Добірка наукової літератури з теми "Dickkopf-3 (DKK3)"
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Статті в журналах з теми "Dickkopf-3 (DKK3)":
Suwa, T., M. Chen, CL Hawks, and PJ Hornsby. "Zonal expression of dickkopf-3 and components of the Wnt signalling pathways in the human adrenal cortex." Journal of Endocrinology 178, no. 1 (July 1, 2003): 149–58. http://dx.doi.org/10.1677/joe.0.1780149.
Zewinger, Stephen, Thomas Rauen, Michael Rudnicki, Giuseppina Federico, Martina Wagner, Sarah Triem, Stefan J. Schunk, et al. "Dickkopf-3 (DKK3) in Urine Identifies Patients with Short-Term Risk of eGFR Loss." Journal of the American Society of Nephrology 29, no. 11 (October 2, 2018): 2722–33. http://dx.doi.org/10.1681/asn.2018040405.
Sciascia, Savino, Alice Barinotti, Massimo Radin, Irene Cecchi, Elisa Menegatti, Edoardo Terzolo, Daniela Rossi, Simone Baldovino, Roberta Fenoglio, and Dario Roccatello. "Dickkopf Homolog 3 (DKK3) as a Prognostic Marker in Lupus Nephritis: A Prospective Monocentric Experience." Journal of Clinical Medicine 11, no. 11 (May 25, 2022): 2977. http://dx.doi.org/10.3390/jcm11112977.
Dziamałek-Macioszczyk, Paulina, Agata Winiarska, Anna Pawłowska, Paweł Wojtacha, and Tomasz Stompór. "Patterns of Dickkopf-3 Serum and Urine Levels at Different Stages of Chronic Kidney Disease." Journal of Clinical Medicine 12, no. 14 (July 15, 2023): 4705. http://dx.doi.org/10.3390/jcm12144705.
Zhang, Yingjie, Huibo Li, Rongyi Cao, Lili Sun, Yan Wang, Shengjin Fan, Yanqiu Zhao та ін. "Suppression of Mir-708 Promotes DKK3 to Inhibit Wnt/β-Catenin Signaling Pathway in Adult B-ALL". Blood 128, № 22 (2 грудня 2016): 5090. http://dx.doi.org/10.1182/blood.v128.22.5090.5090.
Inamoto, Yoshihiro, Paul J. Martin, Stephanie J. Lee, Amin A. Momin, Laura Tabellini, Lynn E. Onstad, Joseph Pidala, et al. "Dickkopf-related protein 3 is a novel biomarker for chronic GVHD after allogeneic hematopoietic cell transplantation." Blood Advances 4, no. 11 (June 3, 2020): 2409–17. http://dx.doi.org/10.1182/bloodadvances.2020001485.
Zhou, Liran, Hongmei Husted, Todd Moore, Mason Lu, Defeng Deng, Yan Liu, Vijaya Ramachandran, et al. "Suppression of stromal-derived Dickkopf-3 (DKK3) inhibits tumor progression and prolongs survival in pancreatic ductal adenocarcinoma." Science Translational Medicine 10, no. 464 (October 24, 2018): eaat3487. http://dx.doi.org/10.1126/scitranslmed.aat3487.
Sciascia, S., M. Radin, A. Barinotti, I. Cecchi, D. Rossi, R. Fenoglio, and D. Roccatello. "POS1448 DICKKOPF HOMOLOG 3 (DKK3) AS A PROGNOSTIC MARKER IN LUPUS NEPHRITIS: A PROSPECTIVE MONOCENTRIC EXPERIENCE." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1069.1–1069. http://dx.doi.org/10.1136/annrheumdis-2022-eular.1254.
Lim, Xinhong, Si Hui Tan, Ka Lou Yu, Sophia Beng Hui Lim та Roeland Nusse. "Axin2 marks quiescent hair follicle bulge stem cells that are maintained by autocrine Wnt/β-catenin signaling". Proceedings of the National Academy of Sciences 113, № 11 (22 лютого 2016): E1498—E1505. http://dx.doi.org/10.1073/pnas.1601599113.
Nguyen, Que Thanh Thanh, Hwang Shin Park, Tae Jin Lee, Kyung-Mi Choi, Joong Yull Park, Daehan Kim, Jae Hyung Kim, Junsoo Park та Eun-Ju Lee. "DKK3, Downregulated in Invasive Epithelial Ovarian Cancer, Is Associated with Chemoresistance and Enhanced Paclitaxel Susceptibility via Inhibition of the β-Catenin-P-Glycoprotein Signaling Pathway". Cancers 14, № 4 (12 лютого 2022): 924. http://dx.doi.org/10.3390/cancers14040924.
Дисертації з теми "Dickkopf-3 (DKK3)":
Mourtada, Jana. "Mécanismes d’activation de la réponse immunitaire par DNp63 dans les cancers des voies aérodigestives supérieures HPV-positifs." Electronic Thesis or Diss., Strasbourg, 2023. http://www.theses.fr/2023STRAJ127.
HPV+ oropharyngeal tumors display both prognostic and molecular heterogeneity. Patients prognosis can be distinguished by the presence or absence of a molecular signature that depends on the ΔNp63 transcription factor. We demonstrated that ΔNp63 inhibits the migratory and invasive capabilities of HPV+ HNSCC cell lines and increases their sensitivity to platinum-based chemotherapy, implying its role in tumor progression. A functional analysis of ΔNp63 revealed its ability to stimulate the phagocytosis of cancer cells by macrophages in vitro. Consistently, a transcriptomic analysis of the same cellular model highlighted that ΔNp63 regulates the expression of secreted factors, including chemokines and interleukins, among which is the DKK3protein. Our findings indicate that DKK3 secretion by cancer cells activates the NF-κB pathway in macrophages, mimicking ΔNp63's effects on phagocytosis regulation. Induction of the NF-κB pathway by DKK3 in macrophages is mediated by its receptor CKAP4. Finally, our analyses suggest that ∆Np63 regulates the expression of factors involved in the inflammasome, as well as those of other cytokines such as TNFRSF11B, CCL26, CCL11, TIMP1 and TIMP2. Altogether, our results show that ΔNp63 plays a unique role in the prognosis of HPV+ patients by regulating secreted molecules involved in the recruitment and immune cell activation
Zheng, Shu-Kai, and 鄭舒凱. "Dickkopf -3 protein ( Dkk3), a novel target gene of zebrafish myf5 intronic microRNA, is involved in the myf5 expression during myogenesis." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/86794154837362841582.
臺灣大學
分子與細胞生物學研究所
95
Myf5, one of myogenesis regulatory factors (MRFs), plays roles in the specification and differentiation of muscular cells during myogenesis. The expression of myf5 is in a somite- and stage-specific manner under a fine-tuned regulation mechanism. Hoi (2006) identified an intronic motif (miR-In, +610/+632) within intron I (+502/+835, I300) of zebrafish myf5. The miR-In can inhibit myf5 expression and regulate muscle development through repressing the expression of myf5. However, the target gene of miR-In is totally unknown. In this study, we found a putative EST sequence of target gene of miR-In by using pull-down assay. Then, the full length of miR-In-putative target gene was identified by using 5’ and 3’ rapid amplification of cDNA ends. The sequence of this clone was blasted with NCBI database and found that it was similar to a Dickkopf 3 protein (dkk3) sequence, named dkk3. Whole mount in situ hybridization showed that the dkk3 transcripts appeared at somites in the 10 hpf zebrafish embryos. The signals of dkk3 at somites were progressively increased and were up to maximum at 16 hpf. But the dkk3 transcripts were gradually decreased after 16 hpf and became quite low after 24 hpf. This expression pattern of dkk3 gene was consistent with that of myf5, suggesting that dkk3 might be involved in the myf5 expression at somites. Knocking down dkk3 with morpholino oligonucleotie (MO) resulted in a down-regulation of myf5 in somites but not in presomitic mesoderm. The phenotype of dkk3-MO injected embryos was similar to the myf5 morphant. At the same time, the embryos of myf5-GFP transgenic zebrafish were injected dkk3 morphant and were observed that fluorescence of GFP was down expression in somites. Co-injection of myf5 mRNA and dkk3-MO could rescue the expression of myogenin in somites, suggesting that dkk3 might influence myf5 expression in somites. The dual-luciferase assay revealed that miR-In enabled to inhibit dkk3 expression through binding to 3’UTR target sequences of dkk3. This is the first report by using pull-down assay to find that dkk3 is a target gene of the miR-In and demonstrate that miR-In could inhibit myf5 expression through repressing dkk3 protein expression during myogenesis in zebrafish.
Fu, Chuan-Yang, та 傅傳揚. "Zebrafish Dickkopf-3-related gene (Dkk3a) regulates thepromoter activity of myf5 through interaction with membranereceptor Integrinα6b". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/56bwx4.
國立臺灣大學
分子與細胞生物學研究所
101
Myogenic regulatory factor Myf5 plays important roles in muscle development. In zebrafish myf5, a microRNA (miR), termed miR-3906 or miR-In300, was reported to silence dickkopf-3-related gene (dkk3r or dkk3a), resulting in repressing myf5 promoter activity. However, the membrane receptor which interacts with ligand Dkk3a to control myf5 expression through signal transduction remains unknown. To address this question, we applied immunoprecipitation and LC-MS/MS mass spectrometry to screen putative membrane receptors of Dkk3a, and Integrin α6b (Itgα6b) was finally identified. To further confirm this, we employed cell-surface binding assays which showed that Dkk3a and Itgα6b co-expressed at the cell membrane of HEK-293T cells. Crosslinking immunoprecipitation data also showed high affinity of Itgα6b for Dkk3a. We further proved that the β-propeller repeated domains of Itgα6b are key segments bound by Dkk3a. Moreover, when dkk3a and itgα6b mRNAs were co-injected into embryos, luciferase activity was upregulated four-fold greater than that of control embryos. In contrast, the luciferase activities of dkk3a-knockdown embryos co-injected with itgα6b mRNA and itgα6b-knockdown embryos co-injected with dkk3a mRNA were decreased in a manner similar to control embryos, respectively. Knockdown of itgα6b resulted in abnormal somite shape, fewer somitic cells, weaker, or absent, myf5 expression, and reduced protein level of phosphorylated p38a in somites. These defective phenotypes of trunk muscular development were similar to those of dkk3a-knockdown embryos. We demonstrated that the secreted ligand Dkk3a binds to the membrane receptor Itgα6b, which increases the protein level of phosphorylated p38a and activates myf5 promoter activity of zebrafish embryos during myogenesis.
Su, Ying-Fang, and 蘇盈方. "Zebrafish Dickkopf-3-related gene (Dkk3r) regulates the promoter activity of myogenic regulatory factor myf5 gene through interaction with membrane receptor of Integrin alpha 6b." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/59233074383649141970.
國立臺灣大學
分子與細胞生物學研究所
99
Myf5, one of the myogenic regulatory factors, plays important roles in the specification and differentiation of muscular cells during myogenesis. In zebrafish, an intronic microRNA (miR), miR-3906, located within myf5 intron I, has been reported to silence the translation of its target gene, dickkopf-3-related (dkk3r) gene. Dkk3r, a secretory protein, regulates the phosporylation of p38a to maintain Smad4 stability, which, in turn, enabling the Smad2/Smad3a/Smad4 complex to form and to activate the myf5 promoter in nucleus. However, the membrane receptor(s) bound by Dkk3r to control signal transduction is still unknown. After recombinant zebrafish Dkk3r tagged with Flag was produced by insect cells, we applied protein immunoprecipitation and mass spectromotry to screen the putative receptors of Dkk3r. We found that Integrin alpha 6b (Itga6b) might be one of receptors to interact with Dkk3r. To further confirm this hypothesis, we used whole-mount in situ hybridization and found that the transcripts of both dkk3r and itga6b were presented in somites at 16 hpf during myogenesis. By in vitro cell surface binding assay, we also observed that Dkk3r and Itga6b were co-expressed at the cell membrane of HEK-293T, indicating that the temporal and spatial expressions of dkk3r and itga6b are co-localized. Furthermore, in vivo luciferase assay demonstrated that the luciferase activity driven by myf5 promoter was 223% and 217% greater than that of control when the excessive dkk3r and itga6b mRNAs were injected into embryos, respectively. Interestingly, when we co-injected dkk3r and itga6b mRNAs into embryos, the luciferase activity was up-regulated as high as 397% greater than that of control embryos. This up-regulation of myf5 promoter activity mediated by interaction between dkk3r and itga6b was dosage-dependent. In contrast, when dkk3r was knockdown and co-injected with itga6b mRNA, the luciferase activity was down-regulated to 69% of control embryos, suggesting that the regulatory effect of Itga6b on the downstream activity is dependent on Dkk3r signal pathway. In addition, knockdown of itga6b by injection of itga6b-morpholinos resulted in abnormal shape of somites and weak or even absent expression of myf5 in somites at 16 hpf. Furthermore, knockdown of itga6b reduced the protein level of the phosphorylated p38a. Taken together, we concluded that it is highly likely that Itga6b functions as a receptor of Dkk3r. Their interactions drive the downstream signal transduction to regulate myf5 promoter activity in somites during the development of zebrafish embryos.
Тези доповідей конференцій з теми "Dickkopf-3 (DKK3)":
Zhou, Liran, Hongmei Husted, Todd Moore, Mason Lu, Defeng Deng, Yan Liu, Vijaya Ramachandran, et al. "Abstract 2961: Targeting stromal-derived Dickkopf-3 (DKK3) for the treatment of pancreatic ductal adenocarcinoma (PDAC)." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2961.
Ueno, Koji, Hiroshi Hirata, Soichiro Yamamura, Sharanjot Saini, Shahana Majid, Peter R. Carroll, and Rajvir Dahiya. "Abstract 5002: Functional significance and mechanisms of inactivation of Secreted Wnt antagonist DICKKOPF-3 (DKK-3) gene in human renal cell carcinoma." 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.am10-5002.