Table S2 Differentially Expressed Genes Between Oncogene-Introduced Wild-Type and Atf4-/- Cells
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Strategies to Increase ß-Cell Mass Expansion
This electronic thesis or dissertation has been downloaded from the King’s Research Portal at https://kclpure.kcl.ac.uk/portal/ Strategies to increase -cell mass expansion Drynda, Robert Lech Awarding institution: King's College London The copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without proper acknowledgement. END USER LICENCE AGREEMENT Unless another licence is stated on the immediately following page this work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International licence. https://creativecommons.org/licenses/by-nc-nd/4.0/ You are free to copy, distribute and transmit the work Under the following conditions: Attribution: You must attribute the work in the manner specified by the author (but not in any way that suggests that they endorse you or your use of the work). Non Commercial: You may not use this work for commercial purposes. No Derivative Works - You may not alter, transform, or build upon this work. Any of these conditions can be waived if you receive permission from the author. Your fair dealings and other rights are in no way affected by the above. Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 Strategies to increase β-cell mass expansion A thesis submitted by Robert Drynda For the degree of Doctor of Philosophy from King’s College London Diabetes Research Group Division of Diabetes & Nutritional Sciences Faculty of Life Sciences & Medicine King’s College London 2017 Table of contents Table of contents ................................................................................................. -
Kinesin Family Member 18B Regulates the Proliferation and Invasion Of
Wu et al. Cell Death and Disease (2021) 12:302 https://doi.org/10.1038/s41419-021-03582-2 Cell Death & Disease ARTICLE Open Access Kinesin family member 18B regulates the proliferation and invasion of human prostate cancer cells Yu-Peng Wu 1,Zhi-BinKe 1, Wen-Cai Zheng 1, Ye-Hui Chen 1,Jun-MingZhu 1,FeiLin 1,Xiao-DongLi 1, Shao-Hao Chen 1,HaiCai 1, Qing-Shui Zheng 1, Yong Wei 1, Xue-Yi Xue 1 and Ning Xu 1 Abstract Expression of kinesin family member 18B (KIF18B), an ATPase with key roles in cell division, is deregulated in many cancers, but its involvement in prostate cancer (PCa) is unclear. Here, we investigated the expression and function of KIF18B in human PCa specimens and cell lines using bioinformatics analyses, immunohistochemical and immunofluorescence microscopy, and RT-qPCR and western blot analyses. KIF18B was overexpressed in PCa specimens compared with paracancerous tissues and was associated with poorer disease-free survival. In vitro, KIF18B knockdown in PCa cell lines promoted cell proliferation, migration, and invasion, and inhibited cell apoptosis, while KIF18B overexpression had the opposite effects. In a mouse xenograft model, KIF18B overexpression accelerated and promoted the growth of PCa tumors. Bioinformatics analysis of control and KIF18B-overexpressing PCa cells showed that genes involved in the PI3K–AKT–mTOR signaling pathway were significantly enriched among the differentially expressed genes. Consistent with this observation, we found that KIF18B overexpression activates the PI3K–AKT–mTOR signaling pathway in PCa cells both in vitro and in vivo. Collectively, our results suggest that KIF18B plays a crucial role – – 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; in PCa via activation of the PI3K AKT mTOR signaling pathway, and raise the possibility that KIF18B could have utility as a novel biomarker for PCa. -
0.5) in Stat3∆/∆ Compared with Stat3flox/Flox
Supplemental Table 2 Genes down-regulated (<0.5) in Stat3∆/∆ compared with Stat3flox/flox Probe ID Gene Symbol Gene Description Entrez gene ID 1460599_at Ermp1 endoplasmic reticulum metallopeptidase 1 226090 1460463_at H60c histocompatibility 60c 670558 1460431_at Gcnt1 glucosaminyl (N-acetyl) transferase 1, core 2 14537 1459979_x_at Zfp68 zinc finger protein 68 24135 1459747_at --- --- --- 1459608_at --- --- --- 1459168_at --- --- --- 1458718_at --- --- --- 1458618_at --- --- --- 1458466_at Ctsa cathepsin A 19025 1458345_s_at Colec11 collectin sub-family member 11 71693 1458046_at --- --- --- 1457769_at H60a histocompatibility 60a 15101 1457680_a_at Tmem69 transmembrane protein 69 230657 1457644_s_at Cxcl1 chemokine (C-X-C motif) ligand 1 14825 1457639_at Atp6v1h ATPase, H+ transporting, lysosomal V1 subunit H 108664 1457260_at 5730409E04Rik RIKEN cDNA 5730409E04Rik gene 230757 1457070_at --- --- --- 1456893_at --- --- --- 1456823_at Gm70 predicted gene 70 210762 1456671_at Tbrg3 transforming growth factor beta regulated gene 3 21378 1456211_at Nlrp10 NLR family, pyrin domain containing 10 244202 1455881_at Ier5l immediate early response 5-like 72500 1455576_at Rinl Ras and Rab interactor-like 320435 1455304_at Unc13c unc-13 homolog C (C. elegans) 208898 1455241_at BC037703 cDNA sequence BC037703 242125 1454866_s_at Clic6 chloride intracellular channel 6 209195 1453906_at Med13l mediator complex subunit 13-like 76199 1453522_at 6530401N04Rik RIKEN cDNA 6530401N04 gene 328092 1453354_at Gm11602 predicted gene 11602 100380944 1453234_at -
Application to Acetaminophen Anaïs Michaut, Dounia Le Guillou, Caroline Moreau, Simon Bucher, Mitchell R
A cellular model to study drug-induced liver injury in nonalcoholic fatty liver disease: application to acetaminophen Anaïs Michaut, Dounia Le Guillou, Caroline Moreau, Simon Bucher, Mitchell R. Mcgill, Sophie Martinais, Thomas Gicquel, Isabelle Morel, Marie-Anne Robin, Hartmut Jaeschke, et al. To cite this version: Anaïs Michaut, Dounia Le Guillou, Caroline Moreau, Simon Bucher, Mitchell R. Mcgill, et al.. A cellular model to study drug-induced liver injury in nonalcoholic fatty liver disease: applica- tion to acetaminophen. Toxicology and Applied Pharmacology, Elsevier, 2016, 292, pp.40-55. 10.1016/j.taap.2015.12.020. hal-01255826 HAL Id: hal-01255826 https://hal-univ-rennes1.archives-ouvertes.fr/hal-01255826 Submitted on 29 Jan 2016 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. ACCEPTED MANUSCRIPT A cellular model to study drug-induced liver injury in nonalcoholic fatty liver disease: application to acetaminophen Anaïs Michauta, Dounia Le Guilloua, Caroline Moreaua,b, Simon Buchera, Mitchell R. McGillc, Sophie Martinaisa, Thomas Gicquela,b, Isabelle Morela,b, Marie-Anne Robina, Hartmut Jaeschkec, and Bernard Fromentya,* aINSERM, U991, Université de Rennes 1, Rennes, France, bService de Biochimie et Toxicologie, CHU Pontchaillou, Rennes, France, cDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA *To whom correspondenceACCEPTED should be addressed MANUSCRIPT at INSERM U991, Université de Rennes 1, 35043 Rennes Cedex, France. -
Original Article Colonic Mucosal Gene Expression in Irritable Bowel Syndrome Rats by the Liquid Chip Technology
Int J Clin Exp Pathol 2016;9(10):10751-10755 www.ijcep.com /ISSN:1936-2625/IJCEP0036079 Original Article Colonic mucosal gene expression in irritable bowel syndrome rats by the liquid chip technology Guanqun Chao1, Yingying Wang2, Shuo Zhang2 1Department of Family Medicine, Sir Run Run Shaw Hospital, Zhejiang University, Zhejiang, China; 2Department of Gastroenterology, The First Affiliated Hospital, Zhejiang Chinese Medical University, Zhejiang, China Received July 18, 2016; Accepted August 27, 2016; Epub October 1, 2016; Published October 15, 2016 Abstract: Background: Irritable bowel syndrome (IBS) is one of the most frequent GI disorders. The etiology and pathogenesis underlying IBS are currently unclear. Gene influence a number of chronic disease processes and may also be involved in regulating disease activity in gastrointestinal disorders, but few studies of IBS have focused on gene expression. Objective: The objective of this study was to screen the differentially expressed colonic mucosal genes in IBS rats to build the expression profile of genes in the colon of IBS rats. Methods: Twenty SD rats were divided randomly into two groups: the rats of control group were normal rats; the rats of model group were induced by conditioned stimulus and unconditioned stimulus. The rats’ visceral sensitivity was evaluated by abdominal with- draw reaction. Then we screened differential expression of colonic mucosal gene by the liquid chip technology and verified by RT-PCR technology. Results: The IBS model was successfully established. Compared with control group, the dose of injection water was decreased in model group (P<0.01). We screened htr4, htr1a, 2rl3, nos1, Calca, npy, crhr2, il1b, p2rx3, nos2, tph1, crhr1, hmox1, trpv1, Vip, f2rl, tgfb1, htr3a, slc6a4, tff2, aqp8 from the colon, but we found that only the expression of nos1, il1b, htr3a in model group was up-regulated (P<0.05). -
Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes
Tohoku J. Exp. Med., 2011,Differential 223, 161-176 Gene Expression in OPCs, Oligodendrocytes and Type II Astrocytes 161 Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes Jian-Guo Hu,1,2,* Yan-Xia Wang,3,* Jian-Sheng Zhou,2 Chang-Jie Chen,4 Feng-Chao Wang,1 Xing-Wu Li1 and He-Zuo Lü1,2 1Department of Clinical Laboratory Science, The First Affiliated Hospital of Bengbu Medical College, Bengbu, P.R. China 2Anhui Key Laboratory of Tissue Transplantation, Bengbu Medical College, Bengbu, P.R. China 3Department of Neurobiology, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China 4Department of Laboratory Medicine, Bengbu Medical College, Bengbu, P.R. China Oligodendrocyte precursor cells (OPCs) are bipotential progenitor cells that can differentiate into myelin-forming oligodendrocytes or functionally undetermined type II astrocytes. Transplantation of OPCs is an attractive therapy for demyelinating diseases. However, due to their bipotential differentiation potential, the majority of OPCs differentiate into astrocytes at transplanted sites. It is therefore important to understand the molecular mechanisms that regulate the transition from OPCs to oligodendrocytes or astrocytes. In this study, we isolated OPCs from the spinal cords of rat embryos (16 days old) and induced them to differentiate into oligodendrocytes or type II astrocytes in the absence or presence of 10% fetal bovine serum, respectively. RNAs were extracted from each cell population and hybridized to GeneChip with 28,700 rat genes. Using the criterion of fold change > 4 in the expression level, we identified 83 genes that were up-regulated and 89 genes that were down-regulated in oligodendrocytes, and 92 genes that were up-regulated and 86 that were down-regulated in type II astrocytes compared with OPCs. -
Microrna-7-5P Mediates the Signaling of Hepatocyte Growth
www.nature.com/scientificreports OPEN MicroRNA-7-5p mediates the signaling of hepatocyte growth factor to suppress oncogenes in the Received: 30 August 2017 Accepted: 2 November 2017 MCF-10A mammary epithelial cell Published: xx xx xxxx Dawoon Jeong1, Juyeon Ham1, Sungbin Park1, Seungyeon Lee 1, Hyunkyung Lee1, Han-Sung Kang2 & Sun Jung Kim1 MicroRNA-7 (miR-7) is a non-coding RNA of 23-nucleotides that has been shown to act as a tumor suppressor in various cancers including breast cancer. Although there have been copious studies on the action mechanisms of miR-7, little is known about how the miR is controlled in the mammary cell. In this study, we performed a genome-wide expression analysis in miR-7-transfected MCF-10A breast cell line to explore the upstream regulators of miR-7. Analysis of the dysregulated target gene pool predicted hepatocyte growth factor (HGF) as the most plausible upstream regulator of miR-7. MiR-7 was upregulated in MCF-10A cells by HGF, and subsequently downregulated upon treatment with siRNA against HGF. However, the expression of HGF did not signifcantly change through either an upregulation or downregulation of miR-7 expression, suggesting that HGF acts upstream of miR-7. In addition, the target genes of miR-7, such as EGFR, KLF4, FAK, PAK1 and SET8, which are all known oncogenes, were downregulated in HGF-treated MCF-10A; in contrast, knocking down HGF recovered their expression. These results indicate that miR-7 mediates the activity of HGF to suppress oncogenic proteins, which inhibits the development of normal cells, at least MCF-10A, into cancerous cells. -
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 -
Identification of Potential Key Genes and Pathway Linked with Sporadic Creutzfeldt-Jakob Disease Based on Integrated Bioinformatics Analyses
medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Identification of potential key genes and pathway linked with sporadic Creutzfeldt-Jakob disease based on integrated bioinformatics analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Abstract Sporadic Creutzfeldt-Jakob disease (sCJD) is neurodegenerative disease also called prion disease linked with poor prognosis. The aim of the current study was to illuminate the underlying molecular mechanisms of sCJD. The mRNA microarray dataset GSE124571 was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened. -
Impaired Angiogenesis and Tumor Development by Inhibition of the Mitotic Kinesin Eg5
Oncotarget, December, Vol.4, No 12 Impaired angiogenesis and tumor development by inhibition of the mitotic kinesin Eg5 Prisca Exertier1,2, Sophie Javerzat1,2, Baigang Wang3,8, Mélanie Franco1,2, John Herbert4, Natalia Platonova1,2, Marie Winandy5, Nadège Pujol1,2, Olivier Nivelles6, Sandra Ormenese7, Virginie Godard1,2, Jürgen Becker8, Roy Bicknell4, Raphael Pineau9, Jörg Wilting8*, Andreas Bikfalvi1,2*, Martin Hagedorn1,2* 1 Univ. Bordeaux, LAMC, UMR 1029, F-33405 Talence, France 2 INSERM, LAMC, UMR 1029, F-33405 Talence, France 3 Ruhr-Universität Bochum, Medizinische Fakultät; Abt. f. Anatomie und Embryologie, D-44780 Bochum, Germany 4 Molecular Angiogenesis Group, Institute of Biomedical Research, Univ Birmingham, Medical School, Edgbaston, Birmingham, UK 5 GIGA, Zebrafish Facility, Tour B34, Université de Liège, Belgium 6 GIGA, Unité de Biologie Moléculaire et Génie Génétique, Tour B34, Université de Liège, Belgium 7 GIGA, Imaging and Flow Cytometry Facility, Tour B34, Université de Liege, Belgium 8 Zentrum Anatomie, Abteilung Anatomie und Zellbiologie, Georg-August-Universität Goettingen, Germany 9 Animalerie mutualisée, University of Bordeaux I, Talence, France * Co-PIs Correspondence to: Martin Hagedorn, email: [email protected] Keywords: Angiogenesis, Eg5 kinesin, Mklp2 kinesin, VEGF, ispinesib Received: October 11, 2013 Accepted: October 24, 2013 Published: October 26, 2013 This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT: Kinesin motor proteins exert essential cellular functions in all eukaryotes. They control mitosis, migration and intracellular transport through interaction with microtubules. Small molecule inhibitors of the mitotic kinesin KiF11/Eg5 are a promising new class of anti-neoplastic agents currently evaluated in clinical cancer trials for solid tumors and hematological malignancies. -
Areca Catechu-(Betel-Nut)-Induced Whole Transcriptome Changes Associated With
bioRxiv preprint doi: https://doi.org/10.1101/2020.08.03.233932; this version posted August 3, 2020. 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 4.0 International license. 1 Areca catechu-(Betel-nut)-induced whole transcriptome changes associated with 2 diabetes, obesity and metabolic syndrome in a human monocyte cell line 3 4 Short title: Betel-nut induced whole transcriptome changes 5 6 7 Shirleny Cardoso1¶ , B. William Ogunkolade1¶, Rob Lowe2, Emanuel Savage3, Charles A 8 Mein3, Barbara J Boucher1, Graham A Hitman1* 9 10 11 1Centre for Genomics and Child Health, Blizard Institute, Barts and the London School of 12 Medicine and Dentistry, Queen Mary University of London, United Kingdom 13 14 2Omnigen Biodata Ltd, Cambridge, United Kingdom 15 16 3Barts and The London Genome Centre, Blizard Institute, Queen Mary University of London, 17 United Kingdom 18 19 * Corresponding author 20 Email: [email protected] 21 22 ¶These authors contributed equally to the work 23 24 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.08.03.233932; this version posted August 3, 2020. 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 4.0 International license. 25 Abstract 26 Betel-nut consumption is the fourth most common addictive habit globally and there is good 27 evidence to link it with obesity, type 2 diabetes and the metabolic syndrome. -
Molecular Features of Triple Negative Breast Cancer Cells by Genome-Wide Gene Expression Profiling Analysis
478 INTERNATIONAL JOURNAL OF ONCOLOGY 42: 478-506, 2013 Molecular features of triple negative breast cancer cells by genome-wide gene expression profiling analysis MASATO KOMATSU1,2*, TETSURO YOSHIMARU1*, TAISUKE MATSUO1, KAZUMA KIYOTANI1, YASUO MIYOSHI3, TOSHIHITO TANAHASHI4, KAZUHITO ROKUTAN4, RUI YAMAGUCHI5, AYUMU SAITO6, SEIYA IMOTO6, SATORU MIYANO6, YUSUKE NAKAMURA7, MITSUNORI SASA8, MITSUO SHIMADA2 and TOYOMASA KATAGIRI1 1Division of Genome Medicine, Institute for Genome Research, The University of Tokushima; 2Department of Digestive and Transplantation Surgery, The University of Tokushima Graduate School; 3Department of Surgery, Division of Breast and Endocrine Surgery, Hyogo College of Medicine, Hyogo 663-8501; 4Department of Stress Science, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503; Laboratories of 5Sequence Analysis, 6DNA Information Analysis and 7Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639; 8Tokushima Breast Care Clinic, Tokushima 770-0052, Japan Received September 22, 2012; Accepted November 6, 2012 DOI: 10.3892/ijo.2012.1744 Abstract. Triple negative breast cancer (TNBC) has a poor carcinogenesis of TNBC and could contribute to the develop- outcome due to the lack of beneficial therapeutic targets. To ment of molecular targets as a treatment for TNBC patients. clarify the molecular mechanisms involved in the carcino- genesis of TNBC and to identify target molecules for novel Introduction anticancer drugs, we analyzed the gene expression profiles of 30 TNBCs as well as 13 normal epithelial ductal cells that were Breast cancer is one of the most common solid malignant purified by laser-microbeam microdissection. We identified tumors among women worldwide. Breast cancer is a heteroge- 301 and 321 transcripts that were significantly upregulated neous disease that is currently classified based on the expression and downregulated in TNBC, respectively.