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KO Kidney.Xlsx
Supplemental Table 18: Dietary Impact on the CGL KO Kidney Sulfhydrome DR/AL Accession Molecular Cysteine Spectral Protein Name Number Alternate ID Weight Residues Count Ratio P‐value Ig gamma‐2A chain C region, A allele P01863 (+1) Ighg 36 kDa 10 C 5.952 0.03767 Heterogeneous nuclear ribonucleoprotein M Q9D0E1 (+1) Hnrnpm 78 kDa 6 C 5.000 0.00595 Phospholipase D3 O35405 Pld3 54 kDa 8 C 4.167 0.04761 Ig kappa chain V‐V region L7 (Fragment) P01642 Gm10881 13 kDa 2 C 2.857 0.01232 UPF0160 protein MYG1, mitochondrial Q9JK81 Myg1 43 kDa 7 C 2.333 0.01613 Copper homeostasis protein cutC homolog Q9D8X1 Cutc 29 kDa 7 C 10.333 0.16419 Corticosteroid‐binding globulin Q06770 Serpina6 45 kDa 3 C 10.333 0.16419 28S ribosomal protein S22, mitochondrial Q9CXW2 Mrps22 41 kDa 2 C 7.333 0.3739 Isoform 3 of Agrin A2ASQ1‐3 Agrn 198 kDa 2 C 7.333 0.3739 3‐oxoacyl‐[acyl‐carrier‐protein] synthase, mitochondrial Q9D404 Oxsm 49 kDa 11 C 7.333 0.3739 Cordon‐bleu protein‐like 1 Q3UMF0 (+3)Cobll1 137 kDa 10 C 5.833 0.10658 ADP‐sugar pyrophosphatase Q9JKX6 Nudt5 24 kDa 5 C 4.167 0.15819 Complement C4‐B P01029 C4b 193 kDa 29 C 3.381 0.23959 Protein‐glutamine gamma‐glutamyltransferase 2 P21981 Tgm2 77 kDa 20 C 3.381 0.23959 Isochorismatase domain‐containing protein 1 Q91V64 Isoc1 32 kDa 5 C 3.333 0.10588 Serpin B8 O08800 Serpinb8 42 kDa 11 C 2.903 0.06902 Heterogeneous nuclear ribonucleoprotein A0 Q9CX86 Hnrnpa0 31 kDa 3 C 2.667 0.5461 Proteasome subunit beta type‐8 P28063 Psmb8 30 kDa 5 C 2.583 0.36848 Ig kappa chain V‐V region MOPC 149 P01636 12 kDa 2 C 2.583 0.36848 -
Active Rac1 Detection Kit 2012 09/20
Active Rac1 Detection Kit 1 Kit Orders n 877-616-CELL (2355) (30 immunoprecipitations) [email protected] Support n 877-678-TECH (8324) [email protected] Web n www.cellsignal.com rev. 09/24/20 #8815 For Research Use Only. Not For Use In Diagnostic Procedures. Species Cross-Reactivity: H, M Components Ship As: 11894S Item # Kit Quantity Storage Temp Description: The Active Rac1 Detection Kit provides all GTPgS 11521 1 X 50 µl –80°C reagents necessary for measuring activation of Rac1 GTPase in the cell. GST-PAK1-PBD fusion protein is used to bind GDP 11522 1 X 50 µl –80°C the activated form of GTP-bound Rac1, which can then be Components Ship As: 11894S Item # Kit Quantity Storage Temp immunoprecipitated with glutathione resin. Rac1 activation levels are then determined by western blot using a Rac1 GST-Human PAK1-PBD 8659 1 X 600 µg –20°C Mouse mAb. Rac1 Mouse mAb 8631 1 X 50 µl –20°C Specificity/Sensitivity: Active Rac1 Detection Kit detects Components Ship As: 11860S Item # Kit Quantity Storage Temp endogenous levels of GTP-bound (active) Rac1 as shown in Lysis/Binding/Wash Buffer 11524 1 X 100 mL 4°C Figure 1. This kit detects proteins from the indicated species, as determined through in-house testing, but may also detect Glutathione Resin 11523 1 X 3 ml 4°C homologous proteins from other species. SDS Sample Buffer 11525 1 X 1.5 ml 4°C Background: The Ras superfamily of small GTP-binding Spin Cup and Collection Tubes 11526 1 X 30 vial RT proteins (G proteins) comprise a large class of proteins (over 150 members) that can be classified into at least five families based on their sequence and functional similarities: 1 2 3 4 Figure 1. -
Mechanical Forces Induce an Asthma Gene Signature in Healthy Airway Epithelial Cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T
www.nature.com/scientificreports OPEN Mechanical forces induce an asthma gene signature in healthy airway epithelial cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T. Kho4, Kelan Tantisira1, Marc Santolini 1,5, Feixiong Cheng6,7,8, Jennifer A. Mitchel3, Maureen McGill3, Michael J. O’Sullivan3, Margherita De Marzio1,3, Amitabh Sharma1, Scott H. Randell9, Jefrey M. Drazen3, Jefrey J. Fredberg3 & Scott T. Weiss1,3* Bronchospasm compresses the bronchial epithelium, and this compressive stress has been implicated in asthma pathogenesis. However, the molecular mechanisms by which this compressive stress alters pathways relevant to disease are not well understood. Using air-liquid interface cultures of primary human bronchial epithelial cells derived from non-asthmatic donors and asthmatic donors, we applied a compressive stress and then used a network approach to map resulting changes in the molecular interactome. In cells from non-asthmatic donors, compression by itself was sufcient to induce infammatory, late repair, and fbrotic pathways. Remarkably, this molecular profle of non-asthmatic cells after compression recapitulated the profle of asthmatic cells before compression. Together, these results show that even in the absence of any infammatory stimulus, mechanical compression alone is sufcient to induce an asthma-like molecular signature. Bronchial epithelial cells (BECs) form a physical barrier that protects pulmonary airways from inhaled irritants and invading pathogens1,2. Moreover, environmental stimuli such as allergens, pollutants and viruses can induce constriction of the airways3 and thereby expose the bronchial epithelium to compressive mechanical stress. In BECs, this compressive stress induces structural, biophysical, as well as molecular changes4,5, that interact with nearby mesenchyme6 to cause epithelial layer unjamming1, shedding of soluble factors, production of matrix proteins, and activation matrix modifying enzymes, which then act to coordinate infammatory and remodeling processes4,7–10. -
Rac1 Accumulates in the Nucleus During the G2 Phase of the Cell
Published Online: 28 April, 2008 | Supp Info: http://doi.org/10.1083/jcb.200801047 JCB: ARTICLE Downloaded from jcb.rupress.org on May 9, 2018 Rac1 accumulates in the nucleus during the G2 phase of the cell cycle and promotes cell division David Michaelson , 2,5 Wasif Abidi , 2,5 Daniele Guardavaccaro , 4,5 Mo Zhou, 3,5 Ian Ahearn , 3,5 Michele Pagano , 4,5 and Mark R. Philips 1,2,3,5 1 Department of Medicine, 2 Department of Cell Biology, 3 Department of Pharmacology, 4 Department of Pathology, and the 5 New York University Cancer Institute, New York University School of Medicine, New York, NY 10016 ac1 regulates a wide variety of cellular processes. zation of cells stably expressing low levels of GFP-Rac1, The polybasic region of the Rac1 C terminus func- and time-lapse microscopy of asynchronous cells revealed Rtions both as a plasma membrane – targeting motif Rac1 accumulation in the nucleus in late G2 and exclu- and a nuclear localization sequence (NLS). We show that sion in early G1. Although constitutively active Rac1 re- a triproline N-terminal to the polybasic region contributes stricted to the cytoplasm inhibited cell division, activated to the NLS, which is cryptic in the sense that it is strongly Rac1 expressed constitutively in the nucleus increased the inhibited by geranylgeranylation of the adjacent cysteine. mitotic rate. These results show that Rac1 cycles in and out Subcellular fractionation demonstrated endogenous Rac1 of the nucleus during the cell cycle and thereby plays a in the nucleus and Triton X-114 partition revealed that this role in promoting cell division. -
Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model
Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. -
IMPDH2: a New Gene Associated with Dominant Juvenile-Onset Dystonia-Tremor Disorder
www.nature.com/ejhg BRIEF COMMUNICATION OPEN IMPDH2: a new gene associated with dominant juvenile-onset dystonia-tremor disorder 1,8 1,8 2 3 1,4 2 5 Anna Kuukasjärvi , Juan✉ C. Landoni , Jyrki Kaukonen , Mika Juhakoski , Mari Auranen , Tommi Torkkeli , Vidya Velagapudi and Anu Suomalainen 1,6,7 © The Author(s) 2021 The aetiology of dystonia disorders is complex, and next-generation sequencing has become a useful tool in elucidating the variable genetic background of these diseases. Here we report a deleterious heterozygous truncating variant in the inosine monophosphate dehydrogenasegene(IMPDH2) by whole-exome sequencing, co-segregating with a dominantly inherited dystonia-tremor disease in a large Finnish family. We show that the defect results in degradation of the gene product, causing IMPDH2 deficiency in patient cells. IMPDH2 is the first and rate-limiting enzyme in the de novo biosynthesis of guanine nucleotides, a dopamine synthetic pathway previously linked to childhood or adolescence-onset dystonia disorders. We report IMPDH2 as a new gene to the dystonia disease entity. The evidence underlines the important link between guanine metabolism, dopamine biosynthesis and dystonia. European Journal of Human Genetics; https://doi.org/10.1038/s41431-021-00939-1 INTRODUCTION The disease-onset was between 9 and 20 years of age. Table 1 Dystonias are rare movement disorders characterised by sustained or summarises the clinical presentations. intermittent muscle contractions causing abnormal, often repetitive, movements and/or postures. Dystonia can manifest as an isolated Case report symptom or combined with e.g. parkinsonism or myoclonus [1]. While Patient II-6 is a 46-year-old woman. -
Identification and Partial Characterization of a Family of Putative Palmitoyltransferases in Dictyostelium Discoideum Brent Elliot Wells
The University of Maine DigitalCommons@UMaine Electronic Theses and Dissertations Fogler Library 2003 Identification and Partial Characterization of a Family of Putative Palmitoyltransferases in Dictyostelium Discoideum Brent Elliot Wells Follow this and additional works at: http://digitalcommons.library.umaine.edu/etd Part of the Biochemistry Commons Recommended Citation Wells, Brent Elliot, "Identification and Partial Characterization of a Family of Putative Palmitoyltransferases in Dictyostelium Discoideum" (2003). Electronic Theses and Dissertations. 301. http://digitalcommons.library.umaine.edu/etd/301 This Open-Access Thesis is brought to you for free and open access by DigitalCommons@UMaine. It has been accepted for inclusion in Electronic Theses and Dissertations by an authorized administrator of DigitalCommons@UMaine. IDENTIFICATION AND PARTIAL CHARACTERIZATION OF A FAMILY OF PUTATIVE PALMITOYLTRANSFERASES IN DICTYOSTELIUM DISCOIDEUM BY Brent Elliott Wells B.S. University of Utah, 1994 A THESIS Submitted in Partial Fulfillment of the Requirements for the Degree of Master of Science (in Biochemistry) The Graduate School The University of Maine December, 2003 Advisory Committee: Robert E. Gundersen, Associate Professor of Biochemistry, Advisor Keith W. Hutchison, Professor of Biochemistry Mary Rumpho-Kennedy, Professor of Biochemistry LIBRARY RIGHTS STATEMENT In presenting this thesis in partial fulfillment of the requirements for an advanced degree at The University of Maine, I agree that the Library shall make it freely available for inspection. I further agree that permission for "fair use" copying of this thesis for scholarly purposes may be granted by the Librarian. It is understood that any copying or publication of this thesis for financial gain shall not be allowed without my written permission. -
Role of Rac1-Pak Pathway in Aggressive B-Cell Lymphoma
University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Spring 5-4-2019 Role of Rac1-Pak pathway in aggressive b-cell lymphoma Tian Tian University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Hemic and Lymphatic Diseases Commons, and the Neoplasms Commons Recommended Citation Tian, Tian, "Role of Rac1-Pak pathway in aggressive b-cell lymphoma" (2019). Theses & Dissertations. 344. https://digitalcommons.unmc.edu/etd/344 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. i Role of Rac1-PAK Pathway in Aggressive B-cell Lymphomas By Tian Tian A DISSERTATION Presented to the Faculty of The University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Pathology & Microbiology Graduate program Under the Supervision of Professor Kai Fu University of Nebraska Medical Center, Omaha, Nebraska Dec, 2018 Supervisory Committee: Ying Yan, Ph.D. John S Davis, Ph.D. Timothy C Greiner, M.D. Javeed Iqbal, Ph.D. ii Role of Rac1-PAK pathway in Aggressive B-cell Lymphomas Tian Tian University of Nebraska Medical Center, 2018 Advisor: Kai Fu, M.D. Ph.D. Aggressive B-cell lymphomas are diverse group of neoplasms that arise at different stages of B-cell development and by various mechanisms of neoplastic transformation. Aggressive B-cell lymphomas include many types, subtypes and variants of diffuse large B-cell lymphoma (DLBCL), Burkitt lymphoma (BL), mantle cell lymphoma (MCL) and B lymphoblastic lymphoma. -
Rac1 Promotes Cell Motility by Controlling Cell Mechanics in Human Glioblastoma
cancers Article Rac1 Promotes Cell Motility by Controlling Cell Mechanics in Human Glioblastoma Jing Xu 1,2, Nicola Galvanetto 1, Jihua Nie 1,3, Yili Yang 2,* and Vincent Torre 1,2,3,4,* 1 International School for Advanced Studies (SISSA), 34136 Trieste, Italy; [email protected] (J.X.); [email protected] (N.G.); [email protected] (J.N.) 2 Joint Laboratory of Biophysics and Translational Medicine, Suzhou Institute of Systems Medicine (ISM)- International School for Advanced Studies (SISSA), Suzhou 215123, China 3 School of Radiation Medicine and Protection, State Key Laboratory of Radiation Medicine and Protection Medical College of Soochow University, Suzhou 215123, China 4 Cixi Institute of Biomedical Engineering, Ningbo Institute of Materials Technology and Engineering Chinese Academy of Sciences, Ningbo 315201, China * Correspondence: [email protected] (Y.Y.);[email protected] (V.T.) Received: 21 May 2020; Accepted: 2 June 2020; Published: 23 June 2020 Abstract: The failure of existing therapies in treating human glioblastoma (GBM) mostly is due to the ability of GBM to infiltrate into healthy regions of the brain; however, the relationship between cell motility and cell mechanics is not well understood. Here, we used atomic force microscopy (AFM), live-cell imaging, and biochemical tools to study the connection between motility and mechanics in human GBM cells. It was found thatRac1 inactivation by genomic silencing and inhibition with EHT 1864 reduced cell motility, inhibited cell ruffles, and disrupted the dynamics of cytoskeleton organization and cell adhesion. These changes were correlated with abnormal localization of myosin IIa and a rapid suppression of the phosphorylation of Erk1/2. -
Chuanxiong Rhizoma Compound on HIF-VEGF Pathway and Cerebral Ischemia-Reperfusion Injury’S Biological Network Based on Systematic Pharmacology
ORIGINAL RESEARCH published: 25 June 2021 doi: 10.3389/fphar.2021.601846 Exploring the Regulatory Mechanism of Hedysarum Multijugum Maxim.-Chuanxiong Rhizoma Compound on HIF-VEGF Pathway and Cerebral Ischemia-Reperfusion Injury’s Biological Network Based on Systematic Pharmacology Kailin Yang 1†, Liuting Zeng 1†, Anqi Ge 2†, Yi Chen 1†, Shanshan Wang 1†, Xiaofei Zhu 1,3† and Jinwen Ge 1,4* Edited by: 1 Takashi Sato, Key Laboratory of Hunan Province for Integrated Traditional Chinese and Western Medicine on Prevention and Treatment of 2 Tokyo University of Pharmacy and Life Cardio-Cerebral Diseases, Hunan University of Chinese Medicine, Changsha, China, Galactophore Department, The First 3 Sciences, Japan Hospital of Hunan University of Chinese Medicine, Changsha, China, School of Graduate, Central South University, Changsha, China, 4Shaoyang University, Shaoyang, China Reviewed by: Hui Zhao, Capital Medical University, China Background: Clinical research found that Hedysarum Multijugum Maxim.-Chuanxiong Maria Luisa Del Moral, fi University of Jaén, Spain Rhizoma Compound (HCC) has de nite curative effect on cerebral ischemic diseases, *Correspondence: such as ischemic stroke and cerebral ischemia-reperfusion injury (CIR). However, its Jinwen Ge mechanism for treating cerebral ischemia is still not fully explained. [email protected] †These authors share first authorship Methods: The traditional Chinese medicine related database were utilized to obtain the components of HCC. The Pharmmapper were used to predict HCC’s potential targets. Specialty section: The CIR genes were obtained from Genecards and OMIM and the protein-protein This article was submitted to interaction (PPI) data of HCC’s targets and IS genes were obtained from String Ethnopharmacology, a section of the journal database. -
Inorganic Pyrophosphatase Is a Component of the Drosophila Nucleosome Remodeling Factor Complex
Downloaded from genesdev.cshlp.org on October 3, 2021 - Published by Cold Spring Harbor Laboratory Press Inorganic pyrophosphatase is a component of the Drosophila nucleosome remodeling factor complex David A. Gdula, Raphael Sandaltzopoulos, Toshio Tsukiyama,1 Vincent Ossipow, and Carl Wu2 Laboratory of Molecular Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4255 USA The Drosophila nucleosome remodeling factor (NURF) is a protein complex consisting of four polypeptides that facilitates the perturbation of chromatin structure in vitro in an ATP-dependent manner. The 140-kD NURF subunit, imitation switch (ISWI), is related to the SWI2/SNF2 ATPase. Another subunit, NURF-55, is a 55-kD WD repeat protein homologous to the human retinoblastoma-associated protein RbAp48. Here, we report the cloning and characterization of the smallest (38 kD) component of NURF. NURF-38 is strikingly homologous to known inorganic pyrophosphatases. Both recombinant NURF-38 alone and the purified NURF complex are shown to have inorganic pyrophosphatase activity. Inhibition of the pyrophosphatase activity of NURF with sodium fluoride has no significant effect on chromatin remodeling, indicating that these two activities may be biochemically uncoupled. Our results suggest that NURF-38 may serve a structural or regulatory role in the complex. Alternatively, because accumulation of unhydrolyzed pyrophosphate during nucleotide incorporation inhibits polymerization, NURF may also have been adapted to deliver pyrophosphatase -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase