Identification of a Family of Camp Response Element-Binding Protein Coactivators by Genome-Scale Functional Analysis in Mammalian Cells
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Gene Symbol Gene Description ACVR1B Activin a Receptor, Type IB
Table S1. Kinase clones included in human kinase cDNA library for yeast two-hybrid screening Gene Symbol Gene Description ACVR1B activin A receptor, type IB ADCK2 aarF domain containing kinase 2 ADCK4 aarF domain containing kinase 4 AGK multiple substrate lipid kinase;MULK AK1 adenylate kinase 1 AK3 adenylate kinase 3 like 1 AK3L1 adenylate kinase 3 ALDH18A1 aldehyde dehydrogenase 18 family, member A1;ALDH18A1 ALK anaplastic lymphoma kinase (Ki-1) ALPK1 alpha-kinase 1 ALPK2 alpha-kinase 2 AMHR2 anti-Mullerian hormone receptor, type II ARAF v-raf murine sarcoma 3611 viral oncogene homolog 1 ARSG arylsulfatase G;ARSG AURKB aurora kinase B AURKC aurora kinase C BCKDK branched chain alpha-ketoacid dehydrogenase kinase BMPR1A bone morphogenetic protein receptor, type IA BMPR2 bone morphogenetic protein receptor, type II (serine/threonine kinase) BRAF v-raf murine sarcoma viral oncogene homolog B1 BRD3 bromodomain containing 3 BRD4 bromodomain containing 4 BTK Bruton agammaglobulinemia tyrosine kinase BUB1 BUB1 budding uninhibited by benzimidazoles 1 homolog (yeast) BUB1B BUB1 budding uninhibited by benzimidazoles 1 homolog beta (yeast) C9orf98 chromosome 9 open reading frame 98;C9orf98 CABC1 chaperone, ABC1 activity of bc1 complex like (S. pombe) CALM1 calmodulin 1 (phosphorylase kinase, delta) CALM2 calmodulin 2 (phosphorylase kinase, delta) CALM3 calmodulin 3 (phosphorylase kinase, delta) CAMK1 calcium/calmodulin-dependent protein kinase I CAMK2A calcium/calmodulin-dependent protein kinase (CaM kinase) II alpha CAMK2B calcium/calmodulin-dependent -
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MEK-7 Polyclonal Antibody Catalog No : YT2725 Reactivity : Human,Mouse,Rat Applications : WB,ELISA Gene Name : MAP2K7 Protein Name : Dual specificity mitogen-activated protein kinase kinase 7 Human Gene Id : 5609 Human Swiss Prot O14733 No : Mouse Gene Id : 26400 Mouse Swiss Prot Q8CE90 No : Rat Gene Id : 363855 Rat Swiss Prot No : Q4KSH7 Immunogen : The antiserum was produced against synthesized peptide derived from human MAP2K7. AA range:241-290 Specificity : MEK-7 Polyclonal Antibody detects endogenous levels of MEK-7 protein. Formulation : Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide. Source : Rabbit Dilution : Western Blot: 1/500 - 1/2000. ELISA: 1/20000. Not yet tested in other applications. Purification : The antibody was affinity-purified from rabbit antiserum by affinity- chromatography using epitope-specific immunogen. Concentration : 1 mg/ml 1 / 3 Storage Stability : -20°C/1 year Molecularweight : 47485 Observed Band : 47 Cell Pathway : MAPK_ERK_Growth,MAPK_G_Protein,ErbB_HER,Toll_Like,T_Cell_Receptor, Fc epsilon RI,Neurotrophin,GnRH, Background : mitogen-activated protein kinase kinase 7(MAP2K7) Homo sapiens The protein encoded by this gene is a dual specificity protein kinase that belongs to the MAP kinase kinase family. This kinase specifically activates MAPK8/JNK1 and MAPK9/JNK2, and this kinase itself is phosphorylated and activated by MAP kinase kinase kinases including MAP3K1/MEKK1, MAP3K2/MEKK2,MAP3K3/MEKK5, and MAP4K2/GCK. This kinase is involved in the signal transduction mediating the cell -
Application of a MYC Degradation
SCIENCE SIGNALING | RESEARCH ARTICLE CANCER Copyright © 2019 The Authors, some rights reserved; Application of a MYC degradation screen identifies exclusive licensee American Association sensitivity to CDK9 inhibitors in KRAS-mutant for the Advancement of Science. No claim pancreatic cancer to original U.S. Devon R. Blake1, Angelina V. Vaseva2, Richard G. Hodge2, McKenzie P. Kline3, Thomas S. K. Gilbert1,4, Government Works Vikas Tyagi5, Daowei Huang5, Gabrielle C. Whiten5, Jacob E. Larson5, Xiaodong Wang2,5, Kenneth H. Pearce5, Laura E. Herring1,4, Lee M. Graves1,2,4, Stephen V. Frye2,5, Michael J. Emanuele1,2, Adrienne D. Cox1,2,6, Channing J. Der1,2* Stabilization of the MYC oncoprotein by KRAS signaling critically promotes the growth of pancreatic ductal adeno- carcinoma (PDAC). Thus, understanding how MYC protein stability is regulated may lead to effective therapies. Here, we used a previously developed, flow cytometry–based assay that screened a library of >800 protein kinase inhibitors and identified compounds that promoted either the stability or degradation of MYC in a KRAS-mutant PDAC cell line. We validated compounds that stabilized or destabilized MYC and then focused on one compound, Downloaded from UNC10112785, that induced the substantial loss of MYC protein in both two-dimensional (2D) and 3D cell cultures. We determined that this compound is a potent CDK9 inhibitor with a previously uncharacterized scaffold, caused MYC loss through both transcriptional and posttranslational mechanisms, and suppresses PDAC anchorage- dependent and anchorage-independent growth. We discovered that CDK9 enhanced MYC protein stability 62 through a previously unknown, KRAS-independent mechanism involving direct phosphorylation of MYC at Ser . -
Kinase Profiling Book
Custom and Pre-Selected Kinase Prof iling to f it your Budget and Needs! As of July 1, 2021 19.8653 mm 128 196 12 Tyrosine Serine/Threonine Lipid Kinases Kinases Kinases Carna Biosciences, Inc. 2007 Carna Biosciences, Inc. Profiling Assays available from Carna Biosciences, Inc. As of July 1, 2021 Page Kinase Name Assay Platform Page Kinase Name Assay Platform 4 ABL(ABL1) MSA 21 EGFR[T790M/C797S/L858R] MSA 4 ABL(ABL1)[E255K] MSA 21 EGFR[T790M/L858R] MSA 4 ABL(ABL1)[T315I] MSA 21 EPHA1 MSA 4 ACK(TNK2) MSA 21 EPHA2 MSA 4 AKT1 MSA 21 EPHA3 MSA 5 AKT2 MSA 22 EPHA4 MSA 5 AKT3 MSA 22 EPHA5 MSA 5 ALK MSA 22 EPHA6 MSA 5 ALK[C1156Y] MSA 22 EPHA7 MSA 5 ALK[F1174L] MSA 22 EPHA8 MSA 6 ALK[G1202R] MSA 23 EPHB1 MSA 6 ALK[G1269A] MSA 23 EPHB2 MSA 6 ALK[L1196M] MSA 23 EPHB3 MSA 6 ALK[R1275Q] MSA 23 EPHB4 MSA 6 ALK[T1151_L1152insT] MSA 23 Erk1(MAPK3) MSA 7 EML4-ALK MSA 24 Erk2(MAPK1) MSA 7 NPM1-ALK MSA 24 Erk5(MAPK7) MSA 7 AMPKα1/β1/γ1(PRKAA1/B1/G1) MSA 24 FAK(PTK2) MSA 7 AMPKα2/β1/γ1(PRKAA2/B1/G1) MSA 24 FER MSA 7 ARG(ABL2) MSA 24 FES MSA 8 AurA(AURKA) MSA 25 FGFR1 MSA 8 AurA(AURKA)/TPX2 MSA 25 FGFR1[V561M] MSA 8 AurB(AURKB)/INCENP MSA 25 FGFR2 MSA 8 AurC(AURKC) MSA 25 FGFR2[V564I] MSA 8 AXL MSA 25 FGFR3 MSA 9 BLK MSA 26 FGFR3[K650E] MSA 9 BMX MSA 26 FGFR3[K650M] MSA 9 BRK(PTK6) MSA 26 FGFR3[V555L] MSA 9 BRSK1 MSA 26 FGFR3[V555M] MSA 9 BRSK2 MSA 26 FGFR4 MSA 10 BTK MSA 27 FGFR4[N535K] MSA 10 BTK[C481S] MSA 27 FGFR4[V550E] MSA 10 BUB1/BUB3 MSA 27 FGFR4[V550L] MSA 10 CaMK1α(CAMK1) MSA 27 FGR MSA 10 CaMK1δ(CAMK1D) MSA 27 FLT1 MSA 11 CaMK2α(CAMK2A) MSA 28 -
CHD7 Represses the Retinoic Acid Synthesis Enzyme ALDH1A3 During Inner Ear Development
CHD7 represses the retinoic acid synthesis enzyme ALDH1A3 during inner ear development Hui Yao, … , Shigeki Iwase, Donna M. Martin JCI Insight. 2018;3(4):e97440. https://doi.org/10.1172/jci.insight.97440. Research Article Development Neuroscience CHD7, an ATP-dependent chromatin remodeler, is disrupted in CHARGE syndrome, an autosomal dominant disorder characterized by variably penetrant abnormalities in craniofacial, cardiac, and nervous system tissues. The inner ear is uniquely sensitive to CHD7 levels and is the most commonly affected organ in individuals with CHARGE. Interestingly, upregulation or downregulation of retinoic acid (RA) signaling during embryogenesis also leads to developmental defects similar to those in CHARGE syndrome, suggesting that CHD7 and RA may have common target genes or signaling pathways. Here, we tested three separate potential mechanisms for CHD7 and RA interaction: (a) direct binding of CHD7 with RA receptors, (b) regulation of CHD7 levels by RA, and (c) CHD7 binding and regulation of RA-related genes. We show that CHD7 directly regulates expression of Aldh1a3, the gene encoding the RA synthetic enzyme ALDH1A3 and that loss of Aldh1a3 partially rescues Chd7 mutant mouse inner ear defects. Together, these studies indicate that ALDH1A3 acts with CHD7 in a common genetic pathway to regulate inner ear development, providing insights into how CHD7 and RA regulate gene expression and morphogenesis in the developing embryo. Find the latest version: https://jci.me/97440/pdf RESEARCH ARTICLE CHD7 represses the retinoic acid synthesis enzyme ALDH1A3 during inner ear development Hui Yao,1 Sophie F. Hill,2 Jennifer M. Skidmore,1 Ethan D. Sperry,3,4 Donald L. -
Oncjuly3 6..6
Oncogene (1999) 18, 4137 ± 4143 ã 1999 Stockton Press All rights reserved 0950 ± 9232/99 $12.00 http://www.stockton-press.co.uk/onc Tax protein of HTLV-1 inhibits CBP/p300-mediated transcription by interfering with recruitment of CBP/p300 onto DNA element of E-box or p53 binding site Takeshi Suzuki1, Masami Uchida-Toita1 and Mitsuaki Yoshida*,1 1Department of Cellular and Molecular Biology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Tax protein of human T-cell leukemia virus type 1 Tax was originally identi®ed as a transcriptional (HTLV-1) is a potent transcriptional regulator which can activator for viral gene expression and then was shown activate or repress speci®c cellular genes and has been to activate a wide variety of cellular genes (Yoshida et proposed to contribute to leukemogenic processes in al., 1995). Tax was also demonstrated to inhibit adult T-cell leukemia. The molecular mechanism of Tax- expression of several genes. In addition to the mediated trans-activation has been well investigated. transcriptional deregulation, we found that Tax binds However, trans-repression by Tax remains to be studied to p16ink4a protein, a cyclin-dependent kinase (CDK) in detail, although it is known to require a speci®c DNA inhibitor, and suppresses its inhibitory activity pre- element such as E-box or p53 binding site. Examining venting the cell from undergoing growth arrest (Suzuki possible mechanisms of trans-repression, we found that et al., 1996). These pleiotropic functions of Tax aect co-expression of E47 and p300 activated E-box multiple regulatory processes of cells and are believed dependent transcription and this activation was eciently to play roles at least in the initial stage of repressed by Tax. -
Transcrip\Onal and Epigene\C Changes During Heart Disease
786/110 Transcrip)onal and Epigene)c Changes during Heart Disease Danish Sayed Unique Features of Heart • Involuntary, rhythmic, cyclic contractions • Terminally differentiated, postnatal myocytes increase in size not numbers for growth • Number of non myocytes (e.g. fibroblasts) is more (60-70%) compared to number of myocytes (~30%). Neonate Heart Postnatal Growth “Physiological” Adult Heart - Exercise - Hypertension - Pregnancy - Aortic Stenosis - Sarcomeric Gene mutation - Myocardial Infarction - Dilated Cardiomyopathy Physiological Pathological Hypertrophy Hypertrophy Dilatation and Failure Compensatory Decompensation Overload • Increase in cardiomyocyte size • Chamber dilatation and mass, resulting in enlarged heart • Decreased Ventricular Wall • Increase in generalized gene Thickness and Increased expression, superimposed with wall tension significant increase in specialized genes, fetal gene • Altered Ca+2 handling program • Increased wall thickness • Increased myocardial • Switch to glucose metabolism apoptosis for energy Compromised Maintained Cardiac Cardiac function and Function and Output Output Modulators of Cardiac Hypertrophy L-Type Ca+2 Ang II, ET-1 Channel α-Adrenergic β-Adrenergic Mechanical Ca+2 Insulin-like Growth Stretch + Factor Na Gq Gs P Ca+2 PKA PLC Adenylyl Integrin Cyclase Ca+2 RAS-GTP Na+ PI3K IP3 DAG cAMP Calcineurine FAK AKT Ca+2 Rho PKC PKA Ras mTOR Rac GSK3β 4EBP1 Rock MLCK NFAT MAPK eIF2B p70S6K eIF4E ME ME ME ME GATA4 GATA4 MEF2 Sarcomere SRF Translation AC AC Transcription HDAC Histone Acetylation HAT Modificatn. Methylation HMT Chromatin Demethylases Remodeling Phosphorylation DNA Methylation Transcriptional Modificatn. General Factors Transcription factors TFIIA, TFIIB, TFIID… Promoter Specific Factors GATA family, NFATc family Activity Recruitment Gene Regulation RNA Polymerase II Dynamics Initiation Elongation Translation factors e.g. -
HCC and Cancer Mutated Genes Summarized in the Literature Gene Symbol Gene Name References*
HCC and cancer mutated genes summarized in the literature Gene symbol Gene name References* A2M Alpha-2-macroglobulin (4) ABL1 c-abl oncogene 1, receptor tyrosine kinase (4,5,22) ACBD7 Acyl-Coenzyme A binding domain containing 7 (23) ACTL6A Actin-like 6A (4,5) ACTL6B Actin-like 6B (4) ACVR1B Activin A receptor, type IB (21,22) ACVR2A Activin A receptor, type IIA (4,21) ADAM10 ADAM metallopeptidase domain 10 (5) ADAMTS9 ADAM metallopeptidase with thrombospondin type 1 motif, 9 (4) ADCY2 Adenylate cyclase 2 (brain) (26) AJUBA Ajuba LIM protein (21) AKAP9 A kinase (PRKA) anchor protein (yotiao) 9 (4) Akt AKT serine/threonine kinase (28) AKT1 v-akt murine thymoma viral oncogene homolog 1 (5,21,22) AKT2 v-akt murine thymoma viral oncogene homolog 2 (4) ALB Albumin (4) ALK Anaplastic lymphoma receptor tyrosine kinase (22) AMPH Amphiphysin (24) ANK3 Ankyrin 3, node of Ranvier (ankyrin G) (4) ANKRD12 Ankyrin repeat domain 12 (4) ANO1 Anoctamin 1, calcium activated chloride channel (4) APC Adenomatous polyposis coli (4,5,21,22,25,28) APOB Apolipoprotein B [including Ag(x) antigen] (4) AR Androgen receptor (5,21-23) ARAP1 ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 1 (4) ARHGAP35 Rho GTPase activating protein 35 (21) ARID1A AT rich interactive domain 1A (SWI-like) (4,5,21,22,24,25,27,28) ARID1B AT rich interactive domain 1B (SWI1-like) (4,5,22) ARID2 AT rich interactive domain 2 (ARID, RFX-like) (4,5,22,24,25,27,28) ARID4A AT rich interactive domain 4A (RBP1-like) (28) ARID5B AT rich interactive domain 5B (MRF1-like) (21) ASPM Asp (abnormal -
Repressor to Activator Switch by Mutations in the First Zn Finger of The
Proc. Nat!. Acad. Sci. USA Vol. 88, pp. 7086-7090, August 1991 Biochemistry Repressor to activator switch by mutations in the first Zn finger of the glucocorticoid receptor: Is direct DNA binding necessary? (interleukin 1 indudbility/dexamethasone modulation/DNA-binding domain mutants/interleukin 6 and c-fos promoters) ANURADHA RAY, K. STEVEN LAFORGE, AND PRAVINKUMAR B. SEHGAL* The Rockefeller University, New York, NY 10021 Communicated by Igor Tamm, May 20, 1991 (receivedfor review March 15, 1991) ABSTRACT Transfection ofHeLa cells with cDNA vectors previous experiments in HeLa cells transfected with cDNA expressing the wild-type human glucocorticoid receptor (GR) vectors constitutively expressing the wild type (wt) but not enabled dexamethasone to strongly repress cytokine- and sec- the inactive carboxyl-terminal truncation mutants of GR, we ond messenger-induced expression of cotransfected chimeric observed that dexamethasone (Dex) strongly repressed the reporter genes containing transcription regulatory DNA ele- induction by interleukin 1 (IL-1), tumor necrosis factor, ments from the human interleukin 6 (IL-6) promoter. Deletion phorbol ester, or forskolin of IL-6-chloramphenicol acetyl- of the DNA-binding domain or of the second Zn finger or a transferase (CAT) constructs containing IL-6 DNA from point mutation in the Zn catenation site in the second finger -225 to +13. Dex also repressed induction of IL-6- blocked the ability of GR to mediate repression of the IL-6 thymidine kinase (TK)-CAT chimeric constructs containing promoter. -
NIH Public Access Provided by Digital.CSIC Author Manuscript Bioessays
View metadata, citation and similar papers at core.ac.uk brought to you by CORE NIH Public Access provided by Digital.CSIC Author Manuscript Bioessays. Author manuscript; available in PMC 2007 October 1. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Bioessays. 2007 April ; 29(4): 356±370. GTP-binding proteins of the Rho/Rac family: regulation, effectors and functions in vivo Xosé R. Bustelo*, Vincent Sauzeau, and Inmaculada M. Berenjeno Centro de Investigación del Cáncer and Instituto de Biología Molecular y Celular del Cáncer (IBMCC), CSIC-University of Salamanca, Salamanca, Spain. Summary Rho/Rac proteins constitute a subgroup of the Ras superfamily of GTP hydrolases. Although originally implicated in the control of cytoskeletal events, it is currently known that these GTPases coordinate diverse cellular functions, including cell polarity, vesicular trafficking, the cell cycle and transcriptomal dynamics. In this review, we will provide an overview on the recent advances in this field regarding the mechanism of regulation and signaling, and the roles in vivo of this important GTPase family. Introduction The isolation of rhoA,(1) the first member of the Rho/Rac family ever identified, was achieved by Richard Axel’s group in 1985 during the search for ras -related genes in Aplysia.(1) The subsequent use of conventional cloning techniques and the more-recent characterization of genomes revealed that the original gene is not alone, having numerous family counterparts in other species including, among many others, S. cerevisiae(7 genes), A. taliana(11 genes), C. elegans(9 genes), D. melanogaster(9 genes) and H. -
Characterization of the Small Molecule Kinase Inhibitor SU11248 (Sunitinib/ SUTENT in Vitro and in Vivo
TECHNISCHE UNIVERSITÄT MÜNCHEN Lehrstuhl für Genetik Characterization of the Small Molecule Kinase Inhibitor SU11248 (Sunitinib/ SUTENT in vitro and in vivo - Towards Response Prediction in Cancer Therapy with Kinase Inhibitors Michaela Bairlein Vollständiger Abdruck der von der Fakultät Wissenschaftszentrum Weihenstephan für Ernährung, Landnutzung und Umwelt der Technischen Universität München zur Erlangung des akademischen Grades eines Doktors der Naturwissenschaften genehmigten Dissertation. Vorsitzender: Univ. -Prof. Dr. K. Schneitz Prüfer der Dissertation: 1. Univ.-Prof. Dr. A. Gierl 2. Hon.-Prof. Dr. h.c. A. Ullrich (Eberhard-Karls-Universität Tübingen) 3. Univ.-Prof. A. Schnieke, Ph.D. Die Dissertation wurde am 07.01.2010 bei der Technischen Universität München eingereicht und durch die Fakultät Wissenschaftszentrum Weihenstephan für Ernährung, Landnutzung und Umwelt am 19.04.2010 angenommen. FOR MY PARENTS 1 Contents 2 Summary ................................................................................................................................................................... 5 3 Zusammenfassung .................................................................................................................................................... 6 4 Introduction .............................................................................................................................................................. 8 4.1 Cancer .............................................................................................................................................................. -
MLK3 (MAP3K11) (NM 002419) Human Tagged ORF Clone Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RC203782 MLK3 (MAP3K11) (NM_002419) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: MLK3 (MAP3K11) (NM_002419) Human Tagged ORF Clone Tag: Myc-DDK Symbol: MAP3K11 Synonyms: MEKK11; MLK-3; MLK3; PTK1; SPRK Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 5 MLK3 (MAP3K11) (NM_002419) Human Tagged ORF Clone – RC203782 ORF Nucleotide >RC203782 representing NM_002419 Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGGAGCCCTTGAAGAGCCTCTTCCTCAAGAGCCCTCTAGGGTCATGGAATGGCAGTGGCAGCGGGGGTG GTGGGGGCGGTGGAGGAGGCCGGCCTGAGGGGTCTCCAAAGGCAGCGGGTTATGCCAACCCGGTGTGGAC AGCCCTGTTCGACTACGAGCCCAGTGGGCAGGATGAGCTGGCCCTGAGGAAGGGTGACCGTGTGGAGGTG CTGTCCCGGGACGCAGCCATCTCAGGAGACGAGGGCTGGTGGGCGGGCCAGGTGGGTGGCCAGGTGGGCA TCTTCCCGTCCAACTATGTGTCTCGGGGTGGCGGCCCGCCCCCCTGCGAGGTGGCCAGCTTCCAGGAGCT GCGGCTGGAGGAGGTGATCGGCATTGGAGGCTTTGGCAAGGTGTACAGGGGCAGCTGGCGAGGTGAGCTG GTGGCTGTGAAGGCAGCTCGCCAGGACCCCGATGAGGACATCAGTGTGACAGCCGAGAGCGTTCGCCAGG AGGCCCGGCTCTTCGCCATGCTGGCACACCCCAACATCATTGCCCTCAAGGCTGTGTGCCTGGAGGAGCC CAACCTGTGCCTGGTGATGGAGTATGCAGCCGGTGGGCCCCTCAGCCGAGCTCTGGCCGGGCGGCGCGTG