For 317 Kinases. Blank Fields Indicate Combinations That Were Tested, but for Which Binding Was Weak (Kd > 10 Um), Or Not Detected in a Primary Screen (10 Um)
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N-Glycan Trimming in the ER and Calnexin/Calreticulin Cycle
Neurotransmitter receptorsGABA and A postsynapticreceptor activation signal transmission Ligand-gated ion channel transport GABAGABA Areceptor receptor alpha-5 alpha-1/beta-1/gamma-2 subunit GABA A receptor alpha-2/beta-2/gamma-2GABA receptor alpha-4 subunit GABAGABA receptor A receptor beta-3 subunitalpha-6/beta-2/gamma-2 GABA-AGABA receptor; A receptor alpha-1/beta-2/gamma-2GABA receptoralpha-3/beta-2/gamma-2 alpha-3 subunit GABA-A GABAreceptor; receptor benzodiazepine alpha-6 subunit site GABA-AGABA-A receptor; receptor; GABA-A anion site channel (alpha1/beta2 interface) GABA-A receptor;GABA alpha-6/beta-3/gamma-2 receptor beta-2 subunit GABAGABA receptorGABA-A receptor alpha-2receptor; alpha-1 subunit agonist subunit GABA site Serotonin 3a (5-HT3a) receptor GABA receptorGABA-C rho-1 subunitreceptor GlycineSerotonin receptor subunit3 (5-HT3) alpha-1 receptor GABA receptor rho-2 subunit GlycineGlycine receptor receptor subunit subunit alpha-2 alpha-3 Ca2+ activated K+ channels Metabolism of ingested SeMet, Sec, MeSec into H2Se SmallIntermediateSmall conductance conductance conductance calcium-activated calcium-activated calcium-activated potassium potassium potassiumchannel channel protein channel protein 2 protein 1 4 Small conductance calcium-activatedCalcium-activated potassium potassium channel alpha/beta channel 1 protein 3 Calcium-activated potassiumHistamine channel subunit alpha-1 N-methyltransferase Neuraminidase Pyrimidine biosynthesis Nicotinamide N-methyltransferase Adenosylhomocysteinase PolymerasePolymeraseHistidine basic -
Profiling Data
Compound Name DiscoveRx Gene Symbol Entrez Gene Percent Compound Symbol Control Concentration (nM) JNK-IN-8 AAK1 AAK1 69 1000 JNK-IN-8 ABL1(E255K)-phosphorylated ABL1 100 1000 JNK-IN-8 ABL1(F317I)-nonphosphorylated ABL1 87 1000 JNK-IN-8 ABL1(F317I)-phosphorylated ABL1 100 1000 JNK-IN-8 ABL1(F317L)-nonphosphorylated ABL1 65 1000 JNK-IN-8 ABL1(F317L)-phosphorylated ABL1 61 1000 JNK-IN-8 ABL1(H396P)-nonphosphorylated ABL1 42 1000 JNK-IN-8 ABL1(H396P)-phosphorylated ABL1 60 1000 JNK-IN-8 ABL1(M351T)-phosphorylated ABL1 81 1000 JNK-IN-8 ABL1(Q252H)-nonphosphorylated ABL1 100 1000 JNK-IN-8 ABL1(Q252H)-phosphorylated ABL1 56 1000 JNK-IN-8 ABL1(T315I)-nonphosphorylated ABL1 100 1000 JNK-IN-8 ABL1(T315I)-phosphorylated ABL1 92 1000 JNK-IN-8 ABL1(Y253F)-phosphorylated ABL1 71 1000 JNK-IN-8 ABL1-nonphosphorylated ABL1 97 1000 JNK-IN-8 ABL1-phosphorylated ABL1 100 1000 JNK-IN-8 ABL2 ABL2 97 1000 JNK-IN-8 ACVR1 ACVR1 100 1000 JNK-IN-8 ACVR1B ACVR1B 88 1000 JNK-IN-8 ACVR2A ACVR2A 100 1000 JNK-IN-8 ACVR2B ACVR2B 100 1000 JNK-IN-8 ACVRL1 ACVRL1 96 1000 JNK-IN-8 ADCK3 CABC1 100 1000 JNK-IN-8 ADCK4 ADCK4 93 1000 JNK-IN-8 AKT1 AKT1 100 1000 JNK-IN-8 AKT2 AKT2 100 1000 JNK-IN-8 AKT3 AKT3 100 1000 JNK-IN-8 ALK ALK 85 1000 JNK-IN-8 AMPK-alpha1 PRKAA1 100 1000 JNK-IN-8 AMPK-alpha2 PRKAA2 84 1000 JNK-IN-8 ANKK1 ANKK1 75 1000 JNK-IN-8 ARK5 NUAK1 100 1000 JNK-IN-8 ASK1 MAP3K5 100 1000 JNK-IN-8 ASK2 MAP3K6 93 1000 JNK-IN-8 AURKA AURKA 100 1000 JNK-IN-8 AURKA AURKA 84 1000 JNK-IN-8 AURKB AURKB 83 1000 JNK-IN-8 AURKB AURKB 96 1000 JNK-IN-8 AURKC AURKC 95 1000 JNK-IN-8 -
Regulation of Skeletal Muscle Metabolism and Development by Small, Non-Coding Rnas: Implications for Insulin Resistance and Type 2 Diabetes Mellitus
From the Department of Molecular Medicine and Surgery Karolinska Institutet, Stockholm, Sweden Regulation of Skeletal Muscle Metabolism and Development by Small, Non-Coding RNAs: Implications for Insulin Resistance and Type 2 Diabetes Mellitus Rasmus Sjögren Stockholm 2018 All previously published papers were reproduced with permission from the publisher. © 2017 by the American Diabetes Association ® Diabetes 2017 Jul; 66(7): 1807-1818 Reprinted with permission from the American Diabetes Association ® Published by Karolinska Institutet. Printed by Eprint AB, 2018. © Rasmus Sjögren, 2018. ISBN 978-91-7831-057-9 Department of Molecular Medicine and Surgery Regulation of Skeletal Muscle Metabolism and Development by Small, Non-Coding RNAs: Implications for Insulin Resistance and Type 2 Diabetes Mellitus THESIS FOR DOCTORAL DEGREE (Ph.D.) by Rasmus Sjögren Defended on: Wednesday the 13th of June 2018, 12:30 pm Hillarpsalen, Retzius väg 8, Stockholm Principal Supervisor: Opponent: Prof Juleen R. Zierath Prof Markus Stoffel Karolinska Institutet Swiss Federal Institute of Technology in Zurich Department of Molecular Medicine and Surgery Department of Biology Division of Integrative Physiology Division of Metabolism and Metabolic Diseases Co-supervisor(s): Examination Board: Prof Anna Krook Prof Ulf Eriksson Karolinska Institutet Karolinska Insitutet Department of Physiology and Pharmacology Department of Medical Biochemistry and Bio- Division of Integrative Physiology physics Division of Vascular Biology Prof Eckardt Treuter Karolinska Insitutet Department of Biosciences and Nutrition Division of Epigenome Regulation Prof Lena Eliasson Lund University Department of Clinical Sciences, Malmö Division of Islet Cell Exocytosis ABSTRACT microRNAs (miRNAs) are a class of epigenetic post-transcriptional regulators. These short (~22 nucleotides) non-coding RNAs can potently reduce protein abundance through direction of the RNA-induced silencing complex to targeted genes. -
Kinaseseeker™ Full-Length Panel (112 Wild-Type Kinases)
KinaseSeeker™ Full-Length Panel (112 Wild-Type Kinases) Kinase Group Kinase Group ABL1 full-length TK DDR1 intracellular module TK ACVR1 intracellular module TKL DDR2 intracellular module TK AKT1 full-length AGC EGFR intracellular module TK AKT2 full-length AGC EPHA1 intracellular module TK AKT3 full-length AGC EPHA2 intracellular module TK AMPKa1 full-length CAMK EPHA3 intracellular module TK BLK full-length TK EPHA4 intracellular module TK BTK full-length TK EPHA5 intracellular module TK CAMK1D full-length CAMK EPHA6 intracellular module TK CAMK1G full-length CAMK EPHA7 intracellular module TK CAMK2A full-length CAMK EPHA8 intracellular module TK CAMK2B full-length CAMK EPHB3 intracellular module TK CAMK2D full-length CAMK EPHB4 intracellular module TK CAMK2G full-length CAMK ERBB2 intracellular module TK CAMKK1 full-length Other ERBB4 intracellular module TK CAMKK2 full-length Other FAK full-length TK CASK full-length CAMK FGFR2 intracellular module TK CDKL5 full-length CMGC FGFR3 intracellular module TK CK1d full-length CK1 FGR full-length TK CLK1 full-length CMGC FLT1 intracellular module TK CLK2 full-length CMGC FLT2 intracellular module TK CLK3 full-length CMGC FLT4 intracellular module TK CSF1R intracellular module TK FRK full-length TK CSK full-length TK FYN full-length TK DAPK1 full-length CAMK GRK7 full-length AGC Legend: Full-Length: Construct contains Full-length kinase Intracellular Module: Construct contains Cytoplasmic Region in Receptor Tyrosine Kinases Page 1 of 3 KinaseSeeker™ Full-Length Panel (112 Wild-Type Kinases) -
Informationpackage.Pdf
TABLE OF CONTENTS Sample Preparation PDF Page No. 1. Introduction ……………………………………………………………………………………….……. 3 2. Quantity of lysate required …………………………………………………………………………… 5 3. Preparation of cell lysates A. Adherent cells ………………………………………………………………………..…….……. 6 B. Suspension cells ………………………………………………………………………...……… 6 4. Preparation of cell pellets …………………………………………………………………….……… 7 5. Tissue preparation ……………………………………………………………………………………. 7 6. Sample buffer preparation …………………………………………………………………………… 8 Shipping & Pricing 7. Preparation for storage and shipping of samples ……………………………………………..…. 8 8. Shipping information ………………………………………………………………………………….. 8 9. Pricing information ……………………………………………………………………………………. 9 Description of Follow Up Services 10. Follow up services ……………………………………………………………………………………. 9 11. Forms to be completed ………………………………………………………………………………. 10 Sample Buffer Protocol 12. Appendix A - KinetworksTM Sample Buffer protocol ………………………………………………. 15 KinetworksTM Phospho-Site Screening Services 13. Appendix B - List of 38 phosphorylation sites in KPSS-1.3 - Broad Signalling Pathway ….… 16 14. Appendix C - List of 44 phosphorylation sites in KPSS-10.1 - Cell Cycle Status Screen….... 17 15. Appendix D - List of 37 phosphorylation sites in KPSS-11.0 - Protein Kinase Screen …....... 18 16. Appendix E - List of 40 phosphorylation sites in KPSS-12.1 - Substrates of Kinases Screen 19 KinetworksTM Expression Level Profiling Services 17. Appendix F - List of 76 proteins tracked in KPKS-1.2 Screen – Protein Kinase Screen ....… 20 18. Appendix G - List -
IRAK-M Associates with Susceptibility to Adult-Onset Asthma and Promotes Chronic Airway Inflammation
IRAK-M Associates with Susceptibility to Adult-Onset Asthma and Promotes Chronic Airway Inflammation This information is current as Yi Liu, Mingqiang Zhang, Lili Lou, Lun Li, Youming of September 28, 2021. Zhang, Wei Chen, Weixun Zhou, Yan Bai and Jinming Gao J Immunol published online 7 January 2019 http://www.jimmunol.org/content/early/2019/01/04/jimmun ol.1800712 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2019/01/04/jimmunol.180071 Material 2.DCSupplemental http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 28, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2019 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published January 7, 2019, doi:10.4049/jimmunol.1800712 The Journal of Immunology IRAK-M Associates with Susceptibility to Adult-Onset Asthma and Promotes Chronic Airway Inflammation Yi Liu,*,†,1 Mingqiang Zhang,*,1 Lili Lou,* Lun Li,* Youming Zhang,‡ Wei Chen,x Weixun Zhou,{ Yan Bai,‖ and Jinming Gao* IL-1R–associated kinase (IRAK)-M regulates lung immunity during asthmatic airway inflammation. -
Supplementary Table 1. in Vitro Side Effect Profiling Study for LDN/OSU-0212320. Neurotransmitter Related Steroids
Supplementary Table 1. In vitro side effect profiling study for LDN/OSU-0212320. Percent Inhibition Receptor 10 µM Neurotransmitter Related Adenosine, Non-selective 7.29% Adrenergic, Alpha 1, Non-selective 24.98% Adrenergic, Alpha 2, Non-selective 27.18% Adrenergic, Beta, Non-selective -20.94% Dopamine Transporter 8.69% Dopamine, D1 (h) 8.48% Dopamine, D2s (h) 4.06% GABA A, Agonist Site -16.15% GABA A, BDZ, alpha 1 site 12.73% GABA-B 13.60% Glutamate, AMPA Site (Ionotropic) 12.06% Glutamate, Kainate Site (Ionotropic) -1.03% Glutamate, NMDA Agonist Site (Ionotropic) 0.12% Glutamate, NMDA, Glycine (Stry-insens Site) 9.84% (Ionotropic) Glycine, Strychnine-sensitive 0.99% Histamine, H1 -5.54% Histamine, H2 16.54% Histamine, H3 4.80% Melatonin, Non-selective -5.54% Muscarinic, M1 (hr) -1.88% Muscarinic, M2 (h) 0.82% Muscarinic, Non-selective, Central 29.04% Muscarinic, Non-selective, Peripheral 0.29% Nicotinic, Neuronal (-BnTx insensitive) 7.85% Norepinephrine Transporter 2.87% Opioid, Non-selective -0.09% Opioid, Orphanin, ORL1 (h) 11.55% Serotonin Transporter -3.02% Serotonin, Non-selective 26.33% Sigma, Non-Selective 10.19% Steroids Estrogen 11.16% 1 Percent Inhibition Receptor 10 µM Testosterone (cytosolic) (h) 12.50% Ion Channels Calcium Channel, Type L (Dihydropyridine Site) 43.18% Calcium Channel, Type N 4.15% Potassium Channel, ATP-Sensitive -4.05% Potassium Channel, Ca2+ Act., VI 17.80% Potassium Channel, I(Kr) (hERG) (h) -6.44% Sodium, Site 2 -0.39% Second Messengers Nitric Oxide, NOS (Neuronal-Binding) -17.09% Prostaglandins Leukotriene, -
MAPK4 Overexpression Promotes Tumor Progression Via Noncanonical Activation of AKT/Mtor Signaling
The Journal of Clinical Investigation RESEARCH ARTICLE MAPK4 overexpression promotes tumor progression via noncanonical activation of AKT/mTOR signaling Wei Wang,1 Tao Shen,1 Bingning Dong,1 Chad J. Creighton,2,3 Yanling Meng,1 Wolong Zhou,1 Qing Shi,1 Hao Zhou,1 Yinjie Zhang,1 David D. Moore,1 and Feng Yang1 1Department of Molecular and Cellular Biology, 2Department of Medicine, and 3Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas, USA. MAPK4 is an atypical MAPK. Currently, little is known about its physiological function and involvement in diseases, including cancer. A comprehensive analysis of 8887 gene expression profiles in The Cancer Genome Atlas (TCGA) revealed that MAPK4 overexpression correlates with decreased overall survival, with particularly marked survival effects in patients with lung adenocarcinoma, bladder cancer, low-grade glioma, and thyroid carcinoma. Interestingly, human tumor MAPK4 overexpression also correlated with phosphorylation of AKT, 4E-BP1, and p70S6K, independent of the loss of PTEN or mutation of PIK3CA. This led us to examine whether MAPK4 activates the key metabolic, prosurvival, and proliferative kinase AKT and mTORC1 signaling, independent of the canonical PI3K pathway. We found that MAPK4 activated AKT via a novel, concerted mechanism independent of PI3K. Mechanistically, MAPK4 directly bound and activated AKT by phosphorylation of the activation loop at threonine 308. It also activated mTORC2 to phosphorylate AKT at serine 473 for full activation. MAPK4 overexpression induced oncogenic outcomes, including transforming prostate epithelial cells into anchorage-independent growth, and MAPK4 knockdown inhibited cancer cell proliferation, anchorage-independent growth, and xenograft growth. We concluded that MAPK4 can promote cancer by activating the AKT/mTOR signaling pathway and that targeting MAPK4 may provide a novel therapeutic approach for cancer. -
The Genetics of Bipolar Disorder
Molecular Psychiatry (2008) 13, 742–771 & 2008 Nature Publishing Group All rights reserved 1359-4184/08 $30.00 www.nature.com/mp FEATURE REVIEW The genetics of bipolar disorder: genome ‘hot regions,’ genes, new potential candidates and future directions A Serretti and L Mandelli Institute of Psychiatry, University of Bologna, Bologna, Italy Bipolar disorder (BP) is a complex disorder caused by a number of liability genes interacting with the environment. In recent years, a large number of linkage and association studies have been conducted producing an extremely large number of findings often not replicated or partially replicated. Further, results from linkage and association studies are not always easily comparable. Unfortunately, at present a comprehensive coverage of available evidence is still lacking. In the present paper, we summarized results obtained from both linkage and association studies in BP. Further, we indicated new potential interesting genes, located in genome ‘hot regions’ for BP and being expressed in the brain. We reviewed published studies on the subject till December 2007. We precisely localized regions where positive linkage has been found, by the NCBI Map viewer (http://www.ncbi.nlm.nih.gov/mapview/); further, we identified genes located in interesting areas and expressed in the brain, by the Entrez gene, Unigene databases (http://www.ncbi.nlm.nih.gov/entrez/) and Human Protein Reference Database (http://www.hprd.org); these genes could be of interest in future investigations. The review of association studies gave interesting results, as a number of genes seem to be definitively involved in BP, such as SLC6A4, TPH2, DRD4, SLC6A3, DAOA, DTNBP1, NRG1, DISC1 and BDNF. -
Monocytes Production in Β -Induced IL-1 Δ Kinase C Associated Kinase-1
IL-1R−Associated Kinase-1 Mediates Protein Kinase C δ-Induced IL-1β Production in Monocytes This information is current as Rajiv Lochan Tiwari, Vishal Singh, Ankita Singh and Manoj of October 1, 2021. Kumar Barthwal J Immunol published online 29 July 2011 http://www.jimmunol.org/content/early/2011/07/29/jimmun ol.1002526 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2011/07/29/jimmunol.100252 Material 6.DC1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on October 1, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published July 29, 2011, doi:10.4049/jimmunol.1002526 The Journal of Immunology IL-1R–Associated Kinase-1 Mediates Protein Kinase Cd-Induced IL-1b Production in Monocytes Rajiv Lochan Tiwari, Vishal Singh, Ankita Singh, and Manoj Kumar Barthwal The role of IL-1R–associated kinase (IRAK)1 and its interaction with protein kinase C (PKC)d in monocytes to regulate IL-1b production has not been reported so far. -
Halogen-Aromatic Π Interactions Modulate Inhibitor Residence Time
bioRxiv preprint doi: https://doi.org/10.1101/255513; this version posted January 29, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Classification: Biophysics and Computational Biology Halogen-aromatic π interactions modulate inhibi- tor residence time Christina Herovena, Victoria Georgib, Gaurav K. Ganotrae, Paul E. Brennana,f, Finn Wolfreysa,f, Rebecca C. Wadee,h,i, Amaury E. Fernández-Montalvánb, Apirat Chaikuada,c,d,1, Stefan Knappa,c,d,g,1 aNuffield Department of Clinical Medicine, Structural Genomics Consortium, University of Oxford, Oxford, OX3 7DQ, UK bBayer AG, Drug Discovery, Pharmaceuticals, Lead Discovery Berlin, 13353 Berlin, Ger- many cBuchmann Institute for Molecular Life Sciences, Johann Wolfgang Goethe-University, D- 60438 Frankfurt am Main, DE dInstitute for Pharmaceutical Chemistry, Johann Wolfgang Goethe-University, D-60438 Frankfurt am Main, DE eMolecular and Cellular Modeling Group, Heidelberg Institute for Theoretical Studies (HITS), 69118 Heidelberg, Germany fTarget Discovery Institute, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7FZ, UK gGerman Cancer Network (DKTK), Frankfurt/Mainz site, D-60438 Frankfurt am Main, DE hZentrum für Molekulare Biologie, DKFZ-ZMBH Alliance, Heidelberg University, 69120 Heidelberg, Germany; IInterdisciplinary Center for Scientific Computing, Heidelberg University, 69120 Heidel- berg, Germany 1 Corresponding authors: Apirat Chaikuad ([email protected]) or Stefan Knapp ([email protected]), Institute for Pharmaceutical Chemis- try, Johann Wolfgang Goethe-University, Max-von-Laue Str. 9, D-60438 Frankfurt am Main, Germany. -
BMC Genomics Biomed Central
BMC Genomics BioMed Central Research article Open Access Global gene expression analysis of early response to chemotherapy treatment in ovarian cancer spheroids Sylvain L'Espérance1,3, Magdalena Bachvarova3, Bernard Tetu2,3, Anne- Marie Mes-Masson4,5 and Dimcho Bachvarov*1,3 Address: 1Department of Medicine, Laval University, Québec (Québec), Canada, 2Department of Pathology, Laval University, Québec (Québec), Canada, 3Cancer Research Centre, Hôpital L'Hotel-Dieu de Québec, Centre Hospitalier Universitaire de Québec (CHUQ), Québec (Québec), Canada, 4Department of Medicine, Université de Montréal, Montreal, (Québec) Canada and 5Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CHUM), Institut du cancer de Montréal, Montréal (Québec), Canada Email: Sylvain L'Espérance - [email protected]; Magdalena Bachvarova - [email protected]; [email protected]; Anne-Marie Mes-Masson - [email protected]; Dimcho Bachvarov* - [email protected] * Corresponding author Published: 26 February 2008 Received: 6 August 2007 Accepted: 26 February 2008 BMC Genomics 2008, 9:99 doi:10.1186/1471-2164-9-99 This article is available from: http://www.biomedcentral.com/1471-2164/9/99 © 2008 L'Espérance et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly