direct Target of the ZNF217/CoREST Complex." Molecular and Cellular Biology 28, no. 19 (2008): 6066–77. http://dx.doi.org/10.1128/mcb.00246-08.

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ABSTRACT The ZNF217 oncoprotein is a constituent of a core transcriptional complex that includes CoREST, histone deacetylase 1/2, lysine demethylase 1, and the C-terminal binding protein 1/2. We have combined genome-wide expression profiling and chromatin immunoprecipitation with directed selection and ligation (ChIP-DSL) to identify a subset of genes directly regulated by ZNF217. Our results establish p15ink4b as a direct target of the ZNF217 complex. Downregulation of ZNF217 in MCF-7 breast cancer cells resulted in a dramatic increase in p15ink4b expression and coincided with increases in di

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13

Chen, Jing, Daniel J. DeAngelo, Jeffery L. Kutok, et al. "PKC412 Inhibits the ZNF198-FGFR1 Fusion Tyrosine Kinase and Is Efficacious in Treatment of t(8;13)(p11;q12) Associated Stem Cell Myeloproliferative Disease." Blood 104, no. 11 (2004): 2549. http://dx.doi.org/10.1182/blood.v104.11.2549.2549.

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Abstract Human stem cell leukemia-lymphoma syndrome usually presents as a myeloproliferative disease (MPD) that evolves to acute myeloid leukemia and/or lymphoma. The syndrome associated with t(8;13)(p11;q12) results in expression of the ZNF198-FGFR1 fusion tyrosine kinase. Current empirically-derived cytotoxic chemotherapy is inadequate treatment of this disease. We hypothesized that small molecule inhibitors of the ZNF198-FGFR1 fusion would have therapeutic efficacy. We characterized the transforming activity of ZNF198-FGFR1 in hematopoietic cells in vitro and in vivo. Expression of ZNF198-F

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Kasyapa, Chitta S., Padmaja Kunapuli, Lesleyann Hawthorn, and John K. Cowell. "Induction of the plasminogen activator inhibitor-2 in cells expressing the ZNF198/FGFR1 fusion kinase that is involved in atypical myeloproliferative disease." Blood 107, no. 9 (2006): 3693–99. http://dx.doi.org/10.1182/blood-2005-04-1505.

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The ZNF198/FGFR1 fusion kinase associated with an atypical myeloproliferative disease is constitutively activated and regulates several STAT transcription factors. We used oligonucleotide microarrays to compare the gene-expression profiles between HEK-293 cells that stably express either the ZNF198/FGFR1 chimeric protein or the wild-type ZNF198 gene. Expression of the plasminogen activator inhibitor-2 (PAI-2/SERPINB2) was highly increased in cells expressing the fusion gene. Western blot analysis demonstrated that HEK-293 cells do not express PAI-2 endogenously, but in ZNF198/FGFR1-expressing

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Wang, Minghao, Qiang Han, Zhe Su, and Xinmiao Yu. "Transcription Factor ZNF326 Upregulates the Expression of ERCC1 and HDAC7 and its Clinicopathologic Significance in Glioma." Laboratory Medicine 51, no. 4 (2020): 377–84. http://dx.doi.org/10.1093/labmed/lmz075.

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Abstract Previous reports that we have coauthored have shown that transcription factor ZNF326 can upregulate the expression of ERCC1 and HDAC7, and downregulate the expression of LTBP4 and ZNF383 in lung-cancer cells. However, whether tissue-specificity of the ZNF326 function exists in glioma tissue remains unclear. In this study, overexpression or knockdown of ZNF326 in glioma cells caused upregulation or downregulation, respectively, of the protein and micro RNA (mRNA) levels of ERCC1 and HDAC7. The levels of LTBP4 and ZNF383 were not significantly changed. Immunohistochemical results showed

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Qin, Xi, Rui Su, Lu Yang, et al. "Identification of ZNF217 As an Essential Oncogenic Gene in B-Cell Acute Lymphoblastic Leukemia By CRISPR/Cas9-Based Library Screening." Blood 134, Supplement_1 (2019): 1465. http://dx.doi.org/10.1182/blood-2019-129849.

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Background and Significance Although the prognosis of pediatric B-cell acute lymphoblastic leukemia (B-ALL) has been significantly improved in recent years, adult patients continue to have dismal survival. This is partially due to the fact that adult patients tend to have more unfavorable cytogenetic characteristics such as MLL-AF4 fusion and BCR-ABL1 fusion. N6-methyladenosine (m6A) is the most prevalent epigenetic modification on eukaryotic messenger RNA (mRNA), which plays important roles in many fundamental bioprocesses. The aberrant regulation of m6A modification is crucial for the initia

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Li, Changhong, Peijun Xia, Yijuan Ma, Xinyue Zhang, and Yijia Liu. "Expression pattern of ZNF33B in bovine ovaries and the effect of its polymorphism on superovulation traits." Archives Animal Breeding 65, no. 1 (2022): 69–77. http://dx.doi.org/10.5194/aab-65-69-2022.

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Abstract. ZNF33B belongs to recently duplicated Krüppel-associated box domain zinc finger proteins (KRAB-ZFPs), which is widely present in various organs, and some evidence showed that its expression is altered in the ovary undergoing superovulation. In this study, the expression of ZNF33B in ovary and early embryo was determined by immunohistochemistry and immunofluorescence techniques. Results showed that the expression of ZNF33B in the ovary was mainly in the cytoplasm of oocytes and granulosa luteal cells of ovarian corpus luteum and significantly reduced during follicular ovulation to lut

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Lu, Zhaojin, Zepeng Zheng, Yufen Xu, et al. "The Associated of the Risk of IVIG Resistance in Kawasaki Disease with ZNF112 Gene and ZNF180 Gene in a Southern Chinese Population." Journal of Inflammation Research Volume 15 (September 2022): 5053–62. http://dx.doi.org/10.2147/jir.s378080.

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Laudadio, Ilaria, Alex Bastianelli, Valerio Fulci та ін. "ZNF281 Promotes Colon Fibroblast Activation in TGFβ1-Induced Gut Fibrosis". International Journal of Molecular Sciences 23, № 18 (2022): 10261. http://dx.doi.org/10.3390/ijms231810261.

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Crohn’s disease (CD) and ulcerative colitis (UC) are chronic inflammatory disorders of the gastrointestinal tract. Chronic inflammation is the main factor leading to intestinal fibrosis, resulting in recurrent stenosis, especially in CD patients. Currently, the underlying molecular mechanisms of fibrosis are still unclear. ZNF281 is a zinc-finger transcriptional regulator that has been characterized as an epithelial-to-mesenchymal transition (EMT)-inducing transcription factor, suggesting its involvement in the regulation of pluripotency, stemness, and cancer. The aim of this study is to inves

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Santos, Katheryn, Qingchun Jin, Peter G. Miller, et al. "Abstract P3-08-01: Clonal hematopoiesis of indeterminate potential (CHIP) in metastatic triple negative breast cancer." Cancer Research 82, no. 4_Supplement (2022): P3–08–01—P3–08–01. http://dx.doi.org/10.1158/1538-7445.sabcs21-p3-08-01.

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Abstract Background. Patients (pts) with metastatic triple negative breast cancer (mTNBC) receive serial cytotoxic chemotherapy regimens, often with cumulative myelosuppressive effects, impairing treatment tolerance. Clonal hematopoiesis of indeterminate potential (CHIP) refers to the detection of somatic mutations in genes recurrently mutated in hematologic malignancies in the blood of adults with no evident hematologic abnormalities. Little is known about the natural history of CHIP after breast cancer treatment. We sought to characterize CHIP in pts undergoing treatment for mTNBC. Methods.

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Nicolai, Sara, Robert Mahen, Giuseppe Raschellà, et al. "ZNF281 is recruited on DNA breaks to facilitate DNA repair by non-homologous end joining." Oncogene 39, no. 4 (2019): 754–66. http://dx.doi.org/10.1038/s41388-019-1028-7.

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Abstract Efficient repair of DNA double-strand breaks (DSBs) is of critical importance for cell survival. Although non-homologous end joining (NHEJ) is the most used DSBs repair pathway in the cells, how NHEJ factors are sequentially recruited to damaged chromatin remains unclear. Here, we identify a novel role for the zinc-finger protein ZNF281 in participating in the ordered recruitment of the NHEJ repair factor XRCC4 at damage sites. ZNF281 is recruited to DNA lesions within seconds after DNA damage through a mechanism dependent on its DNA binding domain and, at least in part, on poly-ADP r

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Reiter, Andreas, Jastinder Sohal, Shashikant Kulkarni, et al. "Consistent Fusion of ZNF198 to the Fibroblast Growth Factor Receptor-1 in the t(8;13)(p11;q12) Myeloproliferative Syndrome." Blood 92, no. 5 (1998): 1735–42. http://dx.doi.org/10.1182/blood.v92.5.1735.

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Abstract The 8p11 myeloproliferative syndrome is a rare, aggressive condition associated with reciprocal translocations of chromosome band 8p11, most commonly the t(8;13)(p11;q12). To identify the genes involved in this translocation, we used fluorescence in situ hybridization (FISH) analysis to show that the chromosome 8 breakpoints fell within YAC 899e2 and that the chromosome 13 breakpoints are clustered in a region flanked by YACs 929f11 and 911h8. FISH using chromosome 13 PAC clones indicated that the t(8;13) is not simply a reciprocal translocation but also involves an inversion of 13q11

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Reiter, Andreas, Jastinder Sohal, Shashikant Kulkarni, et al. "Consistent Fusion of ZNF198 to the Fibroblast Growth Factor Receptor-1 in the t(8;13)(p11;q12) Myeloproliferative Syndrome." Blood 92, no. 5 (1998): 1735–42. http://dx.doi.org/10.1182/blood.v92.5.1735.417k11_1735_1742.

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The 8p11 myeloproliferative syndrome is a rare, aggressive condition associated with reciprocal translocations of chromosome band 8p11, most commonly the t(8;13)(p11;q12). To identify the genes involved in this translocation, we used fluorescence in situ hybridization (FISH) analysis to show that the chromosome 8 breakpoints fell within YAC 899e2 and that the chromosome 13 breakpoints are clustered in a region flanked by YACs 929f11 and 911h8. FISH using chromosome 13 PAC clones indicated that the t(8;13) is not simply a reciprocal translocation but also involves an inversion of 13q11-12. Exon

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Xiao, Sheng, Jennifer G. McCarthy, Jon C. Aster, and Jonathan A. Fletcher. "ZNF198–FGFR1 transforming activity depends on a novel proline-rich ZNF198 oligomerization domain." Blood 96, no. 2 (2000): 699–704. http://dx.doi.org/10.1182/blood.v96.2.699.

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Abstract An acquired chromosomal translocation, t(8;13)(p11;q11-12), observed in a distinctive type of stem cell leukemia/lymphoma syndrome, leads to the fusion of the 5′ portion of ZNF198 and the 3′ portion of FGFR1. ZNF198–FGFR1 fusion transcripts encode 4 to 10 zinc fingers, a proline-rich region, and the intracellular portion of the FGFR1 (fibroblast growth factor receptor 1) receptor tyrosine kinase. We demonstrate that the ZNF198 proline-rich region constitutes a novel self-association domain. When fused to the intracellular domain of FGFR1, the ZNF198 proline-rich region is sufficient t

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Xiao, Sheng, Jennifer G. McCarthy, Jon C. Aster, and Jonathan A. Fletcher. "ZNF198–FGFR1 transforming activity depends on a novel proline-rich ZNF198 oligomerization domain." Blood 96, no. 2 (2000): 699–704. http://dx.doi.org/10.1182/blood.v96.2.699.014k53_699_704.

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An acquired chromosomal translocation, t(8;13)(p11;q11-12), observed in a distinctive type of stem cell leukemia/lymphoma syndrome, leads to the fusion of the 5′ portion of ZNF198 and the 3′ portion of FGFR1. ZNF198–FGFR1 fusion transcripts encode 4 to 10 zinc fingers, a proline-rich region, and the intracellular portion of the FGFR1 (fibroblast growth factor receptor 1) receptor tyrosine kinase. We demonstrate that the ZNF198 proline-rich region constitutes a novel self-association domain. When fused to the intracellular domain of FGFR1, the ZNF198 proline-rich region is sufficient to cause o

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Fang, Yuan, Xu Han, Jianang Li, Tiantao Kuang, and Wenhui Lou. "HEATR1 Deficiency Promotes Chemoresistance via Upregulating ZNF185 and Downregulating SMAD4 in Pancreatic Cancer." Journal of Oncology 2020 (May 26, 2020): 1–10. http://dx.doi.org/10.1155/2020/3181596.

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Objective. To discover the correlated gene with HEATR1 in regulating chemoresistance of gemcitabine. Methods. Gene chip analysis was performed to find out differential genes between HEATR1-KD and control groups. The top 20 genes were subjected to high-content screening, and functional assay was implemented. Gene expression profiling was carried out to find the downstream target. Immunohistochemistry and survival analysis were performed. Results. ZNF185 fold change (4.5285) was the most significant between the HEATR1-KD and control groups. Knocking down ZNF185 could promote the chemosensitivity

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Ramírez-Ramírez, Ruth, Melva Gutiérrez-Angulo, Jorge Peregrina-Sandoval, et al. "Somatic deletion of KDM1A/LSD1 gene is associated to advanced colorectal cancer stages." Journal of Clinical Pathology 73, no. 2 (2019): 107–11. http://dx.doi.org/10.1136/jclinpath-2019-206128.

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AimsKDM1A/LSD1 and ZNF217 are involved in a protein complex that participates in transcriptional regulation. ZNF217 has been analysed in numerous cancers and its amplification has been associated with advanced stages of disease; however, a similar role for KDM1A/LSD1 has not been uncovered. In this study, we estimated the number of KDM1A/LSD1 and ZNF217 gene copies in tissue samples from patients diagnosed with colorectal cancer (CRC), as well as its association with clinicopathological features in patients with CRC.MethodsParaffin-embedded tumour samples from 50 patients with CRC with a histo

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Mantsou, Aglaia, Evangelia Koutsogiannouli, Costas Haitoglou, Athanasios G. Papavassiliou, and Nikolaos A. Papanikolaou. "Regulation of expression of the p21CIP1 gene by the transcription factor ZNF217 and MDM2." Biochemistry and Cell Biology 94, no. 6 (2016): 560–68. http://dx.doi.org/10.1139/bcb-2016-0026.

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Using mouse double minute 2 (MDM2) protein-specific affinity chromatography and mass spectrometry, we have isolated the protein product of the oncogene znf217, which is a transcription factor and a component of a Hela-S-derived HDAC1 complex, as a novel MDM2-interacting protein. When co-expressed in cultured cancer cells, ZNF217 forms a complex with MDM2 and its ectopic over-expression reduces the steady-state levels of acetylated p53 in cell lines, suppressing its ability to activate the expression of a p21 promoter construct. In-silico analysis of the p21 promoter revealed the presence of se

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Zhang, Shulong, Kaihua Zhu, Qi Han, Quan Wang, and Bin Yang. "lncRNA PCAT1 might coordinate ZNF217 to promote CRC adhesion and invasion through regulating MTA2/MTA3/Snai1/E-cadherin signaling." Cellular and Molecular Biology 67, no. 4 (2022): 1–9. http://dx.doi.org/10.14715/cmb/2021.67.4.1.

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LncRNA prostate cancer-associated transcript 1 (PCAT1) is a well-known oncogene, but the mechanisms of exosomes PCAT1 in colorectal cancer (CRC) remain largely unknown. Thus, the mechanisms of exosomes lncRNA PCAT1 were investigated. The expressions of exosomes lncRNA PCAT1 in tissues from stage 0-I and stage II-III CRC patients, and intestinal epithelial cell line FHC and two CRC cell lines, HT29 and HCT8 were measured by real-time quantitative PCR. The effects of lncRNA PCAT1 on adhesion and invasion of two CRC cell lines were investigated by cell-matrix adhesion and transwell assays. In add

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Ren, Mingqiang, Xiurong Li, and John K. Cowell. "Genetic fingerprinting of the development and progression of T-cell lymphoma in a murine model of atypical myeloproliferative disorder initiated by the ZNF198–fibroblast growth factor receptor-1 chimeric tyrosine kinase." Blood 114, no. 8 (2009): 1576–84. http://dx.doi.org/10.1182/blood-2009-03-212704.

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AbstractA mouse model of human ZNF198–fibroblast growth factor receptor-1 (FGFR1) stem cell leukemia lymphoma has been developed to investigate mechanisms of oncogenesis and progression. Using array-based comparative genomic hybridization, we followed disease progression after serial transplantation of ZNF198-FGFR1–transformed stem cells that give rise to a distinct myeloproliferative disorder and T-lymphoblastic leukemia. A consistent, frequently homozygous, chr14:53880459-55011545 deletion, containing the T-cell receptor α and δ genes, was identified in the bone marrow, spleen, and lymph nod

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Gao, Yiwen, Nan Zhang, Chunmei Lv, Na Li, Xueqin Li та Weiwei Li. "lncRNA SNHG1 Knockdown Alleviates Amyloid-β-Induced Neuronal Injury by Regulating ZNF217 via Sponging miR-361-3p in Alzheimer’s Disease". Journal of Alzheimer's Disease 77, № 1 (2020): 85–98. http://dx.doi.org/10.3233/jad-191303.

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Background: Long noncoding RNAs have been proven to play an important role in the progression of Alzheimer’s disease (AD). However, the function of small nucleolar RNA host gene 1 (SNHG1) in AD progression remains to be studied. Objective: To explore the role of SNHG1 in AD progression and clarify its potential mechanism. Methods: Amyloid β-protein (Aβ) was used to construct an AD cell model in vitro. The expression levels of SNHG1 and miR-361-3p were determined by quantitative real-time polymerase chain reaction. Cell viability and apoptosis were measured by cell counting kit 8 assay and flow

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Capon, Francesca, Marie-José Bijlmakers, Natalie Wolf, et al. "Identification of ZNF313 / RNF114 as a novel psoriasis susceptibility gene." Human Molecular Genetics 17, no. 13 (2008): 1938–45. http://dx.doi.org/10.1093/hmg/ddn091.

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Zhu, Hua, Yaojuan Yang, Jun Gao, et al. "Area dependent expression of ZNF312 in human fetal cerebral cortex." Neuroscience Research 68, no. 1 (2010): 73–76. http://dx.doi.org/10.1016/j.neures.2010.05.007.

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El Abdellaoui-Soussi, Fadoua, Paula S. Yunes-Leites, Dolores López-Maderuelo, et al. "Interplay between the Chd4/NuRD Complex and the Transcription Factor Znf219 Control Cardiac Cell Identity." International Journal of Molecular Sciences 23, no. 17 (2022): 9565. http://dx.doi.org/10.3390/ijms23179565.

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The sarcomere regulates striated muscle contraction. This structure is composed of several myofibril proteins, isoforms of which are encoded by genes specific to either the heart or skeletal muscle. The chromatin remodeler complex Chd4/NuRD regulates the transcriptional expression of these specific sarcomeric programs by repressing genes of the skeletal muscle sarcomere in the heart. Aberrant expression of skeletal muscle genes induced by the loss of Chd4 in the heart leads to sudden death due to defects in cardiomyocyte contraction that progress to arrhythmia and fibrosis. Identifying the tra

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Bijlmakers, Marie-jose, Jonathan Barker, Richard Trembath, and Francesca Capon. "F.11. Preliminary Characterization of the RNF114/ZNF313 Psoriasis Susceptibility Gene." Clinical Immunology 131 (2009): S96. http://dx.doi.org/10.1016/j.clim.2009.03.279.

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Lee, Dung-Fang, Martin J. Walsh, and Francesca Aguiló. "ZNF217/ZFP217 Meets Chromatin and RNA." Trends in Biochemical Sciences 41, no. 12 (2016): 986–88. http://dx.doi.org/10.1016/j.tibs.2016.07.013.

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37

Donaldson, Nickett S., Curtis L. Nordgaard, Christina C. Pierre, et al. "Kaiso regulates Znf131-mediated transcriptional activation." Experimental Cell Research 316, no. 10 (2010): 1692–705. http://dx.doi.org/10.1016/j.yexcr.2010.03.011.

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Li, Yongqing, Yuequn Wang, Wuzhou Yuan, Yun Deng, Chuanbing Zhu, and Xiushan Wu. "Advanced studies on human gene ZNF322." Frontiers of Biology in China 2, no. 4 (2007): 379–82. http://dx.doi.org/10.1007/s11515-007-0056-9.

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39

Demiroglu, Asuman, E. Joanna Steer, Carol Heath, et al. "The t(8;22) in chronic myeloid leukemia fuses BCR to FGFR1: transforming activity and specific inhibition of FGFR1 fusion proteins." Blood 98, no. 13 (2001): 3778–83. http://dx.doi.org/10.1182/blood.v98.13.3778.

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Abstract This report describes 2 patients with a clinical and hematologic diagnosis of chronic myeloid leukemia (CML) in chronic phase who had an acquired t(8;22)(p11;q11). Analysis by fluorescence in situ hybridization (FISH) and reverse transcription-polymerase chain reaction (RT-PCR) indicated that both patients were negative for the BCR-ABL fusion, but suggested that the BCR gene was disrupted. Further FISH indicated a breakpoint within fibroblast growth factor receptor 1 (FGFR1), the receptor tyrosine kinase that is known to be disrupted in a distinctive myeloproliferative disorder, most

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40

Bruton, Rachel K., Peter Pelka, Katie L. Mapp, et al. "Identification of a Second CtBP Binding Site in Adenovirus Type 5 E1A Conserved Region 3." Journal of Virology 82, no. 17 (2008): 8476–86. http://dx.doi.org/10.1128/jvi.00248-08.

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ABSTRACT C-terminal binding protein (CtBP) binds to adenovirus early region 1A (AdE1A) through a highly conserved PXDLS motif close to the C terminus. We now have demonstrated that CtBP1 also interacts directly with the transcriptional activation domain (conserved region 3 [CR3]) of adenovirus type 5 E1A (Ad5E1A) and requires the integrity of the entire CR3 region for optimal binding. The interaction appears to be at least partially mediated through a sequence (161RRNTGDP167) very similar to a recently characterized novel CtBP binding motif in ZNF217 as well as other regions of CR3. Using repo

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41

Fisher, Laura. "Retraction: Berberine alleviates amyloid beta-induced injury in Alzheimer’s disease by miR-107/ZNF217." RSC Advances 11, no. 9 (2021): 5001. http://dx.doi.org/10.1039/d1ra90031e.

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42

Rodriguez, Patricia Q., Asmundur Oddsson, Lwaki Ebarasi, et al. "Knockdown of Tmem234 in zebrafish results in proteinuria." American Journal of Physiology-Renal Physiology 309, no. 11 (2015): F955—F966. http://dx.doi.org/10.1152/ajprenal.00525.2014.

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Podocytes are highly specialized epithelial cells located at the outer aspects of the glomerular capillary tuft and critical components of the kidney filtration barrier. To maintain their unique features, podocytes express a number of proteins that are only sparsely found elsewhere in the body. In this study, we have identified four (Tmem234, Znf185, Lrrc49, and Slfn5) new highly podocyte-enriched proteins. The proteins are strongly expressed by podocytes, while other parts of the kidney show only weak or no expression. Tmem234, Slfn5, and Lrrc49 are located in foot processes, whereas Znf185 i

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43

Gianotten, J., F. van der Veen, M. Alders, N. Leschot, M. Mannens, and M. Hoffer. "ZNF214: a candidate gene for impaired spermatogenesis." Fertility and Sterility 76, no. 3 (2001): S155—S156. http://dx.doi.org/10.1016/s0015-0282(01)02457-8.

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Law, David J., Edwin M. Labut, and Juanita L. Merchant. "Intestinal overexpression of ZNF148 suppresses ApcMin/+ neoplasia." Mammalian Genome 17, no. 10 (2006): 999–1004. http://dx.doi.org/10.1007/s00335-006-0052-4.

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Hui, Hong-xia, Zhong-wu Hu, Chao Jiang, Jian Wu, Yong Gao, and Xiao-wei Wang. "ZNF418 overexpression protects against gastric carcinoma and prompts a good prognosis." OncoTargets and Therapy Volume 11 (May 2018): 2763–70. http://dx.doi.org/10.2147/ott.s160802.

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Lee, M. G., J. Han, S. I. Jeong, et al. "XAF1 directs apoptotic switch of p53 signaling through activation of HIPK2 and ZNF313." Proceedings of the National Academy of Sciences 111, no. 43 (2014): 15532–37. http://dx.doi.org/10.1073/pnas.1411746111.

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Jang, S., K. W. Lee, T. K. Magdalene, J. Ahn, M. G. Lee, and S. G. Chi. "XAF1 and ZNF313 complex stimulates ER stress-induced apoptosis via direct GRP78 inhibition." Annals of Oncology 30 (October 2019): v7. http://dx.doi.org/10.1093/annonc/mdz238.021.

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Li, Yongqing, Dan Yang, Yan Bai, et al. "ZNF418, a novel human KRAB/C2H2 zinc finger protein, suppresses MAPK signaling pathway." Molecular and Cellular Biochemistry 310, no. 1-2 (2007): 141–51. http://dx.doi.org/10.1007/s11010-007-9674-4.

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Kasyapa, Chitta S., Padmaja Kunapuli, and John K. Cowell. "HSPA1A is an important regulator of the stability and function of ZNF198 and its oncogenic derivative, ZNF198–FGFR1." Journal of Cellular Biochemistry 102, no. 5 (2007): 1308–17. http://dx.doi.org/10.1002/jcb.21362.

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Dong, Shaozhong, Sumin Kang, Ting-Lei Gu, et al. "14–3-3 integrates prosurvival signals mediated by the AKT and MAPK pathways in ZNF198-FGFR1–transformed hematopoietic cells." Blood 110, no. 1 (2007): 360–69. http://dx.doi.org/10.1182/blood-2006-12-065615.

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Human 8p11 stem cell leukemia/lymphoma syndrome usually presents as a myeloproliferative disorder (MPD) that evolves to acute myeloid leukemia and/or lymphoma. The syndrome associated with t(8;13)(p11;q12) results in expression of the ZNF198-FGFR1 fusion tyrosine kinase that plays a pathogenic role in hematopoietic transformation. We found that ZNF198-FGFR1 activated both the AKT and mitogen activated protein kinase (MAPK) prosurvival signaling pathways, resulting in elevated phosphorylation of the AKT target FOXO3a at T32 and BAD at S112, respectively. These phosphorylated residues subsequent

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