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81 documents found
1: Title: Gene co-expression network analysis identifies the hub genes associated with immune functions for nocturnal hemodialysis in patients with end-stage renal disease.
Authors: Dai, Hongwei, et.al. .
Journal: Medicine (Medicine (baltimore)), Vol. 97 (37): e12018, 2018 .
Snippet: We found that NHD had a significant effect on neutrophil activation and immune response in patients with ESRD.In addition, Our findings suggest that MAPKAPK3, RHOA, ARRB2, FLOT1, MYH9, PRKCD, RHOG, PTPN6, MAPK3, CNPY3, PI3KCG, and PYGL genes maybe potential targets regulated by core transcriptional factors, including ARNT, C/EBPalpha, CEBPA, CREB1, PSG1, DAND5, SP1, GATA1, MYC, EGR2, and EGR3.
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2: Title: The implication from RAS/RAF/ERK signaling pathway increased activation in epirubicin treated triple negative breast cancer.
Authors: Huang, Jianbo, et.al. .
Journal: Oncotarget, Vol. 8 (64): 108249-108260, 2017 .
Snippet: MAPK13, MAP3K1, MAPK12, MAPK11 and MAPKAPK3) were obviously enriched, also, expression of ERK pathway positive regulation genes significantly increased (P<0.05) and negative regulation genes decreased (P<0.05) in epirubicin resistant cells.
Affiliation: Department of Endocrine & Breast Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. Department of Oncology, Yongchuan Hospital of Chongqing Medical University, Chongqing 402160, China. .
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3: Title: The p38-MK2/3 Module Is Critical for IL-33-Induced Signaling and Cytokine Production in Dendritic Cells.
Authors: Göpfert, Christiane, et.al. .
Journal: Journal of immunology (Baltimore, Md. : 1950) (J Immunol), Vol. 200 (3): 1198-1206, 2018 .
Snippet: In addition, GM-CSF, which is critical for the differentiation and proliferation of bone marrow-derived dendritic cells, potentiates the p65-dependent IL-6 and the p38-MK2/3-dependent IL-13 production.
Affiliation: Institute of Immunology, Jena University Hospital, 07743 Jena, Germany. Department of Gynecology, Jena University Hospital, Friedrich-Schiller University, 07743 Jena, Germany; and. Institute for Cell Biochemistry, Medical School Hannover, 30625 Hannover, Germany. Institute of Immunology, Jena University Hospital, 07743 Jena, Germany; Sebastian.Drube@med.uni-jena.de. .
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4: Title: Pharmacological and Genetic Inhibition of Downstream Targets of p38 MAPK in Experimental Nephrotic Syndrome.
Authors: Nie, Xiaojing, et.al. .
Journal: American journal of physiology. Renal physiology (Am J Physiol Renal Physiol), 2017 .
Snippet: We hypothesized that the downstream targets of p38MAPK, MK2 and/or MK3, play an important role in mediating injury in experimental nephrotic syndrome via their actions on their downstream substrates HSPB1 and COX-2.
Affiliation: 1 Fuzhou Dongfang Hospital. 2 The Research Institute at Nationwide Children's Hospital. 3 University of Miami. .
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5: Title: p38(MAPK)/MK2-dependent phosphorylation controls cytotoxic RIPK1 signalling in inflammation and infection.
Authors: Menon, Manoj B, et.al. .
Journal: Nature cell biology (Nat Cell Biol), Vol. 19 (10): 1248-1259, 2017 .
Snippet: p38(MAPK)/MK2 interact with RIPK1 in a cytoplasmic complex and MK2 phosphorylates mouse RIPK1 at Ser321/336 in response to pro-inflammatory stimuli, such as TNF and LPS, and infection with the pathogen Yersinia enterocolitica.
Affiliation: Institute of Cell Biochemistry, Hannover Medical School, Hannover 30625, Germany. Institute for Medical Microbiology, Virology and Hygiene, University Medical Center Eppendorf, Hamburg 20246, Germany. .
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6: Title: MK2/3 Are Pivotal for IL-33-Induced and Mast Cell-Dependent Leukocyte Recruitment and the Resulting Skin Inflammation.
Authors: Drube, Sebastian, et.al. .
Journal: Journal of immunology (Baltimore, Md. : 1950) (J Immunol), Vol. 197 (9): 3662-3668, 2016 .
Snippet: We aimed to define the relevance of the p38-targets, the MAPK-activated protein kinases 2 and 3 (MK2 and MK3) in IL-33-induced signaling and the resulting mast cell effector functions in vitro and in vivo.
Affiliation: Institute of Immunology, Jena University Hospital, 07743 Jena, Germany; Sebastian.Drube@med.uni-jena.de. Institute of Immunology, Jena University Hospital, 07743 Jena, Germany. Institute of Immunology, Technical University Dresden, Medical Faculty Carl Gustav Carus, 01307 Dresden, Germany. Department of Gynecology, Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. Institute of Pharmacology and Toxicology, Jena University Hospital, Friedrich Schiller University Jena, 07747 Jena, Germany; and. Department of Biochemistry, Hannover Medical School, 30623 Hannover, Germany. .
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7: Title: Martinique Crinkled Retinal Pigment Epitheliopathy: Clinical Stages and Pathophysiologic Insights.
Authors: Jean-Charles, Albert, et.al. .
Journal: Ophthalmology, Vol. 123 (10): 2196-204, 2016 .
Snippet: PURPOSE: To reappraise the autosomal dominant Martinique crinkled retinal pigment epitheliopathy (MCRPE) in light of the knowledge of its associated mutated gene mitogen-activated protein kinase-activated protein kinase 3 (MAPKAPK3), an actor in the p38 mitogen-activated protein kinase pathway.
Affiliation: Department of Ophthalmology, University Hospital of Fort de France, Martinique (FWI), France. Fondation Adolphe de Rothschild, Paris, France; CHNO des Quinze-Vingts, DHU Sight Restore, INSERM-DHOS CIC1423, Paris - Sorborne Universités, UPMC Univ Paris 06, INSERM, CNRS, Institut de la Vision, Paris - Institute of Ophthalmology, University College of London, London, United Kingdom. Eye Clinic Ernest Hemingway, Fort de France, Martinique, France. Institute for Neurosciences of Montpellier U1051, University of Montpellier - University Hospital, Genetics of Sensory Diseases, Montpellier, France. Fondation Adolphe de Rothschild, Paris, France. Fondation Adolphe de Rothschild, Paris, France; Eye Clinic, Maison Rouge, Strasbourg, France. Fondation Adolphe de Rothschild, Paris, France; CHNO des Quinze-Vingts, DHU Sight Restore, INSERM-DHOS CIC1423, Paris - Sorborne Universités, UPMC Univ Paris 06, INSERM, CNRS, Institut de la Vision, Paris - Institute of Ophthalmology, University College of London, London, United Kingdom; Académie des Sciences, Institut de France, Paris, France. Department of Ophthalmology, Lariboisière Hospital, Paris, France. Ophthalmic Center for Imaging and Laser, Paris, France; Department of Ophthalmology, Intercity Hospital and University Paris Est, Créteil, France. Institute for Neurosciences of Montpellier U1051, University of Montpellier - University Hospital, Genetics of Sensory Diseases, Montpellier, France. Electronic address: isabelannemeunier@yahoo.fr. .
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8: Title: Heterometallic titanium-gold complexes inhibit renal cancer cells in vitro and in vivo.
Journal: Chemical science (Chem Sci), Vol. 6 (9): 5269-5283, 2015 .
Snippet: Preliminary mechanistic studies in Caki-1 renal cells indicate that the cytotoxic and anti-migration effects of the most active compound 5 ([(η-C5H5)2TiMe(μ-mba)Au(PPh3)] involve inhibition of thioredoxin reductase and loss of expression of protein kinases that drive cell migration (AKT, p90-RSK, and MAPKAPK3).
Affiliation: Department of Chemistry, Brooklyn College and The Graduate Center, The City University of New York, Brooklyn, NY, 11210, US. Biology PhD Program, The Graduate Center, The City University of New York, 365 Fifth Avenue, New York, NY, 10016, US. Department of Pharmaceutics, College of Pharmacy, University of Minnesota, MN, 55455, US. Center for Translational Drug Delivery, University of Minnesota, MN, 55455, US. Departamento de Química Inorgánica, Universidad de Valencia, Burjassot, Valencia, 46100, Spain. Department of Chemistry and Biochemistry, Queens College, The City University of New York, Flushing, NY, 11367, US. Cancer Biology Program, University of Hawaii Cancer Center, University of Hawaii at Manoa, Honolulu, HI, 96813, US. .
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9: Title: Coordination of stress signals by the lysine methyltransferase SMYD2 promotes pancreatic cancer.
Authors: Reynoird, Nicolas, et.al. .
Journal: Genes & development (Genes Dev), Vol. 30 (7): 772-85, 2016 .
Snippet: Inhibition of MAPKAPK3 impedes PDAC growth, identifying a potential new kinase target in PDAC.
Affiliation: Department of Biology, Stanford University, Stanford, California 94305, USA; Institut Albert Bonniot, U1209, Institut National de la Santé et de la Recherche Médicale, UMR5309, Centre National de la Recherche Scientifique, Université Grenoble-Alpes, F-38700 Grenoble, France; Department of Pediatrics, Stanford University School of Medicine, Stanford, California 94305, USA; Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA; Global Drug Discovery, Bayer Pharma AG, 13353 Berlin, Germany; Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA; Institute for Immunity, Transplantation, and Infection, Stanford University School of Medicine, Stanford, California 94305, USA; Department of Biology, Stanford University, Stanford, California 94305, USA; Institut Albert Bonniot, U1209, Institut National de la Santé et de la Recherche Médicale, UMR5309, Centre National de la Recherche Scientifique, Université Grenoble-Alpes, F-38700 Grenoble, France; Faculty of Medicine, Centre for Innovative Research in Medical and Natural Sciences, University of Rzeszów, 35959 Rzeszów, Poland; Structural Genomics Consortium, Princess Margaret Cancer Centre, University of Toronto, Toronto, Ontario M5G 2M9, Canada; Department of Medical Biophysics, University of Toronto, Toronto, Ontario M5G 2M9, Canada. .
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10: Title: A dominant mutation in MAPKAPK3, an actor of p38 signaling pathway, causes a new retinal dystrophy involving Bruch's membrane and retinal pigment epithelium.
Authors: Meunier, Isabelle, et.al. .
Journal: Human molecular genetics (Hum Mol Genet), Vol. 25 (5): 916-26, 2016 .
Snippet: MAPKAPK3 is a serine/threonine protein kinase of the p38 signaling pathway that is activated by a variety of stress stimuli and is implicated in cellular responses and gene regulation.
Affiliation: National Center in Genetic of Sensory Diseases, Institute for Neurosciences of Montpellier, INSERM U1051, University of Montpellier, Montpellier Hospital, Montpellier, France, isabelannemeunier@yahoo.fr. National Center in Genetic of Sensory Diseases, Institute for Neurosciences of Montpellier, INSERM U1051, University of Montpellier, Montpellier Hospital, Montpellier, France, Mitochondrial Medicine Research Center, University of Angers, CNRS 6214, INSERM U1083, Angers, France. National Center in Genetic of Sensory Diseases, Institute for Neurosciences of Montpellier, INSERM U1051, University of Montpellier, Montpellier Hospital, Montpellier, France. Department of Ophthalmology, University Hospital of Fort de France, Martinique (FWI), France. Imaging and Laser Center of Paris, Department of Ophthalmology, Intercity Hospital and University Paris, Creteil, France. Department of Ophthalmology, Lariboisiere Hospital, AP-HP and University Paris 7-Sorbonne Paris, Paris, France. Center for Structural Biochemistry Montpellier, INSERM U1054-CNRS UMR5048, Montpellier, France. National Center in Genetic of Sensory Diseases, Institute for Neurosciences of Montpellier, INSERM U1051, University of Montpellier, Montpellier Hospital, Montpellier, France, Institute for Neurosciences, CRIC/IURC, Montpellier, France. CHRU Lille, Biochemistry and Molecular Biology Department, University Lille North, Lille, France. Institute of Biochemistry, Hannover Medical School, Hannover, Germany and. MRC Protein Phosphorylation Unit, Dundee, UK. .
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11: Title: Treatment of Obese Insulin-Resistant Mice With an Allosteric MAPKAPK2/3 Inhibitor Lowers Blood Glucose and Improves Insulin Sensitivity.
Authors: Ozcan, Lale, et.al. .
Journal: Diabetes, Vol. 64 (10): 3396-405, 2015 .
Snippet: At the hub of this new pathway is a kinase cascade involving calcium/calmodulin-dependent protein kinase II (CaMKII), p38α mitogen-activated protein kinase (MAPK), and MAPKAPK2/3 (MK2/3).
Affiliation: Department of Medicine, Columbia University, New York, NY lo2192@columbia.edu iat1@columbia.edu. Department of Medicine, Columbia University, New York, NY. Department of Pathology and Cell Biology, Columbia University, New York, NY Irving Institute for Clinical and Translational Research, Columbia University, New York, NY. Department of Medicine, Columbia University, New York, NY Department of Pathology and Cell Biology, Columbia University, New York, NY Irving Institute for Clinical and Translational Research, Columbia University, New York, NY. Tabomedex Biosciences, Boxford, MA. Department of Biochemistry, Hannover Medical School, Hannover, Germany. Department of Medicine, Columbia University, New York, NY Department of Pathology and Cell Biology, Columbia University, New York, NY Department of Physiology and Cellular Biophysics, Columbia University, New York, NY lo2192@columbia.edu iat1@columbia.edu. .
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12: Title: MK3 modulation affects BMI1-dependent and independent cell cycle check-points.
Authors: Prickaerts, Peggy, et.al. .
Journal: PloS one, Vol. 10 (4): e0118840, 2015 .
Snippet: We previously identified MK3 as a binding partner of Polycomb Repressive Complex 1 (PRC1) proteins.
Affiliation: Department of Molecular Genetics, Maastricht University Medical Centre, Maastricht, the Netherlands. Department of Pathology, Maastricht University Medical Centre, Maastricht, the Netherlands. Department of Stem Cell Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan. Princess Margaret Cancer Centre and Campbell Family Institute for Cancer Research, Departments of Radiation Oncology and Medical Biophysics, University Health Network, Toronto, Canada, Maastricht Radiation Oncology (MaastRO) Lab, Maastricht University, Maastricht, The Netherlands. .
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13: Title: The stress-responsive kinases MAPKAPK2/MAPKAPK3 activate starvation-induced autophagy through Beclin 1 phosphorylation.
Authors: Wei, Yongjie, et.al. .
Journal: eLife, Vol. 4, 2015 .
Snippet: Here we show that two related stress-responsive kinases, members of the p38 mitogen-activated protein kinase (MAPK) signaling pathway MAPKAPK2 (MK2) and MAPKAPK3 (MK3), positively regulate starvation-induced autophagy by phosphorylating an essential ATG protein, Beclin 1, at serine 90, and that this phosphorylation site is essential for the tumor suppressor function of Beclin 1.
Affiliation: Center for Autophagy Research, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, United States. Department of Chemistry and Biochemistry, North Dakota State University, Fargo, United States. Department of Clinical Sciences, UT Southwestern Medical Center, Dallas, United States. Institute of Physiological Chemistry, Hannover Medical School, Hannover, Germany. .
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14: Title: Theoretical analysis of the binding of potential inhibitors to protein kinases MK2 and MK3.
Authors: Araújo, Pedro M M, et.al. .
Journal: Medicinal chemistry (Shāriqah (United Arab Emirates)) (Med Chem), Vol. 11 (6): 573-9, 2015 .
Snippet: MK2 (or MAPKAPK2) was already known for its role in the inflammatory response, however recent studies indicate the involvement of this protein kinase in the DNA damage response mechanism.
Affiliation: Centro de Investigacao em Química, Departamento de Química e Bioquímica, Faculdade de Ciência da Universidade do Porto, R. Campo Alegre 687, 4169-007 Porto, Portugal.. jcsilva@fc.up.pt. .
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15: Title: Organometallic Titanocene-Gold Compounds as Potential Chemotherapeutics in Renal Cancer. Study of their Protein Kinase Inhibitory Properties.
Journal: Organometallics, Vol. 33 (22): 6669-6681, 2014 .
Snippet: The activity on renal cancer cell lines (for 5 in the nanomolar range) was considerably higher than that of cisplatin and highly active titanocene Y. Initial mechanistic studies in Caki-1 cells in vitro coupled with studies of their inhibitory properties on a panel of 35 kinases of oncological interest indicate that these compounds inhibit protein kinases of the AKT and MAPKAPK families with a higher selectivity toward MAPKAPK3 (IC503 = 91 nM, IC505 = 117 nM).
Affiliation: Department of Chemistry, Brooklyn College and The Graduate Center, The City University of New York , Brooklyn, New York 11210, United States. Cancer Biology Program, University of Hawaii Cancer Center, University of Hawaii at Manoa , Honolulu, Hawaii 96813, United States. Departamento de Química Inorgánica, Universidad de Valencia , Burjassot, Valencia, 46100, Spain. Department of Chemistry, Brooklyn College and The Graduate Center, The City University of New York , Brooklyn, New York 11210, United States ; Cancer Biology Program, University of Hawaii Cancer Center, University of Hawaii at Manoa , Honolulu, Hawaii 96813, United States. .
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16: Title: The MK2/3 cascade regulates AMPAR trafficking and cognitive flexibility.
Authors: Eales, Katherine L, et.al. .
Journal: Nature communications (Nat Commun), Vol. 5, 2014 .
Snippet: Here we provide evidence that MAPK-activated protein kinases 2 and 3 (MK2/3) regulate neuronal spine morphology, synaptic transmission and plasticity.
Affiliation: School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK. Institute of Biochemistry, Hannover Medical University, 30625 Hannover, Germany. Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK. 1] School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK [2] School of Life Sciences, University of Bradford, Bradford BD7 1DP, UK. .
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17: Title: MAPKAP kinase 3 suppresses Ifng gene expression and attenuates NK cell cytotoxicity and Th1 CD4 T-cell development upon influenza A virus infection.
Authors: Köther, Katharina, et.al. .
Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology (Faseb J), Vol. 28 (10): 4235-46, 2014 .
Snippet: Thus, our data describe the protein kinase MK3 as a novel regulator of the innate and adaptive immune responses.-Köther,
Affiliation: Institute of Molecular Virology (IMV), Centre for Molecular Biology of Inflammation (ZMBE), and. Department of Pediatric Rheumatology and Immunology, Westfälische Wilhelms University, Münster, Germany; Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA; Institute of Biochemistry, Hannover Medical School, Hannover, Germany; and. Institute of Molecular Virology (IMV), Centre for Molecular Biology of Inflammation (ZMBE), and Interdisciplinary Center of Clinical Research (IZKF), University of Münster, Münster, Germany. Institute of Molecular Virology (IMV), Centre for Molecular Biology of Inflammation (ZMBE), and Interdisciplinary Center of Clinical Research (IZKF), University of Münster, Münster, Germany ludwigs@uni-muenster.de. .
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18: Title: Private haplotypes can reveal local adaptation.
Authors: Sjöstrand, Agnès E, et.al. .
Journal: BMC genetics (Bmc Genet), Vol. 15, 2014 .
Snippet: For instance, in the Maasai, MFPH reveals a strong signal of selection in a region where other investigated statistics fail to pick up a clear signal that contains the genes DOCK3, MAPKAPK3 and CISH.
Affiliation: Department of Evolutionary Biology, Evolutionary Biology Centre, Uppsala University, Uppsala, Sweden. mattias.jakobsson@ebc.uu.se. .
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19: Title: Monitoring native p38α:MK2/3 complexes via trans delivery of an ATP acyl phosphate probe.
Authors: Okerberg, Eric S, et.al. .
Journal: Journal of the American Chemical Society (J Am Chem Soc), Vol. 136 (12): 4664-9, 2014 .
Snippet: Here we describe a chemical proteomics strategy using ATP acyl phosphates to measure the formation of a protein:protein complex between p38α and mapkap kinases 2 and/or 3. Formation of the protein:protein complex results in a new probe labeling site on p38α that can be used to quantify the extent of interaction in cell lysates and the equilibrium binding constant for the interaction in vitro.
Affiliation: ActivX Biosciences, Inc., 11025 North Torrey Pines Road, La Jolla, California 92037, United States. .
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20: Title: Endoplasmic reticulum-associated ubiquitin-conjugating enzyme Ube2j1 is a novel substrate of MK2 (MAPKAP kinase-2) involved in MK2-mediated TNFα production.
Authors: Menon, Manoj B, et.al. .
Journal: The Biochemical journal (Biochem J), Vol. 456 (2): 163-72, 2013 .
Snippet: The p38 MAPK (mitogen-activated protein kinase)/MK2 [MAPKAP (MAPK-activated protein) kinase-2] signalling pathway is a major regulator of stress- and cytokine-induced gene expression at the transcriptional and post-transcriptional level.
Affiliation: *Institute of Physiological Chemistry, Hannover Medical School, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany. .
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