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Journal articles on the topic 'SNED1'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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El-Mancy, Shereen S., Alaadin E. El-Haddad, Walaa A. Alshareef, Amr M. Saadeldeen, Soad Z. El-Emam, and Osama S. Elnahas. "Enhancement of Antimicrobial and Antiproliferative Activities of Standardized Frankincense Extract Using Optimized Self-Nanoemulsifying Delivery System." Scientia Pharmaceutica 89, no. 3 (August 2, 2021): 36. http://dx.doi.org/10.3390/scipharm89030036.

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Boswellic acids (BAs) are the main bioactive compounds of frankincense, a natural resin obtained from the genus Boswellia. This study aimed to develop a self-nanoemulsifying delivery system (SNEDS) to improve the antimicrobial and antiproliferative activities of standardized frankincense extract (Fr-extract). Fr-extract was standardized, and BA content was quantified using the developed HPLC-UV method. Screening studies of excipients followed by formula optimization using a mixture simplex lattice design was employed. The optimized Fr-SENDS formulation was characterized. Furthermore, microbiological and antiproliferative assessments of the standardized Fr-extract and Fr-SNEDS were evaluated. Quantification demonstrated that the major constituent is 11-keto-boswellic acid (KBA) (16.25%) among BA content (44.96%). The optimized Fr-SENDS (composed of 5% CapryolTM 90, 48.7% Gelucire® 44/14 and 46.3% ethanol) showed spherical nanosized dispersions with DS, PDI, and zeta potential of 17.9 nm, 0.2, and −14.5 mV, respectively. Fr-SNEDS exhibited lower MIC and MBC values compared with Fr-extract against pathogens conjugated with lung cancer and was comparable to reference antimicrobials. Fr-SNEDS showed superior antiproliferative activity over Fr-extract, with IC50 values of 20.49 and 109.5 μg mL−1, respectively. In conclusion, the optimized Fr-SNEDS could be easily developed and manufactured at a low cost and the in vitro results support its use as a potential adjuvant oral therapy for lung cancer. Further in vivo studies could be continued to assess the therapeutic efficiency of the prepared system.

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Tonfack, Libert B., Steven G. Hussey, Adri Veale, Alexander A. Myburg, and Eshchar Mizrachi. "Analysis of Orthologous SECONDARY WALL-ASSOCIATED NAC DOMAIN1 (SND1) Promotor Activity in Herbaceous and Woody Angiosperms." International Journal of Molecular Sciences 20, no. 18 (September 18, 2019): 4623. http://dx.doi.org/10.3390/ijms20184623.

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SECONDARY WALL-ASSOCIATED NAC DOMAIN1 (SND1) is a master regulator of fibre secondary wall deposition in Arabidopsis thaliana (Arabidopsis), with homologs in other angiosperms and gymnosperms. However, it is poorly understood to what extent the fibre-specific regulation of the SND1 promoter, and that of its orthologs, is conserved between diverged herbaceous and woody lineages. We performed a reciprocal reporter gene analysis of orthologous SND1 promoters from Arabidopsis (AthSND1), Eucalyptus grandis (EgrNAC61) and Populus alba × P. grandidentata (PagWND1A) relative to secondary cell wall-specific Cellulose Synthase4 (CesA4) and CesA7 promoters, in both a non-woody (Arabidopsis) and a woody (poplar) system. β-glucuronidase (GUS) reporter analysis in Arabidopsis showed that the SND1 promoter was active in vascular tissues as previously reported and showed interfascicular and xylary fibre-specific expression in inflorescence stems, while reporter constructs of the woody plant-derived promoters were partial to the (pro)cambium-phloem and protoxylem. In transgenic P. tremula × P. alba plants, all three orthologous SND1 promoters expressed the GUS reporter similarly and preferentially in developing secondary xylem, ray parenchyma and cork cambium. Ours is the first study to reciprocally test orthologous SND1 promoter specificity in herbaceous and woody species, revealing diverged regulatory functions in the herbaceous system.

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Zheng, Hongrui, Juan Wang, Wenjie Zhang, Bin He, Yunhua Wang, Xiaotong Zhang, Hui Mao, and Lei Fan. "Mechanism for Bioactive Nanomaterial circ0024831 Regulation of Staphylococcal Nuclease Domain Containing 1 via RNA Methylation Recognition in Osteosarcoma." Journal of Biomedical Nanotechnology 18, no. 2 (February 1, 2022): 453–62. http://dx.doi.org/10.1166/jbn.2022.3256.

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Bioactive nanomaterial circular RNA (circRNA) is an important non-coding RNA with a strong specificity, stable structure and high expression abundance. It can affect many diseases and physiological processes and may become a new way of disease diagnosis and targeted therapy. Recent studies have shown that Staphylococcal Nuclease Domain-Containing Protein 1 (SND1) can recognize N6-methyladenine (M6A) modified mRNA and regulate target mRNA stability. It can then control the expression of a series of downstream genes. However, whether SND1 can directly combine with circRNA and regulate its stability and function are new issues to be discussed. Results showed bioactive nanomaterial circ0024831 could directly bind to the Tudor domain of SND1 in the cytoplasm to block the recognition of SND1 to M6A modified RNA thus reducing the stability of downstream target gene mRNA and inhibiting the expression of downstream regulatory proteins. The down-regulation of circ0024831 expression in osteosarcoma cells relieved inhibition of SND1 which lead to change of tumor-related gene expression profile, promoting the occurrence and development of osteosarcoma.

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Kalofonou, Foteini, Damien Leach, Mark Hamilton, Sean Eric Mcguire, Claire Fletcher, Jonathan Waxman, and Charlotte L. Bevan. "MiR-1271-5p: An AR-modulatory microRNA with a distinct role in prostate cancer progression, through SND1 and MORF4L1 interaction." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e16562-e16562. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e16562.

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e16562 Background: Current screening methodologies for prostate cancer (PCa) are relatively insensitive and there is a need for new treatments for castrate resistant disease. MicroRNAs (miRs) are considered to be master regulators of the genome. We have investigated the role of miRs in modulating androgen receptor function and their potential as treatments of PCa. We report that the AR-modulatory miR-1271-5p also targets SND1 and MORF4L1 and may have a role in PCa progression and screening. Methods: AGO2-PAR-CLIP analysis was performed to ascertain miR-1271-5p target genes in human PCa cell lines. MiR-1271-5p levels were manipulated in cell lines by transfection with miR mimic and or antisense inhibitor. SND1 and MORF4L1 were confirmed as targets by real-time qPCR and western blotting. The functional role of miR-1271-5p and its target genes was assessed by SRB growth assays . Immunohistochemical detection of SND1 and MORF4L1 expression was studied in a cohort of 63 PCa patients and compared with normal controls. Results: MORF4L1 mRNA levels were significantly reduced with the use of miR-1271-5p mimic in 22RV1 cells (p = 0.001), while SND1 mRNA levels were significantly decreased with the use of miR-1271-5p inhibitor in C42 cells (p = 0.0014). Targeting SND1 or MORF4L1, in combination with miR inhibition, significantly reduced C42 (p = 0.0003) and 22RV1 (p = 0.0014) cell growth. MORF4L1 expression was higher in patients with Gleason score (GS) 4+3 relative to those with GS 3+4 and in PCa tissue, as compared with normal prostatic tissue, but did not reach significance. SND1 immunostaining was significantly higher in patients with GS 4+3 or GS 3+4 PCa, compared with normal prostatic tissue (p = 0.0211, p = 0.0007 respectively). SND1 staining was significantly higher in patients with GS 4+3, compared to GS 3+4 (p = 0.0431) or GS 3+3 (p = 0.0251). Conclusions: MiR-1271-5p is an AR-modulatory microRNA, which shows great potential as a biomarker and therapeutic target in PCa. The interaction of miR-1271-5p with its target genes SND1 and MORF4L1 could provide the basis for therapeutic advance in screening and in the treatment of castrate resistant PCa.

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Cheng, Zhiwei, Xuejiao Li, Yongsheng Deng, and Xiaodan Wang. "Life evaluation of rolling element bearings using stochastic neighbor embedding deep regression." Journal of Physics: Conference Series 2396, no. 1 (December 1, 2022): 012053. http://dx.doi.org/10.1088/1742-6596/2396/1/012053.

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Abstract Accurate residual service life (RSL) evaluation of rolling element bearings is significant for prognostics and health management to guarantee rotating machinery safety, availability, and efficiency. This work develops a method called stochastic neighbor embedding deep regression (SNEDR) to enhance the estimation performance of the RSL. First, the appropriate features originating from the vibration data of the tested REB are extracted. The state indicators are subsequently established with the extracted features by introducing the stochastic neighbor embedding. By doing that, the random errors and noises generated from the vibration signals can be minimized, and the evaluation performance may be improved. Finally, the regression model based on the state indicators and the long short-term memory network with time information representation capacity is generated for the RSL evaluation. The availability of the SNEDR is validated by the real data derived from a bear failure experiment. Furthermore, a peer method is introduced for a comparative study. Experimental results show that the SNEDR outperforms the competing method and can yield more reasonable and accurate evaluation results.

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Wright, Tanner, Yalong Wang, and Mark T. Bedford. "The Role of the PRMT5–SND1 Axis in Hepatocellular Carcinoma." Epigenomes 5, no. 1 (January 5, 2021): 2. http://dx.doi.org/10.3390/epigenomes5010002.

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Arginine methylation is an essential post-translational modification (PTM) deposited by protein arginine methyltransferases (PRMTs) and recognized by Tudor domain-containing proteins. Of the nine mammalian PRMTs, PRMT5 is the primary enzyme responsible for the deposition of symmetric arginine methylation marks in cells. The staphylococcal nuclease and Tudor domain-containing 1 (SND1) effector protein is a key reader of the marks deposited by PRMT5. Both PRMT5 and SND1 are broadly expressed and their deregulation is reported to be associated with a range of disease phenotypes, including cancer. Hepatocellular carcinoma (HCC) is an example of a cancer type that often displays elevated PRMT5 and SND1 levels, and there is evidence that hyperactivation of this axis is oncogenic. Importantly, this pathway can be tempered with small-molecule inhibitors that target PRMT5, offering a therapeutic node for cancer, such as HCC, that display high PRMT5–SND1 axis activity. Here we summarize the known activities of this writer–reader pair, with a focus on their biological roles in HCC. This will help establish a foundation for treating HCC with PRMT5 inhibitors and also identify potential biomarkers that could predict sensitivity to this type of therapy.

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Winarni, Indah. "English for Non English Department at Brawijaya University: How Essential?" TEFLIN Journal - A publication on the teaching and learning of English 16, no. 1 (September 3, 2015): 93. http://dx.doi.org/10.15639/teflinjournal.v16i1/93-109.

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For years, English has been a compulsory subject for the students of non-English departments (henceforth English for SNED). The success of English for SNED at the tertiary level of education has largely been questioned due to various constraints in all levels of its operation. Related to the large resources involved, overall evaluation is necessary. This can be started with analysis of needs, which, in a large organization like university, should be done in two stages (Coleman, 1988). While the present sudy does not pretend that it could be regarded as Coleman's first stage of needs analysis, it would offere a significant contribution to such an undertaking. Carried out in Brawijaya University, this study was aimed at describing, through a set of questionnaires, the perception of graduates, English instructors and subject lecturers on (1) the aim of English for SNED, and (2) the role of references written in English in the level of study programs. As previous studies suggested, conflicting aims of English for SNED in the perception of respondents were identified. This study delienated four different groups with regards to the use of references written in English in the level of study programs.

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Zhang, Xia, Qing Zhang, Ke Zhang, Fang Wang, Xiaogai Qiao, and Jinquan Cui. "Circ SMARCA5 Inhibited Tumor Metastasis by Interacting with SND1 and Downregulating the YWHAB Gene in Cervical Cancer." Cell Transplantation 30 (January 1, 2021): 096368972098378. http://dx.doi.org/10.1177/0963689720983786.

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Cervical cancer is one of the diseases that seriously endanger women’s health. Circular RNA plays an important role in regulating the occurrence and development of cervical cancer. Here, we investigated the mechanisms of circ SMARCA5 in the development of cervical cancer. Quantitative reverse transcriptase polymerase chain reaction (RT-qPCR) results showed that the expression of SMARCA5 was downregulated in cervical cancer tissues and cell lines. Then we found that overexpression of SMARCA5 inhibited proliferation and invasion, but promoted apoptosis in cervical cancer cells. These were detected by Cell Counting Kit-8, Transwell, and Annexin V-fluorescein isothiocyanate/propidium iodide detection kit, respectively, and the expression of the apoptosis-related proteins was determined by western blotting. Then we predicted that SMARCA5 combined with Staphylococcal nuclease domain-containing 1 (SND1) by starBase, and verified by RNA pull-down assay. To further reveal the molecular mechanisms of SMARCA5 in the progression of cervical cancer, the interaction protein of SND1 was predicted by STRING, and the interaction was verified by co-immunoprecipitation assay. Then, the effects of SND1 or YWHAB on the development of cervical cancer were detected by the gain and loss function test, and we found that knockdown of SND1 or YWHAB reversed the effects of SMARCA5 short interfering RNA on proliferation, invasion, and apoptosis of cervical cancer cells. Overexpression of SMARCA5 inhibited cervical cancer metastasis in vivo. Our results showed that overexpression of circ SMARCA5 inhibits the binding of SND1 to YWHAB, and inhibits the proliferation and invasion, but promotes apoptosis in cervical cancer cells, thus inhibiting the metastasis of cervical cancer.

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Rouis, Oumayma, Cédric Broussard, François Guillonneau, Jean-Baptiste Boulé, and Emmanuelle Delagoutte. "Identification of hemicatenane-specific binding proteins by fractionation of HeLa nuclei extracts." Biochemical Journal 477, no. 2 (January 31, 2020): 509–24. http://dx.doi.org/10.1042/bcj20190855.

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DNA hemicatenanes (HCs) are four-way junctions in which one strand of a double-stranded helix is catenated with one strand of another double-stranded DNA. Frequently mentioned as DNA replication, recombination and repair intermediates, they have been proposed to participate in the spatial organization of chromosomes and in the regulation of gene expression. To explore potential roles of HCs in genome metabolism, we sought to purify proteins capable of binding specifically HCs by fractionating nuclear extracts from HeLa cells. This approach identified three RNA-binding proteins: the Tudor-staphylococcal nuclease domain 1 (SND1) protein and two proteins from the Drosophila behavior human splicing family, the paraspeckle protein component 1 and the splicing factor proline- and glutamine-rich protein. Since these proteins were partially pure after fractionation, truncated forms of these proteins were expressed in Escherichia coli and purified to near homogeneity. The specificity of their interaction with HCs was re-examined in vitro. The two truncated purified SND1 proteins exhibited specificity for HCs, opening the interesting possibility of a link between the basic transcription machinery and HC structures via SND1.

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20

Al-Amodi, Yasir A., Khaled M. Hosny, Waleed S. Alharbi, Martin K. Safo, and Khalid M. El-Say. "Investigating the Potential of Transmucosal Delivery of Febuxostat from Oral Lyophilized Tablets Loaded with a Self-Nanoemulsifying Delivery System." Pharmaceutics 12, no. 6 (June 10, 2020): 534. http://dx.doi.org/10.3390/pharmaceutics12060534.

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Gout is the most familiar inflammatory arthritis condition caused by the elevation of uric acid in the bloodstream. Febuxostat (FBX) is the latest drug approved by the United States Food and Drug Administration (US FDA) for the treatment of gout and hyperuricemia. FBX is characterized by low solubility resulting in poor gastrointestinal bioavailability. This study aimed at improving the oral bioavailability of FBX by its incorporation into self-nanoemulsifying delivery systems (SNEDS) with minimum globule size and maximum stability index. The SNEDS-incorporated FBX was loaded into a carrier substrate with a large surface area and lyophilized with other excipients to produce a fluffy, porous-like structure tablet for the transmucosal delivery of FBX. The solubility of FBX was studied in various oils, surfactants, and cosurfactants. Extreme vertices design was utilized to optimize FBX-SNEDS, and subsequently loaded into lyophilized tablets along with suitable excipients. The percentages of the main tablet excipients were optimized using a Box–Behnken design to develop self-nanoemulsifying lyophilized tablets (SNELTs) with minimum disintegration time and maximum drug release. The pharmacokinetics parameters of the optimized FBX-SNELTs were tested in healthy human volunteers in comparison with the marketed FBX tablets. The results revealed that the optimized FBX-SNELTs increased the maximum plasma concentration (Cmax) and decreased the time to reach Cmax (Tmax) with a large area under the curve (AUC) as a result of the enhanced relative oral bioavailability of 146.4%. The significant enhancement of FBX bioavailability is expected to lead to reduced side effects and frequency of administration during the treatment of gout.

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Mebius, Francisca. "Acteren op het scherp van de snede." Advocatenblad 99, no. 6 (June 2019): 50. http://dx.doi.org/10.5553/ab/0165-13312019099006024.

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22

Pool, Grieteke. "Psycho-oncologie: op het scherp van de snede." Tijdschrift voor Psychotherapie 39, no. 5 (September 2013): 331–42. http://dx.doi.org/10.1007/s12485-013-0057-x.

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23

Liezers, M., M. C. Endres, A. J. Carman, and G. C. Eiden. "Generating aerodynamic surrogate nuclear explosion debris (SNED)." Journal of Radioanalytical and Nuclear Chemistry 318, no. 1 (August 14, 2018): 71–77. http://dx.doi.org/10.1007/s10967-018-6046-3.

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24

Hardeman, Erik. "'Hier werk ik op het scherpst van de snede'." GZ - Psychologie 13, no. 5 (October 29, 2021): 30–33. http://dx.doi.org/10.1007/s41480-021-0845-9.

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25

Han, Guofen, and Hongyan Dai. "Ectopic Expression of Hawthorn SND1 Gene in Tobacco." International Journal of Environmental and Agriculture Research 3, no. 11 (November 30, 2017): 85–89. http://dx.doi.org/10.25125/agriculture-journal-ijoear-nov-2017-21.

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26

Jiang, Qingwen, and Karuna Ganesh. "Breaking up MTDH–SND1 to break down metastasis." Nature Cancer 3, no. 1 (January 2022): 6–8. http://dx.doi.org/10.1038/s43018-021-00320-7.

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27

Navarro-Imaz, Hiart, Yuri Rueda, and Olatz Fresnedo. "SND1 overexpression deregulates cholesterol homeostasis in hepatocellular carcinoma." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1861, no. 9 (September 2016): 988–96. http://dx.doi.org/10.1016/j.bbalip.2016.05.011.

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28

Casassus, Juan. "School evaluation in Chile: The case of SNED." Prospects 31, no. 4 (December 2001): 565–74. http://dx.doi.org/10.1007/bf03220040.

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29

Li, Q., Y. C. Lin, Y. H. Sun, J. Song, H. Chen, X. H. Zhang, R. R. Sederoff, and V. L. Chiang. "Splice variant of the SND1 transcription factor is a dominant negative of SND1 members and their regulation in Populus trichocarpa." Proceedings of the National Academy of Sciences 109, no. 36 (August 22, 2012): 14699–704. http://dx.doi.org/10.1073/pnas.1212977109.

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30

STRÖM, V. "Ett fall af ankylotiskt, snedt förträngdt bäcken. Partus arte praematurus." Nordiskt Medicinskt Arkiv 14, no. 17 (April 24, 2009): 1–15. http://dx.doi.org/10.1111/j.0954-6820.1882.tb01467.x.

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31

Wei, Yuannan, Esha Sandhu, Xi Yang, Jie Yang, Yuanyuan Ren, and Xingjie Gao. "Bidirectional Functional Effects of Staphylococcus on Carcinogenesis." Microorganisms 10, no. 12 (November 28, 2022): 2353. http://dx.doi.org/10.3390/microorganisms10122353.

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As a Gram-positive cocci existing in nature, Staphylococcus has a variety of species, such as Staphylococcus aureus and Staphylococcus epidermidis, etc. Growing evidence reveals that Staphylococcus is closely related to the occurrence and development of various cancers. On the one hand, cancer patients are more likely to suffer from bacterial infection and antibiotic-resistant strain infection compared to healthy controls. On the other hand, there exists an association between staphylococcal infection and carcinogenesis. Staphylococcus often plays a pathogenic role and evades the host immune system through surface adhesion molecules, α-hemolysin, PVL (Panton-Valentine leukocidin), SEs (staphylococcal enterotoxins), SpA (staphylococcal protein A), TSST-1 (Toxic shock syndrom toxin-1) and other factors. Staphylococcal nucleases (SNases) are extracellular nucleases that serve as genomic markers for Staphylococcus aureus. Interestingly, a human homologue of SNases, SND1 (staphylococcal nuclease and Tudor domain-containing 1), has been recognized as an oncoprotein. This review is the first to summarize the reported basic and clinical evidence on staphylococci and neoplasms. Investigations on the correlation between Staphylococcus and the occurrence, development, diagnosis and treatment of breast, skin, oral, colon and other cancers, are made from the perspectives of various virulence factors and SND1.

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32

Armengol, Sandra, Enara Arretxe, Leire Enzunza, Irati Llorente, Unai Mendibil, Hiart Navarro-Imaz, Begoña Ochoa, Yolanda Chico, and María José Martínez. "SREBP-2-driven transcriptional activation of human SND1 oncogene." Oncotarget 8, no. 64 (November 21, 2017): 108181–94. http://dx.doi.org/10.18632/oncotarget.22569.

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33

Wang, Nan, Xilin Du, Li Zang, Nuan Song, Tao Yang, Rui Dong, Tao Wu, Xianli He, and Jianguo Lu. "Prognostic impact of Metadherin–SND1 interaction in colon cancer." Molecular Biology Reports 39, no. 12 (October 14, 2012): 10497–504. http://dx.doi.org/10.1007/s11033-012-1933-0.

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34

van Opstal, Jan. "Serie Een Bijzondere Casus: Balanceren op het scherp van de snede." Tijdschrift voor Psychotherapie 29, no. 6 (December 2003): 269–73. http://dx.doi.org/10.1007/bf03062043.

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35

Chidambaranathan-Reghupaty, Saranya, Rachel Mendoza, Paul B. Fisher, and Devanand Sarkar. "The multifaceted oncogene SND1 in cancer: focus on hepatocellular carcinoma." Hepatoma Research 4, no. 7 (July 10, 2018): 32. http://dx.doi.org/10.20517/2394-5079.2018.34.

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36

Tsuchiya, Naoto, and Hitoshi Nakagama. "MicroRNA, SND1, and alterations in translational regulation in colon carcinogenesis." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 693, no. 1-2 (November 10, 2010): 94–100. http://dx.doi.org/10.1016/j.mrfmmm.2010.09.001.

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37

Armengol, Sandra, Enara Arretxe, Begoña Ochoa, and María J. Martínez. "Transient overexpression of SREBP-1c represses the human SND1 promoter." Chemistry and Physics of Lipids 160 (August 2009): S20. http://dx.doi.org/10.1016/j.chemphyslip.2009.06.007.

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38

Carnoy, Martin, Iliana Brodziak, Andres Molina, and Miguel Socías. "The Limitations of Teacher Pay Incentive Programs Based on Inter-Cohort Comparisons: The Case of Chile's SNED." Education Finance and Policy 2, no. 3 (July 2007): 189–227. http://dx.doi.org/10.1162/edfp.2007.2.3.189.

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Since 1996, the Chilean government has awarded teachers pay bonuses based on school performance using a complex formula that combines absolute average student test scores and inter-cohort gains from test year to test year. In this paper, we compared the bonuses schools actually received on the basis of this formula to how they would have fared under a hypothetical alternative measure of school performance—intra-cohort gains between the 4th and 8th grades in 1996–2000. We show that schools that received monetary premiums for “good performance” under the SNED program were more likely to be schools that had scored higher on the 4th grade 1996 test, but, on average, they were not the schools that made the highest cohort gains as students progressed from 4th grade in 1996 to 8th grade in 2000. Given what we have found, to get more SNED awards, the wise school would do much better to raise 4th grade and 8th grade scores every two years (even years for 4th grade and odd years for 8th grade) and not focus on the more difficult task of helping students make greater progress from 4th to 8th grades. Although we have data on only one cohort's gain scores from 4th to 8th grades, our limited analysis demonstrates the possible constraints of a school-based incentive program when the available student performance data for awarding pay bonuses are inter-cohort rather than intra-cohort test score gains.

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39

Qin, Gaoping, Yong Song, Yadong Guo, Yaowen Sun, and Weihui Zeng. "LincRNA TINCR facilitates excessive proliferation and inflammation in post-burn skin fibroblasts by directly binding with SND1 protein and inducing SND1-mediated TGF-β1 expression." Biochemical and Biophysical Research Communications 509, no. 4 (February 2019): 903–10. http://dx.doi.org/10.1016/j.bbrc.2019.01.013.

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40

Li, Peng, Yunjiao He, Teng Chen, Kit-Ying Choy, Tsun Sing Chow, Iris L. K. Wong, Xinqing Yang, et al. "Disruption of SND1–MTDH Interaction by a High Affinity Peptide Results in SND1 Degradation and Cytotoxicity to Breast Cancer Cells In Vitro and In Vivo." Molecular Cancer Therapeutics 20, no. 1 (December 2, 2020): 76–84. http://dx.doi.org/10.1158/1535-7163.mct-20-0130.

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41

Liu, Jing, Jie Yang, Lin Yu, Chun Rao, Qian Wang, Cuiyun Sun, Cuijuan Shi, et al. "miR-361-5p inhibits glioma migration and invasion by targeting SND1." OncoTargets and Therapy Volume 11 (August 2018): 5239–52. http://dx.doi.org/10.2147/ott.s171539.

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42

KANOJIA, SUKRATI, REBECCA K. DAVIDSON, NOLAN CASEY, and JASON SPAETH. "1247-P: The SND1 Coregulator Controls ß-Cell Function and Identity." Diabetes 70, Supplement 1 (June 2021): 1247—P. http://dx.doi.org/10.2337/db21-1247-p.

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43

Jariwala, Nidhi, Devaraja Rajasekaran, Rachel G. Mendoza, Xue-Ning Shen, Ayesha Siddiq, Maaged A. Akiel, Chadia L. Robertson, et al. "Oncogenic Role of SND1 in Development and Progression of Hepatocellular Carcinoma." Cancer Research 77, no. 12 (April 20, 2017): 3306–16. http://dx.doi.org/10.1158/0008-5472.can-17-0298.

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44

Gu, Xi, Jinqi Xue, Liping Ai, Lisha Sun, Xudong Zhu, Yulun Wang, and Caigang Liu. "SND1 expression in breast cancer tumors is associated with poor prognosis." Annals of the New York Academy of Sciences 1433, no. 1 (September 14, 2018): 53–60. http://dx.doi.org/10.1111/nyas.13970.

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45

Tabué Youmbi, Jean Ghislain, Dénis Ntamack, Roger Feumba, Emmanuel Ngnikam, Joseph Wéthé, and Émile Tanawa. "Vulnérabilité des eaux souterraines et périmètres de protection dans le bassin versant de la Mingoa (Yaoundé, Cameroun)." Articles 40, no. 2 (March 24, 2011): 71–96. http://dx.doi.org/10.7202/1001389ar.

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La présente étude traite de la vulnérabilité des nappes phréatiques et de la proposition d’un périmètre de protection dans le bassin versant de la Mingoa, menacées par les foyers de pollution notamment les latrines traditionnelles représentant 83 % des ouvrages d’assainissement individuel. Ces nappes phréatiques sont fortement sollicitées par près de 63 % des ménages non raccordés au réseau SNEC1 (LESEAU2, 2004). Le coefficient d’occupation des sols est de 90 %. La méthode repose sur les enquêtes, les observations directes et les analyses en laboratoire. Les résultats indiquent que l’épuration totale en zone non saturée selon la méthode Rehse est effectuée à plus de 3 mètres, les eaux souterraines sont de mauvaise qualité microbiologique. Deux zones de protection sont définies en tenant compte du contexte sociodémographique, pédologique et environnemental.

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46

Chen, Wei, Zhixian Yu, Weiping Huang, Yu Yang, Feng Wang, and Hang Huang. "LncRNA LINC00665 Promotes Prostate Cancer Progression via miR-1224-5p/SND1 Axis." OncoTargets and Therapy Volume 13 (March 2020): 2527–35. http://dx.doi.org/10.2147/ott.s241578.

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47

Kim, Dae-Myung. "The Multifunctional Protein, Snd1, Involved in tRNA Splicing of the Fission Yeast." Journal of the Korea Entertainment Industry Association 10, no. 6 (December 31, 2016): 439. http://dx.doi.org/10.21184/jkeia.2016.12.10.6.439.

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48

CHEN, Ke-qin, Yun-na GUO, Meng-ru SONG, Hong-yan DAI, and Zhi-hong ZHANG. "Isolation and characterization of the secondary wall-related SND1 gene in hawthorn." Journal of Integrative Agriculture 17, no. 9 (September 2018): 2007–14. http://dx.doi.org/10.1016/s2095-3119(17)61791-x.

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49

Navarro-Imaz, Hiart, Begoña Ochoa, Itsaso García-Arcos, María José Martínez, Yolanda Chico, Olatz Fresnedo, and Yuri Rueda. "Molecular and cellular insights into the role of SND1 in lipid metabolism." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1865, no. 5 (May 2020): 158589. http://dx.doi.org/10.1016/j.bbalip.2019.158589.

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50

Garcia-Arcos, I., Y. Rueda, P. González-Kother, L. Palacios, B. Ochoa, and O. Fresnedo. "Association of SND1 protein to low density lipid droplets in liver steatosis." Journal of Physiology and Biochemistry 66, no. 1 (March 2010): 73–83. http://dx.doi.org/10.1007/s13105-010-0011-0.

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