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147 documents found
1: Title: Proteome analysis of hypoxic glioblastoma cells reveals sequential metabolic adaptation  of one-carbon metabolic pathways.
Authors: Zhang, Kangling, et.al. .
Journal: Molecular & cellular proteomics : MCP (Mol Cell Proteomics), 2017 .
Snippet: We found that hypoxia affects cancer cells in multiple intertwined ways: inflammation, typically with over-expressed glucose transporter (GLUT1), DUSP4/ MKP2, and RelA proteins; a metabolic adaptation with overexpression of all glycolytic pathway enzymes for pyruvate/lactate synthesis; and the EMT (epithelial-mesenchymal transition) and cancer stem cell (CSC) renewal with characteristic morphological changes and mesenchymal/CSC protein expression profiles.
Affiliation: Pharmacology and Toxicology, University of Texas Madical Branch, United States of America kazhang@utmb.edu. Neuroscience and Cell biology, UTMB. UTMB. Univerisy of Texas Medical Branch, United States of America. Pharmacology, University of Texas Medical Branch. University of Texas Medical Branch. Institute for Translational Sciences, University of Texas Medical Branch. .
2: Title: Germline Stem Cell Activity Is Sustained by SALL4-Dependent Silencing of Distinct Tumor Suppressor Genes.
Authors: Chan, Ai-Leen, et.al. .
Journal: Stem cell reports, Vol. 9 (3): 956-971, 2017 .
Snippet: Mechanistically, SALL4 associated with the NuRD co-repressor and repressed expression of the tumor suppressor genes Foxl1 and Dusp4.
Affiliation: Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC 3800, Australia; Development and Stem Cells Program, Monash Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC 3800, Australia. Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC 3800, Australia. Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC 3800, Australia; Systems Biology Institute Australia, Monash University, Melbourne, VIC 3800, Australia. Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC 3800, Australia; Development and Stem Cells Program, Monash Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC 3800, Australia. Electronic address: robin.hobbs@monash.edu. .
3: Title: Expression Profiling of the MAP Kinase Phosphatase Family Reveals a Role for DUSP1 in the Glioblastoma Stem Cell Niche.
Authors: Mills, Bradley N, et.al. .
Journal: Cancer microenvironment : official journal of the International Cancer Microenvironment Society (Cancer Microenviron), 2017 .
Snippet: Interrogation of the REpository for Molecular BRAin Neoplasia DaTa (REMBRANDT) revealed induction (DUSP4, DUSP6), repression (DUSP2, DUSP7-9), or mixed (DUSP1, DUSP5, DUSP10, DUSP15) DUSP transcription of select DUSPs in bulk tumor specimens.
Affiliation: Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, 14642, USA. Center for Neurotherapeutics Discovery, University of Rochester Medical Center, 601 Elmwood Avenue, Box 645, Rochester, NY, 14642, USA. Center for Neurotherapeutics Discovery, University of Rochester Medical Center, 601 Elmwood Avenue, Box 645, Rochester, NY, 14642, USA. Marc_Halterman@urmc.rochester.edu. Department of Neurology, University of Rochester Medical Center, Rochester, NY, 14642, USA. Marc_Halterman@urmc.rochester.edu. Department of Neuroscience, University of Rochester Medical Center, Rochester, NY, 14642, USA. Marc_Halterman@urmc.rochester.edu. .
4: Title: Metalloprotease-dependent activation of EGFR modulates CD44(+)/CD24(-) populations in triple negative breast cancer cells through the MEK/ERK pathway.
Authors: Wise, Randi, et.al. .
Journal: Breast cancer research and treatment (Breast Cancer Res Treat), 2017 .
Snippet: Furthermore, our findings highlight the role of ligand-mediated EGFR signaling in the control of MEK/ERK pathway output in TNBC tumors without DUSP4 loss.
Affiliation: Department of Biochemistry and Molecular Biophysics, Kansas State University, 141 Chalmers Hall, Manhattan, KS, 66506, USA. Department of Biochemistry and Molecular Biophysics, Kansas State University, 141 Chalmers Hall, Manhattan, KS, 66506, USA. zolkiea@ksu.edu. .
5: Title: Nimbolide suppresses non-small cell lung cancer cell invasion and migration via manipulation of DUSP4 expression and ERK1/2 signaling.
Authors: Lin, Hua, et.al. .
Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie (Biomed Pharmacother), Vol. 92, 2017 .
Snippet: Therefore, nimbolide may act as a novel drug to inhibit NSCLC invasion and metastasis through manipulation of ERK1/2 signaling and DUSP4 expression.
Affiliation: Department of Respiratory Medicine, The Third Xiangya Hospital of Central South University, Changsha 410013, Hunan, China. Department of Clinical Laboratory, The Xiangya Hospital of Central South University, Changsha 410008, Hunan, China. Department of Respiratory Medicine, The Third Xiangya Hospital of Central South University, Changsha 410013, Hunan, China. Electronic address: shenghuasunny@126.com. .
6: Title: Establishment of a Strong Link Between Smoking and Cancer Pathogenesis through DNA Methylation Analysis.
Authors: Ma, Yunlong, et.al. .
Journal: Scientific reports (Sci Rep), Vol. 7 (1): 1811, 2017 .
Snippet: Of these, genes such as DUSP4 and AKT3 are well documented as being involved in smoking-related lung cancer.
Affiliation: State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. Research Center for Air Pollution and Health, Zhejiang University, Hangzhou, China. State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. limd586@outlook.com. Research Center for Air Pollution and Health, Zhejiang University, Hangzhou, China. limd586@outlook.com. Institute for NeuroImmune Pharmacology, Seton Hall University, South Orange, NJ, United States. limd586@outlook.com. .
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7: Title: Dual-Specificity Phosphatase 4 Overexpression in Cells Prevents Hypoxia/Reoxygenation-Induced Apoptosis via the Upregulation of eNOS.
Authors: Dougherty, Julie A, et.al. .
Journal: Frontiers in cardiovascular medicine (Front Cardiovasc Med), Vol. 4, 2017 .
Snippet: These results further support our hypothesis that DUSP4 is an antioxidant gene and a key phosphatase in modulating MAPKs, especially p38, during oxidative stress, which regulates ROS generation and eNOS expression and thus protects against oxidant-induced injury or apoptosis.
Affiliation: Department of Emergency Medicine, College of Medicine, The Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, USA. .
8: Title: IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition.
Authors: Gaggianesi, Miriam, et.al. .
Journal: Cancer research (Cancer Res), Vol. 77 (12): 3268-3279, 2017 .
Snippet: Mechanistically, RNAi-mediated attenuation of DUSP4 activated the ERK and p38 MAPK pathways, increased stem-like properties, and spawned metastatic capacity.
Affiliation: Department of Surgical, Oncological and Stomatological Sciences, University of Palermo, Palermo, Italy. Regina Elena National Cancer Institute, Rome, Italy. Central Laboratory of Advanced Diagnosis and Biomedical Research (CLADIBIOR), University of Palermo, Palermo, Italy. Department of Biopathology and Biomedical Methodologies, University of Palermo, Palermo, Italy. Department of DIBIMIS, University of Palermo, Palermo, Italy. Department of Emergency, General Surgery and Organ Transplants, University of Palermo, Palermo, Italy. Central Laboratory of Advanced Diagnosis and Biomedical Research (CLADIBIOR), University of Palermo, Palermo, Italy. matilde.todaro@gmail.com. .
9: Title: Impaired Dual-Specificity Protein Phosphatase DUSP4 Reduces Corticosteroid Sensitivity.
Authors: Kobayashi, Yoshiki, et.al. .
Journal: Molecular pharmacology (Mol Pharmacol), Vol. 91 (5): 475-481, 2017 .
Snippet: The nuclear/cytoplasmic GR, phosphorylation levels of GR-Ser(226) and JNK1, coimmunoprecipitated GR-JNK1-DUSP4, and DUSP4 expression were analyzed by western blotting and/or imaging flow cytometry.
Affiliation: Airway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom (Y.K., K.I., N.M., P.J.B.); and Airway Disease Section, Department of Otolaryngology, Kansai Medical University, Moriguchi, Osaka, Japan (Y.K., A.K., K.T.). Airway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom (Y.K., K.I., N.M., P.J.B.); and Airway Disease Section, Department of Otolaryngology, Kansai Medical University, Moriguchi, Osaka, Japan (Y.K., A.K., K.T.) p.j.barnes@imperial.ac.uk. .
10: Title: Sanguinarine inhibits growth and invasion of gastric cancer cells via regulation of the DUSP4/ERK pathway.
Authors: Zhang, Rui, et.al. .
Journal: Journal of cellular and molecular medicine (J Cell Mol Med), Vol. 21 (6): 1117-1127, 2017 .
Snippet: Further observation demonstrated that sanguinarine up-regulated the expression of DUSP4 and Bcl-2-associated X protein (Bax), but down-regulated phosphorylated extracellular signal-regulated kinase (p-ERK), proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 2 (MMP-2) and B-cell lymphoma 2 (Bcl-2) expression.
Affiliation: Department of Gastroenterology, Shanghai Jiao Tong University Affiliated Shanghai Sixth People's Hospital, Shanghai, China. .
11: Title: Statins affect ETS1-overexpressing triple-negative breast cancer cells by restoring DUSP4 deficiency.
Authors: Jung, Hae Hyun, et.al. .
Journal: Scientific reports (Sci Rep), Vol. 6, 2016 .
Snippet: Accordingly, our study indicates that simvastatin potentially affects the activity of transcriptional factors such as ets-1 and dusp4 through the MAPK pathway.
Affiliation: Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Korea. Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Korea. Biomedical Research Institute, Samsung Medical Center, Seoul 06351, Korea. .
12: Title: Analysis of phosphatases in ER-negative breast cancers identifies DUSP4 as a critical regulator of growth and invasion.
Authors: Mazumdar, Abhijit, et.al. .
Journal: Breast cancer research and treatment (Breast Cancer Res Treat), Vol. 158 (3): 441-54, 2016 .
Snippet: Our studies show that induced DUSP4 expression blocks the cell cycle at the G1/S checkpoint; inhibits ERK1/2, p38, JNK1, RB, and NFkB p65 phosphorylation; and inhibits invasiveness of TNBC cells.
Affiliation: Department of Clinical Cancer Prevention, The University of Texas M.D. Anderson Cancer Center, Houston, TX, 77030, USA. Department of Medicine and the Dan L. Duncan Cancer Center, Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, USA. Methodist Cancer Center, The Methodist Hospital Research Institute, Houston, USA. Department of Systems Biology, The University of Texas M.D. Anderson Cancer Center, Houston, USA. Department of Clinical Cancer Prevention, The University of Texas M.D. Anderson Cancer Center, Houston, TX, 77030, USA. phbrown@mdanderson.org. .
13: Title: Regulatory Roles of MAPK Phosphatases in Cancer.
Authors: Low, Heng Boon, et.al. .
Journal: Immune network (Immune Netw), Vol. 16 (2): 85-98, 2016 .
Snippet: Studies using mice deficient in specific MKPs including MKP1/DUSP1, PAC-1/DUSP2, MKP2/DUSP4, MKP5/DUSP10 and MKP7/DUSP16 demonstrated that these molecules are important not only for both innate and adaptive immune responses, but also for metabolic homeostasis.
Affiliation: Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, Singapore.; Immunology Programme, The Life Science Institute, National University of Singapore, Singapore 117597, Singapore. .
14: Title: DUSP4/MKP2 overexpression is associated with BRAF(V600E) mutation and aggressive behavior of papillary thyroid cancer.
Authors: Ma, Ben, et.al. .
Journal: OncoTargets and therapy (Unknown Journal), Vol. 9, 2016 .
Snippet: Initially, we compared PTC tissues with paired normal tissues in DUSP4 expression using Student's t-test, and then analyzed the correlation of DUSP4 with clinicopathological variables and BRAF(V600E) mutation in PTC using Mann-Whitney U, Kruskal-Wallis, χ (2), and Fisher's exact tests.
Affiliation: Department of Head and Neck Surgery, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China; Department of Oncology, Shanghai Medical College, Fudan University, Minhang Hospital, Shanghai, People's Republic of China. Department of Head and Neck Surgery, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China; Department of Oncology, Shanghai Medical College, Fudan University, Minhang Hospital, Shanghai, People's Republic of China; Department of General Surgery, Fudan University, Minhang Hospital, Shanghai, People's Republic of China. .
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15: Title: A novel EGR-1 dependent mechanism for YB-1 modulation of paclitaxel response in a triple negative breast cancer cell line.
Authors: Lasham, Annette, et.al. .
Journal: International journal of cancer (Int J Cancer), Vol. 139 (5): 1157-70, 2016 .
Snippet: We found that low EGR1 mRNA levels are associated with poor breast cancer patient prognosis, and that EGR1 and YBX1 mRNA expression was inversely correlated in a TNBC line and in a proportion of TNBC tumours.
Affiliation: Department of Molecular Medicine and Pathology, School of Medical Sciences, University of Auckland, Auckland, New Zealand. Maurice Wilkins Centre, University of Auckland, Auckland, New Zealand. Department of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand. Bioinformatics Institute, University of Auckland, Auckland, New Zealand. Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand. Systems Biology Laboratory, Melbourne School of Engineering, University of Melbourne, Melbourne, Australia. Department of Obstetrics and Gynaecology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand. .
16: Title: Genomic Loss of DUSP4 Contributes to the Progression of Intraepithelial Neoplasm of Pancreas to Invasive Carcinoma.
Authors: Hijiya, Naoki, et.al. .
Journal: Cancer research (Cancer Res), Vol. 76 (9): 2612-25, 2016 .
Snippet: revealed that DUSP4, an MAPK phosphatase, was significantly downregulated in cells lacking 8p11.22-ter as well as in invasive carcinomas due to genomic loss.
Affiliation: Department of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan. Department of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan. Department of Hepatogastroenterology, Military Central Hospital, Hanoi, Vietnam. Department of Gastroenterological and Pediatric Surgery, Faculty of Medicine, Oita University, Oita, Japan. Department of Forensic Medicine, Faculty of Medicine, Oita University, Oita, Japan. Department of Human Anatomy, Faculty of Medicine, Oita University, Oita, Japan. Department of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan. Department of Medical Oncology and Hematology, Faculty of Medicine, Oita University, Oita, Japan. Department of Medical Oncology and Hematology, Faculty of Medicine, Oita University, Oita, Japan. Department of Radiology, Faculty of Medicine, Oita University, Oita, Japan. Department of Computer Science/Scientific and Engineering Simulation, Nagoya Institute of Technology, Nagoya, Japan. Division of Molecular Medicine, Aichi Cancer Center, Nagoya, Japan. Division of Molecular Pathology, Aichi Cancer Center, Nagoya, Japan. Division of Cell Signaling and Molecular Medicine, Institute of Medical Sciences, University of Tokyo, Tokyo, Japan. Department of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan. mmoriyam@oita-u.ac.jp. .
17: Title: Ulcerative Colitis-Associated Long Noncoding RNA, BC012900, Regulates Intestinal Epithelial Cell Apoptosis.
Authors: Wu, Feng, et.al. .
Journal: Inflammatory bowel diseases (Inflamm Bowel Dis), Vol. 22 (4): 782-95, 2016 .
Snippet: Furthermore, BC012900 overexpression in epithelial cells results in a significant inhibition of cell proliferation and an increased susceptibility to apoptosis, which differ from its adjacent gene DUSP4.
Affiliation: *Section of Gastroenterology and Hepatology, Department of Medicine, University of Chicago, Chicago, Illinois; and †Division of Digestive and Liver Diseases, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas. .
18: Title: Mitogen-Activated Protein Kinase Phosphatase-2 Deletion Impairs Synaptic Plasticity and Hippocampal-Dependent Memory.
Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci), Vol. 36 (8): 2348-54, 2016 .
Snippet: Here, using transgenic mice where the Dusp4 gene encoding MKP-2 has been knocked out (MKP-2(-/-) mice), we show that long-term potentiation is impaired in MKP-2(-/-) mice compared with MKP-2(+/+) controls whereas neuronal excitability, evoked synaptic transmission, and paired-pulse facilitation remain unaltered.
Affiliation: Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow G4 0RE, United Kingdom, and. Medical Research Council Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom. Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow G4 0RE, United Kingdom, and trevor.bushell@strath.ac.uk. .
19: Title: Differential Roles for DUSP Family Members in Epithelial-to-Mesenchymal Transition and Cancer Stem Cell Regulation in Breast Cancer.
Authors: Boulding, Tara, et.al. .
Journal: PloS one, Vol. 11 (2): e0148065, 2016 .
Snippet: Here we show that DUSP1, DUSP4, and DUSP6 are involved in epithelial-to-mesenchymal transition (EMT) and breast cancer stem cell (CSC) regulation.
Affiliation: Health Research Institute, Faculty of ESTeM, University of Canberra, Bruce, ACT, 2617, Australia. Anatomical Pathology, ACT Pathology, The Canberra Hospital, Garran ACT, 2605, Australia. ANU Medical School, Australian National University, Acton, ACT, 2601, Australia. Department of Medical Oncology, The Canberra Hospital, ACT, Garran, 2605 Australia. .
20: Title: Does mouse embryo primordial germ cell activation start before implantation as suggested by single-cell transcriptomics dynamics?
Authors: Gerovska, Daniela, et.al. .
Journal: Molecular human reproduction (Mol Hum Reprod), Vol. 22 (3): 208-25, 2016 .
Snippet: Among the transitory E3.5 PE markers (Dnmt3l, Dusp4, Cpne8, Akap13, Dcaf12l1, Aaed1, B4galt6, BC100530, Rnpc3, Tfpi, Lgalsl, Ckap4 and Fbxl20), several (Dusp4, Akap13, Cpn8, Dcaf12l1 and Tfpi) are related to the extracellular regulated kinase pathway.
Affiliation: Group of Computational Biology and Systems Biomedicine, Biodonostia Health Research Institute, Calle Doctor Beguiristain s/n, 20014 San Sebastián - Donostia, Spain. Group of Computational Biology and Systems Biomedicine, Biodonostia Health Research Institute, Calle Doctor Beguiristain s/n, 20014 San Sebastián - Donostia, Spain IKERBASQUE, Basque Foundation for Science, Bilbao, Spain mararabra@yahoo.co.uk. .
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