Littérature scientifique sur le sujet « DUSP28 »
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Articles de revues sur le sujet "DUSP28"
Chen, Hsueh-Fen, Huai-Chia Chuang et Tse-Hua Tan. « Regulation of Dual-Specificity Phosphatase (DUSP) Ubiquitination and Protein Stability ». International Journal of Molecular Sciences 20, no 11 (30 mai 2019) : 2668. http://dx.doi.org/10.3390/ijms20112668.
Texte intégralChuang et Tan. « MAP4K Family Kinases and DUSP Family Phosphatases in T-Cell Signaling and Systemic Lupus Erythematosus ». Cells 8, no 11 (13 novembre 2019) : 1433. http://dx.doi.org/10.3390/cells8111433.
Texte intégralLim, S., J. A. Green, H. Wong, M. E. VanderBurg et T. Crook. « DUSP7 and DUSP8 promoter hypermethylations : Predictors of clinical outcomes in advanced epithelial ovarian carcinoma ». Journal of Clinical Oncology 25, no 18_suppl (20 juin 2007) : 5501. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.5501.
Texte intégralBermudez, O., G. Pagès et C. Gimond. « The dual-specificity MAP kinase phosphatases : critical roles in development and cancer ». American Journal of Physiology-Cell Physiology 299, no 2 (août 2010) : C189—C202. http://dx.doi.org/10.1152/ajpcell.00347.2009.
Texte intégralJeong, Dae-Gwin, Song-Yi Kim, Jeong-Hun Yun et Jae-Hoon Kim. « Characterization of a Dual-Specificity Protein Phosphatase, Human DUSP28 ». Journal of Life Science 21, no 1 (30 janvier 2011) : 31–35. http://dx.doi.org/10.5352/jls.2011.21.1.31.
Texte intégralHahn, Cynthia K., Rachel J. West, Elizabeth R. Macari, Emily K. Schaeffer et Christopher H. Lowrey. « Dual-Specificity Phosphatases (DUSPs) Are Potential Targets for Pharmacologic Induction of Fetal Hemoglobin ». Blood 116, no 21 (19 novembre 2010) : 2075. http://dx.doi.org/10.1182/blood.v116.21.2075.2075.
Texte intégralDe Roock, W., M. Janssens, B. Biesmans, B. Jacobs, J. De Schutter, S. Fieuws, E. Van Cutsem et S. Tejpar. « DUSPs as markers of MEK/Erk activation in primary colorectal cancer ». Journal of Clinical Oncology 27, no 15_suppl (20 mai 2009) : 4064. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.4064.
Texte intégralThompson, Elliott M., et Andrew W. Stoker. « A Review of DUSP26 : Structure, Regulation and Relevance in Human Disease ». International Journal of Molecular Sciences 22, no 2 (14 janvier 2021) : 776. http://dx.doi.org/10.3390/ijms22020776.
Texte intégralWANG, DONG, SHENG HAN, RUI PENG, CHENYU JIAO, XING WANG, ZEGUANG HAN et XIANGCHENG LI. « DUSP28 contributes to human hepatocellular carcinoma via regulation of the p38 MAPK signaling ». International Journal of Oncology 45, no 6 (16 septembre 2014) : 2596–604. http://dx.doi.org/10.3892/ijo.2014.2653.
Texte intégralCooper, Lisa M., Rita C. West, Caleb S. Hayes et David S. Waddell. « Dual-specificity phosphatase 29 is induced during neurogenic skeletal muscle atrophy and attenuates glucocorticoid receptor activity in muscle cell culture ». American Journal of Physiology-Cell Physiology 319, no 2 (1 août 2020) : C441—C454. http://dx.doi.org/10.1152/ajpcell.00200.2020.
Texte intégralThèses sur le sujet "DUSP28"
Patterson, Kate Isabel Garvan Institute of Medical Research Faculty of Medicine UNSW. « Characterisation of the atypical dual specificity phosphatase DUSP26 ». Publisher:University of New South Wales. Garvan Institute of Medical Research, 2009. http://handle.unsw.edu.au/1959.4/43594.
Texte intégralCain, Erica L. « An investigation of the oncogenic potential and function of the dual specificity phosphatase 12 ». Diss., Kansas State University, 2012. http://hdl.handle.net/2097/16694.
Texte intégralDepartment of Biology
Alexander Beeser
Large-scale genomic approaches have demonstrated many atypical dual specificity phosphatases (DUSPs) are differentially expressed or mutated in cancer. DUSPs are proteins predicted to have the ability to dephosphorylate Ser/Thr and Tyr residues, and the atypical DUSP subgroup contains at least 16 members with diverse substrates that include proteins, nucleic acids, and sugars, and some of the atypical DUSPs function in the cell not as phosphatases but as scaffolds in signal transduction pathways. Of the atypical DUSPs, DUSP12 is one of the most evolutionarily conserved with homologs found in organisms ranging from yeast to humans. DUSP12 is of particular interest as it has been identified to be one of only two candidate genes for the target of a genetic amplification found in liposarcomas. Furthermore, DUSP12 may be an oncogene in that over-expression of dusp12 in cell culture promotes apoptosis resistance, cell motility, and the up-regulation of two established oncogenes, the hepatocyte growth factor receptor (c-met) and integrin alpha 1 (itga1). Additionally, DUSP12 may protect from apoptosis by functioning as a regulator of stress-induced translation repression and stress granule formation that may be due to its interaction with the DEAD Box RNA Helicase, DDX3.
Buffet, Camille. « Anomalies moléculaires de la voie MAPK et cancer papillaire de la thyroïde : étude de deux phosphatases spécifiques de ERK, DUSP5 et DUSP6 ». Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T049/document.
Texte intégralPapillary thyroid cancer (PTC) is the most common endocrine malignancy. Mutually exclusive and activating alterations of the MAPK pathway (Mitogen-Activated Protein Kinases) are identified in 70% of cases. Common mutations found in PTCs are point mutation of the B-RAF (50%) and RAS genes (10%) as well as RET/PTC chromosomal rearrangements (10%). The hot spot B-RAFV600E mutation is the most frequently alteration identified and is connected with agressive clinical characteristics (high stage at diagnosis, high recurrence risk and death). These molecular events lead to constitutive activation of the MAPK pathway, resulting in MEK (Mitogen-activated Extracellular signal-Regulated Kinase) and ERK (Extracellular signal-Regulated Kinase) phosphorylation. ERK is negatively regulated by phosphatases and among them, Dual Specificity Phosphatases (DUSPs), ubiquitary expressed, in particular two ERK-specific phosphatases DUSP5 (nuclear) and DUSP6 (cytosolic). We hypothesized that these phosphatases could have tumor supressor properties (i.e. their loss would be associated with an increase in MAPK pathway activation) or may serve as a surrogate marker of MAPK pathway activation in the context of a negative feedback loop. We analysed regulation and expression of both phosphatases in 3 models: three PCCL3 cell lines (rat thyroid cells) expressing one of the most common oncogene identified in PTCs (RET/PTC3 or H-RASV12 or B-RAFV600E) under the control of a doxycycline-inducible promoter, human PTC-derived cell lines and human PTC. We demonstrated that MAPK pathway activation was correlated with induction of DUSP5 and DUSP6. These phosphatases are involved in a negative feedback loop that contributes to a tight regulation of phospho-ERK levels. DUSP5 and DUSP6 mRNA are overexpressed in human PTCs, especially in B-RAF mutated tumors suggesting a higher MAPK signaling output in these agressive PTCs. Silencing of DUSP5 and/or DUSP6 by small interfering RNA does not affect proliferation of human B-RAFV600E thyroid carcinoma-derived cell lines, suggesting the lack of tumor suppressor gene role. Compensatory changes in expression of DUSPs when a specific one is inactivated may explain this lack of effect. On the opposite, a DUSP6 pharmacological inhibitor induced a concentration dependent decrease in proliferation of human B-RAFV600E cells, suggesting « off-target » effect of this inhibitor. In a second part, we analysed the regulation of DUSP5 expression, which is a target of the MAPK pathway activation. We demonstrated, using pharmacological inhibitors, that DUSP5 is an early response gene, regulated mostly by the MAPK pathway, at the transcriptional level. Two contiguous CArG boxes that bind serum response factor (SRF) were found in a 1Kb promoter region, as well as several E twenty-six transcription factor family binding sites (EBS). These sites potentially bind Elk-1, a transcription factor activated by ERK1/2. Using wild type or mutated DUSP5 promoter reporters, we demonstrated that SRF plays a crucial role in serum induction of DUSP5 promoter activity, the proximal CArG box being important for SRF binding in vitro and in living cells. Moreover Elk-1 was bound in vitro to a promoter region containing the proximal CArG box and a putative EBS. Its specific binding to SRF was necessary to elicit promoter response to dominant positive Elk-VP16 and to enhance the response to serum stimulation. Altogether our results suggest that the MAPK pathway is more active in B-RAFV600E PTC than in PTC with other genetic alteration and could explain their clinical agressivity. DUSP5 and DUSP6, as well as phosphorylated MEK, are markers of activation of the MAPK pathway. Neither phosphatase has tumor suppressor properties in our thyroid cancer cell models. Our results suggest redundancy and functional compensation among DUSPs. (...)
Manley, Grace C. A. « The roles of DUSPs in respiratory viral infection ». Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/19257/.
Texte intégralEmond-Boisjoly, Marc-Alexandre. « Rôle de la protéine DUSP5 dans l’autophagie des cardiomyocytes ». Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/8908.
Texte intégralAbstract: Autophagy is a process essential to the maintenance of cellular homeostasis. It helps degrade and recycle whole organelles and nonfunctional cytoplasmic components. In addition, the adaptative up regulation of autophagy in stress condition promotes cell survival. In cardiomyocytes basal autophagy is essential to the renewal of, among others, mitochondria and proteins forming sarcomeres. In addition, stresses such as ischemic heart or nutrient deficiency induce an increase in protective autophagy. In extreme conditions, it has been suggested that autophagy may exacerbate cardiac disease causing the death of cardiomyocytes. Considering the importance of this process in cardiac pathophysiology, identify ing safety mechanisms regulating autophagy in cardiomyocytes has been the subject of intense research. To this end, activation of mitogen-activated protein kinase (MAPK) has been demonstrated to regulate, with other signaling pathways, autophagy and cardiomyocyte apoptosis. It is therefore likely that Dual-Specificity Phosphatases (DUSPs), key enzymes that control the activity of MAPKs, also participate in the regulation of autophagy. To test this hypothesis, we have induced autophagy in isolated cardiomyocytes of newborn rats in culture. Analysis of autophagy markers by immunoblotting demonstrated that the activation of MAPKs ERK1/2 and p38 correlates with autophagic activity in cardiomyocytes. Under these conditions, the decrease in expression of the majority of mRNAs encoding different DUSPs found in cardiomyocytes contrast sharply with the increase mRNA expression of Dusp5. Furthermore, we demonstrated by again of function study that sustained activation of p38 by overexpression of a constitutively active MKK6 mutant stimulates autophagy in cardiomyocytes. Surprisingly, the loss of p38 function obtained by overexpression of a dominant negative p38 mutant does not affect the autophagic response in our in vitro model, but increases the lipidation of autophagosomes marker LC3. Our results suggest that DUSPs can regulate, through their actions on MAPKs, important stages of autophagy in cardiomyocytes.
Moreaux, Guenievre. « Investigating downstream effectors of KRas signalling in vivo : Dusp6 and Fra1 ». Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/4056/.
Texte intégralArkell, Rebecca Sarah. « Investigations into the regulation of DUSP6 expression in normal and tumour cells ». Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611087.
Texte intégralLi, Weiling. « Genetic changes in melanoma progression ». Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5595.
Texte intégralCasteel, Maximilian Wilhelm. « Bedeutung von DUSP1 und Expression MAPKinasen-spezifischer Transkriptionsfaktoren während der zellulären Antwort auf Deoxynivalenol ». Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-128239.
Texte intégralIntriago, Rachel Elizabeth. « Role and regulation of DUSP-1 in GnRH signaling ». Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1465076.
Texte intégralTitle from first page of PDF file (viewed June 19, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 55-57).
Chapitres de livres sur le sujet "DUSP28"
Lukas, Thomas J., Daniela V. Rosa, Luiz Alexandre V. Magno, Bruno R. Souza, Marco A. Romano-Silva, Hisao Masai, Kazuhisa Kohda et al. « DUSP24 ». Dans Encyclopedia of Signaling Molecules, 538. New York, NY : Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100372.
Texte intégralMonteiro, Lucas Falcão, Pault Yeison Minaya Ferruzo, Lilian Cristina Russo, Jessica Oliveira Farias et Fábio Luís Forti. « DUSP3/VHR : A Druggable Dual Phosphatase for Human Diseases ». Dans Reviews of Physiology, Biochemistry and Pharmacology, 1–35. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/112_2018_12.
Texte intégral« DUSP24 ». Dans Encyclopedia of Signaling Molecules, 1447. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101058.
Texte intégral« DUSP1 ». Dans Encyclopedia of Pain, 1082. Berlin, Heidelberg : Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_100662.
Texte intégral« DUSP6 ». Dans Encyclopedia of Pain, 1082. Berlin, Heidelberg : Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_100663.
Texte intégral« Dual-specificity Phosphatases (DUSP) ». Dans Encyclopedia of Pain, 1081. Berlin, Heidelberg : Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_100657.
Texte intégralFurukawa, Toru, et Akira Horii. « The Role of DUSP6/MKP-3 in Pancreatic Carcinoma ». Dans Handbook of Immunohistochemistry and in situ Hybridization of Human Carcinomas, Volume 3 - Molecular Genetics, Liver Carcinoma, and Pancreatic Carcinoma, 335–39. Elsevier, 2005. http://dx.doi.org/10.1016/s1874-5784(05)80038-8.
Texte intégralUpadhyay, HC, MA Lawson et B. Gangapurkar. « Regulation of DUSP1 Translation by GnRH in the LβT2 Pituitary Gonadotrope Cell Line. » Dans The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P3–224—P3–224. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part3.p5.p3-224.
Texte intégralChen, Chien-Cheng, et Carole R. Mendelson. « Sp1 Response Elements within the MAPK Phosphatase-1 (MKP-1/DUSP1) Promoter Mediate Progesterone Receptor (PR) Induced MKP-1 Expression in Breast Cancer Cells. » Dans Posters I, P3–13—P3–13. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part3.p1.p3-13.
Texte intégral« Table II : Material composition of dust and feedstuff from pig and hen houses. Results from 1)= AENGST (33), 2) = HARTUNG (34), 3)= KOON et al. (21), 4)= HAR-TUNG (32). n.r. = not reported. pig hoi js e (no 1 bedding] hen hou se(b components dust” dust2) feed1) dust3> ; dust4) •/. •/. •/. •/. dry matter 87 87 88 92 89 92 crude protein 24 24 19 60 50 17 fa t4549 10 15 crude fibre 3554 nr. 2 ash 15 nr 5nr nr. 4 Table III : Number of particles collected by the Andersen Sampler and weight of settled dust in an experi mental piggery at different conditions from HONEY and McQUITTY (17) number of particles / 0.028 n3 treatment particle size settled dust 7 -16 jjm <5jjm g/rrfd ay rel humidity (low ) 51 370 119920 13.42 rel humidity (high) 32450 85230 10.03 pen volume 22.1 nf 38200 86420 12.38 pen volume 11.1m3 45630 118 730 11.08 floor feeding 42 770 883 90 15.85 self feeding 41050 116760 7.62 a irflo w 595rr?/h 38650 93820 12.08 a irflo w 297rr?/h 45170 111 330 11.37 average 41900 102580 11.37 ^ TJa ». Dans Odour Prevention and Control of Organic Sludge and Livestock Farming, 343. CRC Press, 1986. http://dx.doi.org/10.1201/9781482286311-137.
Texte intégralActes de conférences sur le sujet "DUSP28"
Andrade, Pamela V., Mariana T. Ruckert, Carlos Alberto O. Biagi Junior et Vanessa S. Silveira. « Abstract C51 : Targeted inhibition of DUSP1 and DUSP6 suppresses pancreatic adenocarcinoma cells’ growth and glucose metabolism via SAPK/JNK pathway activation ». Dans Abstracts : AACR Special Conference on Pancreatic Cancer : Advances in Science and Clinical Care ; September 6-9, 2019 ; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-c51.
Texte intégralMa, Irene T., Yihui Fan, Roma H. Patel, Jin Cheng, Eugene S. Kim, Jason M. Shohet, Jianhua Yang et Sanjeev A. Vasudevan. « Abstract LB-352 : DUSP26 inhibition : a new therapeutic pathway in neuroblastoma. » Dans 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-lb-352.
Texte intégralTsai, Shaw-Jenq, Chu-An Wang et I.-Heng Chang. « Abstract 1786 : Effect of DUSP2 on pancreatic cancer lymphatic dissemination ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1786.
Texte intégralTsai, Shaw-Jenq, Chu-An Wang et I.-Heng Chang. « Abstract 1786 : Effect of DUSP2 on pancreatic cancer lymphatic dissemination ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1786.
Texte intégralWang, CA, IH Chang, CF Li, PC Hou et SJ Tsai. « PO-177 The novel function of DUSP2/VEGF-C axis in pancreatic cancer progression ». Dans Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.216.
Texte intégralKarakashev, Sergey. « Abstract 1824 : Hypoxia induces lapatinib resistance in ErbB2-positive breast cancer cells via regulation of DUSP2 ». Dans Proceedings : AACR Annual Meeting 2014 ; April 5-9, 2014 ; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1824.
Texte intégralKarakashev, Sergey V., et Reginato J. Mauricio. « Abstract PR15 : Hypoxia induces lapatinib resistance in ErbB2-positive breast cancer cells via regulation of DUSP2 ». Dans Abstracts : Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013 ; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-pr15.
Texte intégralLin, Shih-Chieh, et Shaw-Jenq Tsai. « Abstract 3083 : Dual-specificity phosphatase-2 (DUSP2) negatively control cyclooxygenase-2 (COX-2) expression in cancer cells ». Dans Proceedings : AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012 ; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3083.
Texte intégralMurray, James T., Jason Seely, Jeff Plath, Eric Gotfreson, John Engel, Bill Ryder, Neil Van Lieu et al. « Dust-Penetrating (DUSPEN) “see-through” lidar for helicopter situational awareness in DVE ». Dans SPIE Defense, Security, and Sensing, sous la direction de Kenneth L. Bernier et Jeff J. Güell. SPIE, 2013. http://dx.doi.org/10.1117/12.2016439.
Texte intégralMurray, James T., Jason Seely, Jeff Plath, Eric Gotfredson, John Engel, Bill Ryder, Neil Van Lieu et al. « Dust-penetrating (DUSPEN) see-through lidar for helicopter situational awareness in DVE ». Dans SPIE Security + Defence, sous la direction de Gary W. Kamerman, Ove K. Steinvall, Gary J. Bishop et John D. Gonglewski. SPIE, 2013. http://dx.doi.org/10.1117/12.2033921.
Texte intégralRapports d'organisations sur le sujet "DUSP28"
Morse, Alexander. Bioinformatics experiments. Exp 1. Analysis of mechanisms of Cd+2 impact on MAPK-signalling through DUSPs. Part 1. Theory. ResearchHub Technologies, Inc., septembre 2022. http://dx.doi.org/10.55277/researchhub.9y5bc33g.
Texte intégral