Relevant bibliographies by topics / SNED1

Academic literature on the topic 'SNED1'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "SNED1"

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Vallet, Sylvain D., Martin N. Davis, Anna Barqué, Ali H. Thahab, Sylvie Ricard-Blum, and Alexandra Naba. "Computational and experimental characterization of the novel ECM glycoprotein SNED1 and prediction of its interactome." Biochemical Journal 478, no. 7 (April 16, 2021): 1413–34. http://dx.doi.org/10.1042/bcj20200675.

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The extracellular matrix (ECM) is a complex meshwork of proteins and an essential component of multicellular life. We have recently reported the characterization of a novel ECM protein, SNED1, and showed that it promotes breast cancer metastasis and regulates craniofacial development. However, the mechanisms by which it does so remain unknown. ECM proteins exert their functions by binding to cell surface receptors and interacting with other ECM proteins, actions that we can predict using knowledge of protein's sequence, structure, and post-translational modifications. Here, we combined in-silico and in-vitro approaches to characterize the physico-chemical properties of SNED1 and infer its putative functions. To do so, we established a mammalian cell system to produce and purify SNED1 and its N-terminal fragment, which contains a NIDO domain, and demonstrated experimentally SNED1's potential to be glycosylated, phosphorylated, and incorporated into an insoluble ECM. We also determined the secondary and tertiary structures of SNED1 and its N-terminal fragment and obtained a model for its NIDO domain. Using computational predictions, we identified 114 proteins as putative SNED1 interactors, including the ECM protein fibronectin. Pathway analysis of the predicted SNED1 interactome further revealed that it may contribute to signaling through cell surface receptors, such as integrins, and participate in the regulation of ECM organization and developmental processes. Last, using fluorescence microscopy, we showed that SNED1 forms microfibrils within the ECM and partially colocalizes with fibronectin. Altogether, we provide a wealth of information on an understudied yet important ECM protein with the potential to decipher its pathophysiological functions.
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Tong, Liping, Chao Wang, Xuebin Hu, Bo Pang, Zhonghui Yang, Zhangxiu He, Meihui He, Lanlan Wei, and Ming Chu. "Correlated overexpression of metadherin and SND1 in glioma cells." Biological Chemistry 397, no. 1 (January 1, 2016): 57–65. http://dx.doi.org/10.1515/hsz-2015-0174.

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Abstract Glioma is the most common primary brain tumor with poor prognosis. Effective treatment of glioma remains a big challenge due to complex pathogenic mechanisms. Previous studies have shown that metadherin (MTDH) and its interacting protein staphylococcal nuclease domain containing 1 (SND1) are overexpressed in many solid tumors. To elucidate the role of MDTH and SND1 in the pathogenesis of glioma, we examined the expression of MTDH and SND1 in primary glioma tissues and found that both MTDH and SND1 were highly expressed, with similar expression patterns. Co-expression of MTDH and SND1 was associated with advanced glioma grades. In addition, we detected the interaction between MTDH and SND1 in cultured glioma cell lines. MTDH could promote the expression of p65 and SND1 in glioma cells. However, enhanced SND1 expression by MTDH was abolished by the inhibition of p65. In conclusion, we demonstrated high expression levels MTDH and SND1 in primary glioma tissues. MTDH might promote glioma by inducing SND1 expression through the activation of NF-κB pathway. MTDH and SND1 may serve as the indicator of malignancy and prognosis as well as therapeutic targets for patients with glioma.
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Zhou, Ying, Qingyu Li, Jianfeng Zheng, and Nengming Lin. "N-Glycosylation on Asn50 of SND1 Is Required for Glioma U87 Cell Proliferation and Metastasis." Journal of Immunology Research 2022 (September 29, 2022): 1–10. http://dx.doi.org/10.1155/2022/5239006.

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Staphylococcal nuclease domain-containing protein 1 (SND1) is an evolutionarily conserved multidomain protein, which has gained attention recently due to its positive regulation in several cancer progression and metastatic spread. However, the specific contribution of SND1 glycosylation in glioma remains uncertain. In the current study, we confirmed that SND1 was highly expressed in human glioma. Using site-directed mutagenesis, we created four predicted N-glycosylation site mutants for SND1 and provided the first evidence that SND1 undergoes N-glycosylation on its Asn50, Asn168, Asn283, and Asn416 residues in human glioma U87 cells. In addition, we found that removing the N-glycans on the Asn50 site destabilized SND1 and led to its endoplasmic reticulum-associated degradation. Furthermore, destabilized SND1 inhibits the glioma cell proliferation and metastasis. Collectively, our results reveal that N-glycosylation at Asn50 is essential for SND1 folding and trafficking, thus essential for the glioma process, providing new insights for SND1 as a potential disease biomarker for glioma.
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Zhu, Weifang, and Shiyun Tan. "Tudor-SN protein expression in colorectal cancer and its association with clinical characteristics." Open Life Sciences 12, no. 1 (October 5, 2017): 237–42. http://dx.doi.org/10.1515/biol-2017-0028.

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AbstractObjectivesTudor-SN protein (SND1) is known to be up-regulated in some types of human malignancies and functions as an oncogene. The objective of our study was to investigate the expression and prognostic value of SND1 in human colorectal cancer (CRC).MethodsReal-time PCR and western blot were performed to examine the SND1 expression in human CRC and their corresponding non-cancerous colon tissues from 42 patients. Its clinical significance was evaluated by analyzing its expression with multiple pathological characters of CRC patients. Finally, a Kaplan-Meier survival curve was derived for SND1 gene expression among these CRC patients.ResultsWe found a significantly increased expression of SND1 mRNA and protein in tissue samples of CRC when compared to those in the paired normal adjacent colon tissues. High SND1 expression was positively correlated with higher tumor grades, aggressive N1+N2 nodal status and poor differentiation. Additionally, the overall survival rate in CRC patients with higher expression of SND1 was significantly shorter than that with lower SND1 expression.ConclusionOur findings suggested that SND1 might act as an important agent in the CRC carcinogenesis and predicted worse outcomes. The high expression of SND1 could be used as a novel predictive and prognostic marker of CRC.
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Wang, Xinting, Chunyan Zhang, Shuhe Wang, Rasheduzzaman Rashu, Rony Thomas, Jie Yang, and Xi Yang. "SND1 promotes Th1/17 immunity against chlamydial lung infection through enhancing dendritic cell function." PLOS Pathogens 17, no. 2 (February 26, 2021): e1009295. http://dx.doi.org/10.1371/journal.ppat.1009295.

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To date, no reports have linked the multifunctional protein, staphylococcal nuclease domain-containing protein 1 (SND1), to host defense against intracellular infections. In this study, we investigated the role and mechanisms of SND1, by using SND1 knockout (SND1-/-) mice, in host defense against the lung infection of Chlamydia muridarum, an obligate intracellular bacterium. Our data showed that SND1-/- mice exhibited significantly greater body weight loss, higher organism growth, and more severe pathological changes compared with wild-type mice following the infection. Further analysis showed significantly reduced Chlamydia-specific Th1/17 immune responses in SND1-/- mice after infection. Interestingly, the dendritic cells (DCs) isolated from SND1-/- mice showed lower costimulatory molecules expression and IL-12 production, but higher IL-10 production compared with those from wild-type control mice. In the DC-T cell co-culture system, DCs isolated from SND1-/- infected mice showed significantly reduced ability to promote Chlamydia-specific IFN-γ producing Th1 cells but enhanced capacity to induce CD4+T cells into Foxp3+ Treg cells. Adoptive transfer of DCs isolated from SND1-/- mice, unlike those from wild-type control mice, failed to protect the recipients against challenge infection. These findings provide in vivo evidence that SND1 plays an important role in host defense against intracellular bacterial infection, and suggest that SND1 can promote Th1/17 immunity and inhibit the expansion of Treg cells through modulation of the function of DCs.
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Chen, Shenglan, Ai Jiang, Yan Wang, and Yina Wang. "Long Non-Coding RNA X Inactive Specific Transcript Suppressed the Proliferation and Invasion of Ovarian Cancer Cells by Restricting the Expression of Staphylococcal Nuclease Domain Containing 1." Journal of Biomaterials and Tissue Engineering 10, no. 12 (December 1, 2020): 1793–99. http://dx.doi.org/10.1166/jbt.2020.2490.

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Ovarian cancer is one kind of a deadly gynecological malignancy. Recent study has shown that SND1 was associated with the development of ovarian cancer. Furthermore, the expression of lncRNA XIST in ovarian cancer was down-regulated. However, it is unclear whether lncRNA XIST could affect the occurrence and development of ovarian cancer by targeting SND1. In this study, we used the lentivirus to establish the overexpression and knockdown SND1 ovarian cancer cells. And we next detected the proliferation and invasion of these cells in diverse groups. Then, the luciferase assays were performed to detect the targeted effect of lncRNA XIST on SND1 and determined the expression of SND1 in the overexpressed lncRNA XIST ovarian cancer cells. We found that SND1 promoted the proliferation and invasion of ovarian cancer cells. And the lncRNA XIST targeted and suppressed the expression of SND1. Overexpression of lncRNA XIST inhibited the proliferation and invasion of ovarian cancer cells. However, the overexpression of SND1 alleviated the inhibitory efficacy of lncRNA XIST on the proliferation and invasion of ovarian cancer cells. LncRNA XIST inhibited the proliferation and invasion of ovarian cancer by suppressing the expression of SND1.
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Cooper, Garrett, Benjamin Lee, Nate Smyth, Karuna Mittal, Taylor Lawrence, Hunter Jonus, Jenny Shim, Kelly Goldsmith, and Andrew Hong. "Abstract 1674: FGF8 as a modulator of Wilms' tumor in vitro growth and longevity." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1674. http://dx.doi.org/10.1158/1538-7445.am2022-1674.

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Abstract Wilms’ tumor is the most common pediatric renal tumor accounting for 6-7% of all childhood cancers. Development of faithful Wilms’ tumor cell lines is needed to identify novel therapeutics. Currently, established Wilms’ tumor cell lines that are suitable for high throughput studies only represent anaplastic Wilms, a rare subtype. In contrast, cell lines representing the more common favorable histology Wilms’ tumor (FHWT) often have poor proliferative capacity and are unable to passage long-term (e.g. >20 passages). For this reason, there is a need to establish robust cell lines representing FHWT. We hypothesize that there are core factors missing from the cell culture medium which prevent proper growth signaling and proliferation. We first performed bulk RNA-sequencing from patients and associated cell lines at Aflac Cancer and Blood Disorders Center with an underlying diagnosis of FHWT. Transcriptomic analyses showed that the reduced growth and proliferation in these FHWT cell lines may be due to reduced presence of the mitogenic fibroblast growth factor 8 (FGF8) in the cell culture environment as compared to the tumor environment. Wilms’ tumor has notably high FGF8 expression levels compared to all other pediatric tumors, implicating FGF8 as a potential driving factor in tumor maintenance. To characterize the phenotypic effects of FGF8 reintroduction in short term FHWT cell lines, we both endogenously overexpressed FGF8 via a lentiviral vector and ectopically added recombinant FGF8 to the cell culture medium. Qualitatively, endogenous overexpression of FGF8 induced distinct morphological changes in cells, converting the enlarged and flattened cells into more focal cells resembling proliferative early passage cells. Quantitatively, overexpression of FGF8 in one favorable histology cell line led to an increased rate of cellular proliferation and extended the cellular longevity by seven passages (47% above baseline). RNA-sequencing analysis of these FGF8 overexpressing cells implicated the anti-apoptotic gene, NTSR1, and an extracellular matrix protein, SNED1, as potential downstream targets of FGF8 overexpression. However, ectopic addition of recombinant FGF8 protein to the cellular medium had less pronounced effects, with seemingly cell-line specific effects. These data demonstrate FGF8 as possibly being required for survival in certain Wilms’ tumor cell lines that can be modulated to influence in vitro proliferation and longevity. Citation Format: Garrett Cooper, Benjamin Lee, Nate Smyth, Karuna Mittal, Taylor Lawrence, Hunter Jonus, Jenny Shim, Kelly Goldsmith, Andrew Hong. FGF8 as a modulator of Wilms' tumor in vitro growth and longevity [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1674.
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Lehmusvaara, Saara, Teemu Haikarainen, Juha Saarikettu, Guillermo Martinez Nieto, and Olli Silvennoinen. "Inhibition of RNA Binding in SND1 Increases the Levels of miR-1-3p and Sensitizes Cancer Cells to Navitoclax." Cancers 14, no. 13 (June 24, 2022): 3100. http://dx.doi.org/10.3390/cancers14133100.

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SND1 is an RNA-binding protein overexpressed in large variety of cancers. SND1 has been proposed to enhance stress tolerance in cancer cells, but the molecular mechanisms are still poorly understood. We analyzed the expression of 372 miRNAs in the colon carcinoma cell line and show that SND1 silencing increases the expression levels of several tumor suppressor miRNAs. Furthermore, SND1 knockdown showed synergetic effects with cancer drugs through MEK-ERK and Bcl-2 family-related apoptotic pathways. To explore whether the SND1-mediated RNA binding/degradation is responsible for the observed effect, we developed a screening assay to identify small molecules that inhibit the RNA-binding function of SND1. The screen identified P2X purinoreceptor antagonists as the most potent inhibitors. Validation confirmed that the best hit, suramin, inhibits the RNA binding ability of SND1. The binding characteristics and mode of suramin to SND1 were characterized biophysically and by molecular docking that identified positively charged binding cavities in Staphylococcus nuclease domains. Importantly, suramin-mediated inhibition of RNA binding increased the expression of miR-1-3p, and enhanced sensitivity of cancer cells to Bcl-2 inhibitor navitoclax treatment. Taken together, we demonstrate as proof-of-concept a mechanism and an inhibitor compound for SND1 regulation of the survival of cancer cells through tumor suppressor miRNAs.
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Wang, Yuan, Xinting Wang, Xiaoteng Cui, Yue Zhuo, Hongshuai Li, Chuanbo Ha, Lingbiao Xin, et al. "Oncoprotein SND1 hijacks nascent MHC-I heavy chain to ER-associated degradation, leading to impaired CD8+ T cell response in tumor." Science Advances 6, no. 22 (May 2020): eaba5412. http://dx.doi.org/10.1126/sciadv.aba5412.

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SND1 is highly expressed in various cancers. Here, we identify oncoprotein SND1 as a previously unidentified endoplasmic reticulum (ER) membrane–associated protein. The amino-terminal peptide of SND1 predominantly associates with SEC61A, which anchors on ER membrane. The SN domain of SND1 catches and guides the nascent synthesized heavy chain (HC) of MHC-I to ER-associated degradation (ERAD), hindering the normal assembly of MHC-I in the ER lumen. In mice model bearing tumors, especially in transgenic OT-I mice, deletion of SND1 promotes the presentation of MHC-I in both B16F10 and MC38 cells, and the infiltration of CD8+ T cells is notably increased in tumor tissue. It was further confirmed that SND1 impaired tumor antigen presentation to cytotoxic CD8+ T cells both in vivo and in vitro. These findings reveal SND1 as a novel ER-associated protein facilitating immune evasion of tumor cells through redirecting HC to ERAD pathway that consequently interrupts antigen presentation.
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Blanco, Mario Andres, Maša Alečković, Yuling Hua, Tuo Li, Yong Wei, Zhen Xu, Ileana M. Cristea, and Yibin Kang. "Identification of Staphylococcal Nuclease Domain-containing 1 (SND1) as a Metadherin-interacting Protein with Metastasis-promoting Functions." Journal of Biological Chemistry 286, no. 22 (April 8, 2011): 19982–92. http://dx.doi.org/10.1074/jbc.m111.240077.

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Metastasis is the deadliest and most poorly understood feature of malignant diseases. Recent work has shown that Metadherin (MTDH) is overexpressed in over 40% of breast cancer patients and promotes metastasis and chemoresistance in experimental models of breast cancer progression. Here we applied mass spectrometry-based screen to identify staphylococcal nuclease domain-containing 1 (SND1) as a candidate MTDH-interacting protein. After confirming the interaction between SND1 and MTDH, we tested the role of SND1 in breast cancer and found that it strongly promotes lung metastasis. SND1 was further shown to promote resistance to apoptosis and to regulate the expression of genes associated with metastasis and chemoresistance. Analyses of breast cancer clinical microarray data indicated that high expression of SND1 in primary tumors is strongly associated with reduced metastasis-free survival in multiple large scale data sets. Thus, we have uncovered SND1 as a novel MTDH-interacting protein and shown that it is a functionally and clinically significant mediator of metastasis.
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Dissertations / Theses on the topic "SNED1"

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Jariwala, Nidhi. "SND1 mediated downregulation of PTPN23 in HCC." VCU Scholars Compass, 2014. https://scholarscompass.vcu.edu/etd/3648.

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SND1 MEDIATED DOWNREGULATION OF PTPN23 IN HEPATOCELLULAR CARCINOMA By Nidhi Jariwala, MS A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at Virginia Commonwealth University, 2014. ADVISOR: Dr. Devanand Sarkar Associate Professor, Department of Human and Molecular Genetics Blick Scholar Associate Scientific Director, Cancer Therapeutics VCU Institute of Molecular Medicine Massey Cancer Center ABSTRACT Staphyloccocal nuclease domain containing protein 1 (SND1) is identified as an oncogene in multiple cancers, including hepatocellular carcinoma (HCC). SND1 regulates gene expression at transcriptional as well as post-transcriptional level and mediates molecular pathways that culminate into carcinogenesis. SND1 is a component of RNA-induced silencing complex (RISC) and functions as a nuclease for RNAi-mediated mRNA degradation. On the other hand SND1 also binds to specific mRNAs, increasing their stability and hence expression. The aim of the present study is to identify mRNAs to which SND1 binds and modulates them either by degradation or increasing stability which might facilitate promotion of HCC by SND1. We performed RNA immunoprecipitation followed by RNA sequencing (RIP-Seq) using anti-SND1 antibody and human HCC cell line QGY-7703. More than 350 mRNAs were identified to be interacting with SND1, of which Protein tyrosine phosphatase non-receptor 23 (PTPN23) was of particular interest, since PTPN23 has been identified to be a tumor suppressor and its role in HCC has not been studied. We document that SND1 can bind to PTPN23 mRNA and induce its degradation. There is an inverse correlation between SND1 and PTPN23 levels in human HCC cell lines and PTPN23 level is downregulated in HCC. Our study thus identifies a novel mechanism by which SND1 promotes hepatocarcinogenesis and identifies PTPN23 as a potential tumor suppressor in HCC. Further studies need to be performed to explore the relationship of these two molecules in in vivo models and to develop PTPN23 overexpression as a potential therapeutic approach for HCC.
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Mckiver, Bryan D. "SND1-Targeted Gene Therapy for Hepatocellular Carcinoma." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5676.

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Staphylococcal nuclease and tudor-domain containing 1 (SND1) is an oncogene for a wide variety of cancers, including hepatocellular carcinoma (HCC). SND1 is a multifunctional protein regulating gene expression of proto-oncogenes and tumor suppressor genes, making SND1 a prime target for developing cancer therapeutics. This notion is especially attributed to HCC as most patients are diagnosed in advanced stages and the therapeutic options available for these patients are severely limited. In this study, we evaluated the therapeutic potential of a replication-defective adenovirus vector delivering SND1 shRNA (Ad.SND1sh) to human HCC cell lines, HepG3, HuH-7, and Hep3B. Adenovirus infection in HCC cells was confirmed by Western blotting and immunofluorescence. The efficacy of Ad.SND1sh to knockdown SND1 expression was confirmed via Western blot, qRT-PCR, and immunofluorescence. Ad.SND1sh did not significantly affect proliferation of the three human HCC cells but significantly inhibited their invasive and migratory capacities, as determined by wound healing and Matrigel invasion assays, respectively. As a corollary, Ad.SND1sh treatment resulted in a decrease in mesenchymal markers, such as N-cadherin, Twist, Snail, and Slug, without affecting levels of epithelial marker E-Cadherin, indicating that SND1 knockdown induces mesenchymal conversion in HCC cells. Additionally, reductions in liver cancer stem cell marker CD133 and HCC marker α-fetoprotein (AFP) were observed with SND1 knockdown. HCC cells with aberrant expression of these markers are associated with tumor initiation, recurrence, and multi-drug resistance. Our findings indicate that Ad.SND1sh may potentially be an effective therapy for advanced HCC and needs to be studied further for its clinical application.
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Jariwala, Nidhi H. "Characterization of Staphylococcal nuclease and tudor domain containing protein 1 (SND1) as a molecular target in Hepatocellular carcinoma and Non-alcoholic steatohepatitis." VCU Scholars Compass, 2017. https://scholarscompass.vcu.edu/etd/5183.

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CHARACTERIZATION OF STAPHYLOCOCCAL NUCLEASE AND TUDOR DOMAIN CONTAINING PROTEIN 1 (SND1) AS A MOLECULAR TARGET IN HEPATOCELLULAR CARCINOMA AND NON-ALCOHOLIC STEATOHEPATITIS Nidhi Jariwala, PhD A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Integrative Life Sciences Virginia Commonwealth University, 2017 Devanand Sarkar, M.B.B.S., PhD. Associate Professor, Department of Human and Molecular Genetics Virginia Commonwealth University Richmond, Virginia SND1, a subunit of the miRNA regulatory complex RISC, has been implicated as an oncogene in hepatocellular carcinoma (HCC). Oncoprotein SND1 regulates gene expression at a post-transcriptional level in multiple cancers including hepatocellular carcinoma (HCC). In the present study, we characterize oncogenic functions of SND1 in HCC employing a novel transgenic mouse model (Alb/SND1) and present SND1 as a potential molecular target in HCC management. We show that Alb/SND1 mice develop spontaneous HCC with partial penetrance and exhibit more highly aggressive HCC induced by chemical carcinogenesis. Livers from Alb/SND1 mice exhibit a relative increase in inflammatory markers and spheroid-generating tumor initiating cells (TiC). Mechanistic investigations defined roles for Akt and NF-κB signaling pathways in promoting TiC formation in Alb/SND1 mice. Intravenous administration of the selective SND1 inhibitor 3', 5'-deoxythymidine bisphosphate (pdTp) inhibited tumor formation without effects on body weight or liver function. We conclude that SND1 drives pro-oncogenic transcriptomic and proteomic changes in hepatocyte resulting in aggressive HCC. SND1 specific RNA interactome is identified with RNA immunoprecipitation sequencing (RIPSeq) approach. With an adjusted p value of2-fold enrichment over control, 282 mRNAs were identified to significantly associate with SND1 protein. We focused on the tumor suppressor Protein Tyrosine Phosphatase non-receptor type 23 (PTPN23) because its regulation by SND1 and its role in HCC are not known. In current study, we confirm that SND1 post-transcriptionally downregulates PTPN23. Pursuing functional studies with tetracycline inducible overexpression system, we validate that PTPN23 inhibits tyrosine kinase signaling, proliferation, epithelial to mesenchymal transition, migration, invasion and in vivo tumorigenesis. Alb/SND1 mice also manifest steatosis and fibrosis at one year of age. Coupled with a pro-inflammatory hepatic phenotype, we conclude that Alb/SND1 livers present NASH. High fat diet causes severe NASH and aggressive NASH induced HCC in Alb/SND1 mice. Serum and hepatic lipid profiling shows that hepatocyte specific SND1 overexpression associate with elevated triglyceride and cholesterol LDL levels. Contrarily, hepatocyte specific deletion of SND1 (SND1ΔHEP) in vivo, significantly protects against age dependent steatosis. Association of SND1 in NASH pathology is novel discovery and we present preliminary evidence confirming role of SND1 in promoting NASH.
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Rubiano, de la Cruz Julia María. "Los Programas de Incentivos Vinculados a Resultados Educativos. Exploración de una Opción de Política para Colombia." Tesis, Universidad de Chile, 2007. http://repositorio.uchile.cl/handle/2250/102882.

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El presente estudio exploró los incentivos colectivos como una opción de política hacia el fomento de la calidad educativa con el objetivo de proponer lineamientos de política para una propuesta de esta naturaleza en Colombia. Para ellos, se analizaron cuatro experiencias internacionales (Chile, El Salvador, y los estados de Florida y Carolina del Norte en EU); más los incentivos para el fomento a la calidad dentro de la institucionalidad actual y la herramienta que podría utilizarse para un programa de esta naturaleza. Las principales lecciones de las experiencias internacionales son: i) Se dan señales más claras cuando los incentivos se vinculan a resultados, aunque no deben descartarse otras variables dadas las limitaciones de las pruebas estandarizadas. ii) Lo más adecuado para evaluar el desempeño es el seguimiento por cohortes. De no ser posible hay que combinar opciones que controlen el efecto del nivel socioeconómico y la variabilidad de resultados; iii) La existencia de sanciones también tiene un impacto positivo; iv) Los programas de incentivos no actúan solos y necesitan articularse a políticas de accountability y de apoyo y asistencia a las escuelas más rezagadas. La propuesta para Colombia pretende reconocer el logro de metas definidas; aportar al fortalecimiento del rol de la institución en la gestión de su proceso educativo y fortalecer la planeación educativa local. Se propone un incentivo mixto, cuyos beneficios lleguen a las instituciones, a sus docentes y directivos, pero que involucre al municipio como unidad de asignación.
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Books on the topic "SNED1"

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(Mariëlla), Snel Mariëlla, ed. Het scherp van de snede. 3rd ed. Amsterdam: Poema Pocket, 1997.

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(Mariëlla), Snel Mariëlla, ed. Het scherp van de snede. Utrecht: Luitingh-Sijthoff, 1992.

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Caris, Gerard. De Gulden snede en het werk van Caris. Eindhoven: Technische Hogeschool Eindhoven, 1986.

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Bousset, Hugo. De Gulden Snede: Over Nederlands proza na 1980. Amsterdam: Meulenhoff, 1993.

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Vuurstenen werktuigen: Technologie op het scherp van de snede. Leiden: Sidestone Press, 2010.

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Smalhout, B. De erfenis van Pim: Op het scherp van de snede. 's-Gravenhage: BZZTôH, 2003.

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René, Steenhorst, ed. De onderbuik van Nederland: Op het scherp van de snede. 's-Gravenhage: Bzztôh, 2005.

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Het scherp van de snede: De Nederlandse literatuur in meer dan honderd polemieken. Amsterdam: Prometheus, 2010.

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Oostra, Margriet. Sjoerd de Vries: Op het scherp van de snede : op 'n skerpsten : on the cutting edge. Gersloot: Drijvende Dobber, 1992.

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Op het scherp van de snede: Achtergronden en ontwikkeling van de volksbeweging in China : Beijing, voorjaar 1989. Kampen: Kok Agora, 1990.

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Conference papers on the topic "SNED1"

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Gil–Pon, Pilar, Jordi Gutiérrez, and Enrique García–Berro. "Is There a Chance for SNeI1/2?" In FIRST STARS III: First Stars II Conference. American Institute of Physics, 2008. http://dx.doi.org/10.1063/1.2905552.

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Gil-Pons, Pilar. "Is there a chance for primordial SNeI1/2?" In Supernovae: lights in the darkness. Trieste, Italy: Sissa Medialab, 2008. http://dx.doi.org/10.22323/1.060.0013.

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Jariwala, Nidhi H., Rachel G. Mendoza, Garcia Dawn, Lai Zhao, Mark A. Subler, Jolene J. Windle, Paul B. Fisher, Chen Yidong, and Devanand Sarkar. "Abstract 4445: Post-transcriptional inhibition of PTPN23 by SND1: Potential mechanism for hepatocellular carcinoma." 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.am2018-4445.

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Jariwala, Nidhi, Devaraja Rajasekaran, Rachel Gredler, Maaged Akiel, Chadia Robertson, Paul Fisher, Arun Sanyal, and Devanand Sarkar. "Abstract 3823: Staphylococcal nuclease and tudor domain containing 1 (SND1) in development and progression of hepatocellular 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.am2016-3823.

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Lee, Nathan V., Keith Ching, Maruja Lira, Adam Pavlicek, Roslyn Dillon, Sreesha P. Srinivasa, Carol Nilsson, et al. "Abstract 628: A novel SND1-BRAF fusion confers resistance to the cMet inhibitor PF-04217903 in GTL16 cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-628.

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Santhekadur, Prasanna K., Rachel Gredler, Maaged Akiel, Paul Dent, Paul B. Fisher, and Devanand Sarkar. "Abstract 2628: The multifunctional protein staphylococcal nuclease domain containing-1 (SND1) promotes migration and invasion of hepatocellular carcinoma (HCC) cells by modulating angiotensin II type 1 receptor (AT1R) and transforming growth factor-β (TGF-β) s." 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.am2013-2628.

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