Literatura académica sobre el tema "DUSP28"
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Artículos de revistas sobre el tema "DUSP28"
Chen, Hsueh-Fen, Huai-Chia Chuang y Tse-Hua Tan. "Regulation of Dual-Specificity Phosphatase (DUSP) Ubiquitination and Protein Stability". International Journal of Molecular Sciences 20, n.º 11 (30 de mayo de 2019): 2668. http://dx.doi.org/10.3390/ijms20112668.
Texto completoChuang y Tan. "MAP4K Family Kinases and DUSP Family Phosphatases in T-Cell Signaling and Systemic Lupus Erythematosus". Cells 8, n.º 11 (13 de noviembre de 2019): 1433. http://dx.doi.org/10.3390/cells8111433.
Texto completoLim, S., J. A. Green, H. Wong, M. E. VanderBurg y T. Crook. "DUSP7 and DUSP8 promoter hypermethylations: Predictors of clinical outcomes in advanced epithelial ovarian carcinoma". Journal of Clinical Oncology 25, n.º 18_suppl (20 de junio de 2007): 5501. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.5501.
Texto completoBermudez, O., G. Pagès y C. Gimond. "The dual-specificity MAP kinase phosphatases: critical roles in development and cancer". American Journal of Physiology-Cell Physiology 299, n.º 2 (agosto de 2010): C189—C202. http://dx.doi.org/10.1152/ajpcell.00347.2009.
Texto completoJeong, Dae-Gwin, Song-Yi Kim, Jeong-Hun Yun y Jae-Hoon Kim. "Characterization of a Dual-Specificity Protein Phosphatase, Human DUSP28". Journal of Life Science 21, n.º 1 (30 de enero de 2011): 31–35. http://dx.doi.org/10.5352/jls.2011.21.1.31.
Texto completoHahn, Cynthia K., Rachel J. West, Elizabeth R. Macari, Emily K. Schaeffer y Christopher H. Lowrey. "Dual-Specificity Phosphatases (DUSPs) Are Potential Targets for Pharmacologic Induction of Fetal Hemoglobin". Blood 116, n.º 21 (19 de noviembre de 2010): 2075. http://dx.doi.org/10.1182/blood.v116.21.2075.2075.
Texto completoDe Roock, W., M. Janssens, B. Biesmans, B. Jacobs, J. De Schutter, S. Fieuws, E. Van Cutsem y S. Tejpar. "DUSPs as markers of MEK/Erk activation in primary colorectal cancer". Journal of Clinical Oncology 27, n.º 15_suppl (20 de mayo de 2009): 4064. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.4064.
Texto completoThompson, Elliott M. y Andrew W. Stoker. "A Review of DUSP26: Structure, Regulation and Relevance in Human Disease". International Journal of Molecular Sciences 22, n.º 2 (14 de enero de 2021): 776. http://dx.doi.org/10.3390/ijms22020776.
Texto completoWANG, DONG, SHENG HAN, RUI PENG, CHENYU JIAO, XING WANG, ZEGUANG HAN y XIANGCHENG LI. "DUSP28 contributes to human hepatocellular carcinoma via regulation of the p38 MAPK signaling". International Journal of Oncology 45, n.º 6 (16 de septiembre de 2014): 2596–604. http://dx.doi.org/10.3892/ijo.2014.2653.
Texto completoCooper, Lisa M., Rita C. West, Caleb S. Hayes y 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, n.º 2 (1 de agosto de 2020): C441—C454. http://dx.doi.org/10.1152/ajpcell.00200.2020.
Texto completoTesis sobre el tema "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.
Texto completoCain, 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.
Texto completoDepartment 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.
Texto completoPapillary 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/.
Texto completoEmond-Boisjoly, Marc-Alexandre. "Rôle de la protéine DUSP5 dans l’autophagie des cardiomyocytes". Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/8908.
Texto completoAbstract: 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/.
Texto completoArkell, 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.
Texto completoLi, Weiling. "Genetic changes in melanoma progression". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5595.
Texto completoCasteel, 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.
Texto completoIntriago, 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.
Texto completoTitle from first page of PDF file (viewed June 19, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 55-57).
Capítulos de libros sobre el tema "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". En Encyclopedia of Signaling Molecules, 538. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100372.
Texto completoMonteiro, Lucas Falcão, Pault Yeison Minaya Ferruzo, Lilian Cristina Russo, Jessica Oliveira Farias y Fábio Luís Forti. "DUSP3/VHR: A Druggable Dual Phosphatase for Human Diseases". En Reviews of Physiology, Biochemistry and Pharmacology, 1–35. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/112_2018_12.
Texto completo"DUSP24". En Encyclopedia of Signaling Molecules, 1447. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101058.
Texto completo"DUSP1". En Encyclopedia of Pain, 1082. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_100662.
Texto completo"DUSP6". En Encyclopedia of Pain, 1082. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_100663.
Texto completo"Dual-specificity Phosphatases (DUSP)". En Encyclopedia of Pain, 1081. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_100657.
Texto completoFurukawa, Toru y Akira Horii. "The Role of DUSP6/MKP-3 in Pancreatic Carcinoma". En 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.
Texto completoUpadhyay, HC, MA Lawson y B. Gangapurkar. "Regulation of DUSP1 Translation by GnRH in the LβT2 Pituitary Gonadotrope Cell Line." En 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.
Texto completoChen, Chien-Cheng y 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." En Posters I, P3–13—P3–13. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part3.p1.p3-13.
Texto completo"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". En Odour Prevention and Control of Organic Sludge and Livestock Farming, 343. CRC Press, 1986. http://dx.doi.org/10.1201/9781482286311-137.
Texto completoActas de conferencias sobre el tema "DUSP28"
Andrade, Pamela V., Mariana T. Ruckert, Carlos Alberto O. Biagi Junior y Vanessa S. Silveira. "Abstract C51: Targeted inhibition of DUSP1 and DUSP6 suppresses pancreatic adenocarcinoma cells’ growth and glucose metabolism via SAPK/JNK pathway activation". En 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.
Texto completoMa, Irene T., Yihui Fan, Roma H. Patel, Jin Cheng, Eugene S. Kim, Jason M. Shohet, Jianhua Yang y Sanjeev A. Vasudevan. "Abstract LB-352: DUSP26 inhibition: a new therapeutic pathway in neuroblastoma." En 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.
Texto completoTsai, Shaw-Jenq, Chu-An Wang y I.-Heng Chang. "Abstract 1786: Effect of DUSP2 on pancreatic cancer lymphatic dissemination". En 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.
Texto completoTsai, Shaw-Jenq, Chu-An Wang y I.-Heng Chang. "Abstract 1786: Effect of DUSP2 on pancreatic cancer lymphatic dissemination". En 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.
Texto completoWang, CA, IH Chang, CF Li, PC Hou y SJ Tsai. "PO-177 The novel function of DUSP2/VEGF-C axis in pancreatic cancer progression". En 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.
Texto completoKarakashev, Sergey. "Abstract 1824: Hypoxia induces lapatinib resistance in ErbB2-positive breast cancer cells via regulation of DUSP2". En 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.
Texto completoKarakashev, Sergey V. y Reginato J. Mauricio. "Abstract PR15: Hypoxia induces lapatinib resistance in ErbB2-positive breast cancer cells via regulation of DUSP2". En 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.
Texto completoLin, Shih-Chieh y Shaw-Jenq Tsai. "Abstract 3083: Dual-specificity phosphatase-2 (DUSP2) negatively control cyclooxygenase-2 (COX-2) expression in cancer cells". En 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.
Texto completoMurray, 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". En SPIE Defense, Security, and Sensing, editado por Kenneth L. Bernier y Jeff J. Güell. SPIE, 2013. http://dx.doi.org/10.1117/12.2016439.
Texto completoMurray, 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". En SPIE Security + Defence, editado por Gary W. Kamerman, Ove K. Steinvall, Gary J. Bishop y John D. Gonglewski. SPIE, 2013. http://dx.doi.org/10.1117/12.2033921.
Texto completoInformes sobre el tema "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., septiembre de 2022. http://dx.doi.org/10.55277/researchhub.9y5bc33g.
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