Wnt5a Modulates Integrin Expression in a Receptor-Dependent Manner In
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Identification of a WNT5A-Responsive Degradation Domain in the Kinesin
G C A T T A C G G C A T genes Article Identification of a WNT5A-Responsive Degradation Domain in the Kinesin Superfamily Protein KIF26B Edith P. Karuna ID , Shannon S. Choi, Michael K. Scales, Jennie Hum, Michael Cohen, Fernando A. Fierro and Hsin-Yi Henry Ho * ID Department of Cell Biology and Human Anatomy, School of Medicine, University of California, Davis, CA 95616, USA; [email protected] (E.P.K.); [email protected] (S.S.C.); [email protected] (M.K.S.); [email protected] (J.H.); [email protected] (M.C.); ffi[email protected] (F.A.F.) * Correspondence: [email protected]; Tel.: +1-530-752-8857 Received: 19 February 2018; Accepted: 26 March 2018; Published: 5 April 2018 Abstract: Noncanonical WNT pathways function independently of the β-catenin transcriptional co-activator to regulate diverse morphogenetic and pathogenic processes. Recent studies showed that noncanonical WNTs, such as WNT5A, can signal the degradation of several downstream effectors, thereby modulating these effectors’ cellular activities. The protein domain(s) that mediates the WNT5A-dependent degradation response, however, has not been identified. By coupling protein mutagenesis experiments with a flow cytometry-based degradation reporter assay, we have defined a protein domain in the kinesin superfamily protein KIF26B that is essential for WNT5A-dependent degradation. We found that a human disease-causing KIF26B mutation located at a conserved amino acid within this domain compromises the ability of WNT5A to induce KIF26B degradation. Using pharmacological perturbation, we further uncovered a role of glycogen synthase kinase 3 (GSK3) in WNT5A regulation of KIF26B degradation. -
Expression of Wnt5a and Wnt10b in Non-Immortalized Breast Cancer Cells
903-907 24/2/07 13:56 Page 903 ONCOLOGY REPORTS 17: 903-907, 2007 903 Expression of Wnt5A and Wnt10B in non-immortalized breast cancer cells MARIANA FERNANDEZ-COBO1, FRANCESCA ZAMMARCHI3, JOHN MANDELI4, JAMES F. HOLLAND1 and BEATRIZ G.T. POGO1,2 Departments of 1Medicine, 2Microbiology and Community, and 4Preventive Medicine, Mount Sinai School of Medicine; 3Department of Molecular Pharmacology and Chemistry, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA Received October 23, 2006; Accepted November 7, 2006 Abstract. Wnt signaling is usually divided into two path- transcriptional factors of the LEF/TCF family and the TCF/ ways: the ‘canonical’, acting through ß-catenin, and the ‘non- ß-catenin complexes regulate expression of specific target canonical’ acting through the Ca2+ and planar cell polarity genes. In the non-canonical pathway there are mainly two alter- pathway. Both pathways have been implicated in different native ways of Wnt signaling which do not involve ß-catenin: types of cancer. Most results obtained with established cell the Wnt/Ca2+ pathway, which acts via calmodulin kinase II and lines have been contradictory. Here, we have investigated the protein kinase C, and the planar cell polarity pathway, which expression of Wnt10B (canonical) and Wnt5A (non-canonical) controls cytoskeletal rearrangements through Jun N-terminal in a panel of finite life-span and established normal and kinase (2). breast cancer cells using quantitative RT-PCR. It was found The role of Wnt genes in breast cancer has been studied that there were both significant overexpression of Wnt5A and since 1982, when the first Wnt member (called int-1) was underexpression of Wnt10B in the metastasis-derived finite identified as the gene activated by integration of the mouse life-span breast cancer cells when they were compared to the mammary tumor virus, resulting in the development of finite life-span normal and established normal and breast mammary tumors in mice (3). -
PTPRA Phosphatase Regulates GDNF-Dependent RET Signaling and Inhibits the RET Mutant MEN2A Oncogenic Potential
Journal Pre-proof PTPRA phosphatase regulates GDNF-dependent RET signaling and inhibits the RET mutant MEN2A oncogenic potential Leena Yadav, Elina Pietilä, Tiina Öhman, Xiaonan Liu, Arun K. Mahato, Yulia Sidorova, Kaisa Lehti, Mart Saarma, Markku Varjosalo PII: S2589-0042(20)30055-9 DOI: https://doi.org/10.1016/j.isci.2020.100871 Reference: ISCI 100871 To appear in: ISCIENCE Received Date: 3 August 2019 Revised Date: 15 January 2020 Accepted Date: 26 January 2020 Please cite this article as: Yadav, L., Pietilä, E., Öhman, T., Liu, X., Mahato, A.K., Sidorova, Y., Lehti, K., Saarma, M., Varjosalo, M., PTPRA phosphatase regulates GDNF-dependent RET signaling and inhibits the RET mutant MEN2A oncogenic potential, ISCIENCE (2020), doi: https://doi.org/10.1016/ j.isci.2020.100871. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2020 Growth factor RET PTPRA Cell surface Ras P P Complex formation RAF MEK ERK Growth Nucleus Proliferation Gene expression Migration 1 PTPRA phosphatase regulates GDNF-dependent RET signaling and inhibits the RET mutant MEN2A oncogenic potential Authors Leena Yadav 1, Elina Pietilä 3# , Tiina Öhman 1# , Xiaonan Liu 1, Arun K. -
Supplemental Tables4.Pdf
Yano_Supplemental_Table_S4 Gene ontology – Biological process 1 of 9 Fold List Pop Pop GO Term Count % PValue Bonferroni Benjamini FDR Genes Total Hits Total Enrichment DLC1, CADM1, NELL2, CLSTN1, PCDHGA8, CTNNB1, NRCAM, APP, CNTNAP2, FERT2, RAPGEF1, PTPRM, MPDZ, SDK1, PCDH9, PTPRS, VEZT, NRXN1, MYH9, GO:0007155~cell CTNNA2, NCAM1, NCAM2, DDR1, LSAMP, CNTN1, 50 5.61 2.14E-08 510 311 7436 2.34 4.50E-05 4.50E-05 3.70E-05 adhesion ROR2, VCAN, DST, LIMS1, TNC, ASTN1, CTNND2, CTNND1, CDH2, NEO1, CDH4, CD24A, FAT3, PVRL3, TRO, TTYH1, MLLT4, LPP, NLGN1, PCDH19, LAMA1, ITGA9, CDH13, CDON, PSPC1 DLC1, CADM1, NELL2, CLSTN1, PCDHGA8, CTNNB1, NRCAM, APP, CNTNAP2, FERT2, RAPGEF1, PTPRM, MPDZ, SDK1, PCDH9, PTPRS, VEZT, NRXN1, MYH9, GO:0022610~biological CTNNA2, NCAM1, NCAM2, DDR1, LSAMP, CNTN1, 50 5.61 2.14E-08 510 311 7436 2.34 4.50E-05 4.50E-05 3.70E-05 adhesion ROR2, VCAN, DST, LIMS1, TNC, ASTN1, CTNND2, CTNND1, CDH2, NEO1, CDH4, CD24A, FAT3, PVRL3, TRO, TTYH1, MLLT4, LPP, NLGN1, PCDH19, LAMA1, ITGA9, CDH13, CDON, PSPC1 DCC, ENAH, PLXNA2, CAPZA2, ATP5B, ASTN1, PAX6, ZEB2, CDH2, CDH4, GLI3, CD24A, EPHB1, NRCAM, GO:0006928~cell CTTNBP2, EDNRB, APP, PTK2, ETV1, CLASP2, STRBP, 36 4.04 3.46E-07 510 205 7436 2.56 7.28E-04 3.64E-04 5.98E-04 motion NRG1, DCLK1, PLAT, SGPL1, TGFBR1, EVL, MYH9, YWHAE, NCKAP1, CTNNA2, SEMA6A, EPHA4, NDEL1, FYN, LRP6 PLXNA2, ADCY5, PAX6, GLI3, CTNNB1, LPHN2, EDNRB, LPHN3, APP, CSNK2A1, GPR45, NRG1, RAPGEF1, WWOX, SGPL1, TLE4, SPEN, NCAM1, DDR1, GRB10, GRM3, GNAQ, HIPK1, GNB1, HIPK2, PYGO1, GO:0007166~cell RNF138, ROR2, CNTN1, -
Ptk7-Deficient Mice Have Decreased Hematopoietic Stem Cell Pools As a Result of Deregulated Proliferation and Migration
Ptk7-Deficient Mice Have Decreased Hematopoietic Stem Cell Pools as a Result of Deregulated Proliferation and Migration This information is current as Anne-Catherine Lhoumeau, Marie-Laure Arcangeli, Maria of September 24, 2021. De Grandis, Marilyn Giordano, Jean-Christophe Orsoni, Frédérique Lembo, Florence Bardin, Sylvie Marchetto, Michel Aurrand-Lions and Jean-Paul Borg J Immunol 2016; 196:4367-4377; Prepublished online 18 April 2016; Downloaded from doi: 10.4049/jimmunol.1500680 http://www.jimmunol.org/content/196/10/4367 Supplementary http://www.jimmunol.org/content/suppl/2016/04/16/jimmunol.150068 http://www.jimmunol.org/ Material 0.DCSupplemental References This article cites 55 articles, 24 of which you can access for free at: http://www.jimmunol.org/content/196/10/4367.full#ref-list-1 Why The JI? Submit online. by guest on September 24, 2021 • 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 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 -
Functional Analysis of Somatic Mutations Affecting Receptor Tyrosine Kinase Family in Metastatic Colorectal Cancer
Author Manuscript Published OnlineFirst on March 29, 2019; DOI: 10.1158/1535-7163.MCT-18-0582 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Functional analysis of somatic mutations affecting receptor tyrosine kinase family in metastatic colorectal cancer Leslie Duplaquet1, Martin Figeac2, Frédéric Leprêtre2, Charline Frandemiche3,4, Céline Villenet2, Shéhérazade Sebda2, Nasrin Sarafan-Vasseur5, Mélanie Bénozène1, Audrey Vinchent1, Gautier Goormachtigh1, Laurence Wicquart6, Nathalie Rousseau3, Ludivine Beaussire5, Stéphanie Truant7, Pierre Michel8, Jean-Christophe Sabourin9, Françoise Galateau-Sallé10, Marie-Christine Copin1,6, Gérard Zalcman11, Yvan De Launoit1, Véronique Fafeur1 and David Tulasne1 1 Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T – Mechanisms of Tumorigenesis and Target Therapies, F-59000 Lille, France. 2 Univ. Lille, Plateau de génomique fonctionnelle et structurale, CHU Lille, F-59000 Lille, France 3 TCBN - Tumorothèque Caen Basse-Normandie, F-14000 Caen, France. 4 Réseau Régional de Cancérologie – OncoBasseNormandie – F14000 Caen – France. 5 Normandie Univ, UNIROUEN, Inserm U1245, IRON group, Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine, F-76000 Rouen, France. 6 Tumorothèque du C2RC de Lille, F-59037 Lille, France. 7 Department of Digestive Surgery and Transplantation, CHU Lille, Univ Lille, 2 Avenue Oscar Lambret, 59037, Lille Cedex, France. 8 Department of hepato-gastroenterology, Rouen University Hospital, Normandie Univ, UNIROUEN, Inserm U1245, IRON group, F-76000 Rouen, France. 9 Department of Pathology, Normandy University, INSERM 1245, Rouen University Hospital, F 76 000 Rouen, France. 10 Department of Pathology, MESOPATH-MESOBANK, Centre León Bérard, Lyon, France. 11 Thoracic Oncology Department, CIC1425/CLIP2 Paris-Nord, Hôpital Bichat-Claude Bernard, Paris, France. -
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 -
Loss of Receptor Tyrosine Kinase-Like Orphan Receptor 2 Impairs The
Lei et al. Stem Cell Research & Therapy (2020) 11:137 https://doi.org/10.1186/s13287-020-01646-2 RESEARCH Open Access Loss of receptor tyrosine kinase-like orphan receptor 2 impairs the osteogenesis of mBMSCs by inhibiting signal transducer and activator of transcription 3 Lizhen Lei1,2, Zhuwei Huang1,2, Jingyi Feng1,2, Zijing Huang1,2, Yiwei Tao1,2, Xiaoli Hu1,2* and Xiaolei Zhang1,2* Abstract Background: Receptor tyrosine kinase-like orphan receptor 2 (Ror2) plays a key role in bone formation, but its signaling pathway is not completely understood. Signal transducer and activator of transcription 3 (Stat3) takes part in maintaining bone homeostasis. The aim of this study is to reveal the role and mechanism of Ror2 in the osteogenic differentiation from mouse bone marrow mesenchymal stem cells (mBMSCs) and to explore the effect of Stat3 on Ror2-mediated osteogenesis. Methods: Ror2 CKO mice were generated via the Cre-loxp recombination system using Prrx1-Cre transgenic mice. Quantitative real-time PCR and western blot were performed to assess the expression of Stat3 and osteogenic markers in Ror2-knockdown mBMSCs (mBMSC-sh-Ror2). After being incubated in osteogenic induction medium for 3 weeks, Alizarin Red staining and western blot were used to examine the calcium deposit and osteogenic markers in Stat3 overexpression in mBMSC-sh-Ror2. Results: Loss of Ror2 in mesenchymal or osteoblast progenitor cells led to a dwarfism phenotype in vivo. The mRNA expression of osteogenic markers (osteocalcin, osteopontin (OPN), and collagen I) in the ulna proximal epiphysis of Ror2 CKO mice was significantly decreased (P < 0.05). -
WNT2 and WNT7B Cooperative Signaling in Lung Development
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2012 WNT2 and WNT7B Cooperative Signaling in Lung Development Mayumi Miller University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Developmental Biology Commons, and the Molecular Biology Commons Recommended Citation Miller, Mayumi, "WNT2 and WNT7B Cooperative Signaling in Lung Development" (2012). Publicly Accessible Penn Dissertations. 674. https://repository.upenn.edu/edissertations/674 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/674 For more information, please contact [email protected]. WNT2 and WNT7B Cooperative Signaling in Lung Development Abstract The development of a complex organ, such as the lung, relies upon precisely controlled temporal and spatial expression patterns of signaling pathways for proper specification and differentiation of the cell types required to build a lung. While progress has been made in dissecting the network of signaling pathways and the integration of their positive and negative feedback mechanisms, there is still much to discover. For example, the Wnt signaling pathway is required for lung specification and growth, but a combinatorial role for Wnt ligands has not been investigated. In this dissertation, I combine mouse genetic models and in vitro and ex vivo lung culture assays, to determine a cooperative role for Wnt2 and Wnt7b in the developing lung. This body of work reveals the requirement of cooperative signaling between Wnt2 and Wnt7b for smooth muscle development and proximal to distal patterning of the lung. Additional findings er veal a role for the Pdgf pathway and homeobox genes in potentiating this cooperation. -
Wnt5a-ROR Signaling Is Essential for Alveologenesis
cells Article WNT5a-ROR Signaling Is Essential for Alveologenesis Changgong Li 1,* , Susan M Smith 1, Neil Peinado 1, Feng Gao 1, Wei Li 1, Matt K Lee 1, Beiyun Zhou 2, Saverio Bellusci 1,3 , Gloria S Pryhuber 4, Hsin-Yi Henry Ho 5 , Zea Borok 2 and Parviz Minoo 1,* 1 Division of Neonatology, Departments of Pediatrics, LAC+USC Medical Center and Childrens Hospital, Los Angeles, CA 90033, USA; [email protected] (S.M.S.); [email protected] (N.P.); [email protected] (F.G.); [email protected] (W.L.); [email protected] (M.K.L.); [email protected] (S.B.) 2 Hastings Center for Pulmonary Research and Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Keck School of Medicine of USC, Los Angeles, CA 90033, USA; [email protected] (B.Z.); [email protected] (Z.B.) 3 Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University Giessen, German Center for Lung Research (DZL), Giessen 35390, Germany 4 Division of Neonatology, Department of Pediatrics, University of Rochester Medical Center, Rochester, NY 14642, USA; [email protected] 5 Department of Cell Biology and Human Anatomy, School of Medicine, University of California, Davis, CA 95616, USA; [email protected] * Correspondence: [email protected] (C.L.); [email protected] (P.M.); Tel.: 3234420383 (C.L.); 3234093406 (P.M.) Received: 20 December 2019; Accepted: 6 February 2020; Published: 7 February 2020 Abstract: WNT5a is a mainly “non-canonical” WNT ligand whose dysregulation is observed in lung diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and asthma. -
Global Regulation of Differential Gene Expression by C-Abl/Arg Oncogenic
LAB/IN VITRO RESEARCH e-ISSN 1643-3750 © Med Sci Monit, 2017; 23: 2625-2635 DOI: 10.12659/MSM.904888 Received: 2017.04.16 Accepted: 2017.05.08 Global Regulation of Differential Gene Published: 2017.05.30 Expression by c-Abl/Arg Oncogenic Kinases Authors’ Contribution: ABCE 1 Qincai Dong* 1 Laboratory of Genetic Engineering, Beijing Institute of Biotechnology, Beijing, Study Design A BC 2 Chenggong Li* P.R. China Data Collection B 2 Institute of Health Sciences, Anhui University, Hefei, Anhui, P.R. China Statistical Analysis C BC 3 Xiuhua Qu 3 Center of Basic Medical Sciences, Navy General Hospital of PLA, Beijing, Data Interpretation D AFG 1 Cheng Cao P.R. China Manuscript Preparation E AEG 1 Xuan Liu Literature Search F Funds Collection G * These 2 authors contributed equally to this work Corresponding Authors: Xuan Liu, e-mail: [email protected], Cheng Cao, e-mail: [email protected] Source of support: This work was supported by the National Natural Science Foundation of China [31070674] Background: Studies have found that c-Abl oncogenic kinases may regulate gene transcription by RNA polymerase II phos- phorylation or by direct regulation of specific transcription factors or coactivators. However, the global regu- lation of differential gene expression by c-Abl/Arg is largely unknown. In this study, differentially expressed genes (DEGs) regulated by c-Abl/Arg were identified, and related cellular functions and associated pathways were investigated. Material/Methods: RNA obtained from wild-type and c-Abl/Arg gene-silenced MCF-7 cells was analyzed by RNA-Seq. DEGs were identified using edgeR software and partially validated by qRT-PCR. -
Ror2 Functions As a Noncanonical Wnt Receptor That Regulates NMDAR-Mediated Synaptic Transmission
RoR2 functions as a noncanonical Wnt receptor that regulates NMDAR-mediated synaptic transmission Waldo Cerpaa,1, Elena Latorre-Estevesa,b, and Andres Barriaa,2 aDepartment of Physiology and Biophysics and bMolecular and Cellular Biology Program, University of Washington, Seattle, WA 98195 Edited* by Richard L. Huganir, The Johns Hopkins University School of Medicine, Baltimore, MD, and approved March 6, 2015 (received for review September 16, 2014) Wnt signaling has a well-established role as a regulator of nervous receptor for noncanonical Wnt ligands capable of regulating syn- system development, but its role in the maintenance and regula- aptic NMDARs. In hippocampal neurons, activation of RoR2 by tion of established synapses in the mature brain remains poorly noncanonical Wnt ligand Wnt5a activates PKC and JNK, two understood. At excitatory glutamatergic synapses, NMDA receptors kinases involved in the regulation of NMDAR currents. In ad- (NMDARs) have a fundamental role in synaptogenesis, synaptic dition, we show that signaling through RoR2 is necessary for plasticity, and learning and memory; however, it is not known what the maintenance of basal NMDAR-mediated synaptic trans- controls their number and subunit composition. Here we show that mission and the acute regulation of NMDAR synaptic responses the receptor tyrosine kinase-like orphan receptor 2 (RoR2) func- by Wnt5a. tions as a Wnt receptor required to maintain basal NMDAR- Identification of RoR2 as a Wnt receptor that regulates syn- aptic NMDARs provides a mechanism for Wnt signaling to mediated synaptic transmission. In addition, RoR2 activation by a control synaptic transmission and synaptic plasticity acutely, and noncanonical Wnt ligand activates PKC and JNK and acutely en- is a critical first step toward understanding the role played by hances NMDAR synaptic responses.