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A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
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 -
Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association Between BMI and Adult-Onset Non- Atopic
Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association between BMI and Adult-Onset Non- Atopic Asthma Ayoung Jeong 1,2, Medea Imboden 1,2, Akram Ghantous 3, Alexei Novoloaca 3, Anne-Elie Carsin 4,5,6, Manolis Kogevinas 4,5,6, Christian Schindler 1,2, Gianfranco Lovison 7, Zdenko Herceg 3, Cyrille Cuenin 3, Roel Vermeulen 8, Deborah Jarvis 9, André F. S. Amaral 9, Florian Kronenberg 10, Paolo Vineis 11,12 and Nicole Probst-Hensch 1,2,* 1 Swiss Tropical and Public Health Institute, 4051 Basel, Switzerland; [email protected] (A.J.); [email protected] (M.I.); [email protected] (C.S.) 2 Department of Public Health, University of Basel, 4001 Basel, Switzerland 3 International Agency for Research on Cancer, 69372 Lyon, France; [email protected] (A.G.); [email protected] (A.N.); [email protected] (Z.H.); [email protected] (C.C.) 4 ISGlobal, Barcelona Institute for Global Health, 08003 Barcelona, Spain; [email protected] (A.-E.C.); [email protected] (M.K.) 5 Universitat Pompeu Fabra (UPF), 08002 Barcelona, Spain 6 CIBER Epidemiología y Salud Pública (CIBERESP), 08005 Barcelona, Spain 7 Department of Economics, Business and Statistics, University of Palermo, 90128 Palermo, Italy; [email protected] 8 Environmental Epidemiology Division, Utrecht University, Institute for Risk Assessment Sciences, 3584CM Utrecht, Netherlands; [email protected] 9 Population Health and Occupational Disease, National Heart and Lung Institute, Imperial College, SW3 6LR London, UK; [email protected] (D.J.); [email protected] (A.F.S.A.) 10 Division of Genetic Epidemiology, Medical University of Innsbruck, 6020 Innsbruck, Austria; [email protected] 11 MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, W2 1PG London, UK; [email protected] 12 Italian Institute for Genomic Medicine (IIGM), 10126 Turin, Italy * Correspondence: [email protected]; Tel.: +41-61-284-8378 Int. -
Supplementary Material and Methods
Supplementary material and methods Generation of cultured human epidermal sheets Normal human epidermal keratinocytes were isolated from human breast skin. Keratinocytes were grown on a feeder layer of irradiated human fibroblasts pre-seeded at 4000 cells /cm² in keratinocyte culture medium (KCM) containing a mix of 3:1 DMEM and HAM’s F12 (Invitrogen, Carlsbad, USA), supplemented with 10% FCS, 10ng/ml epidermal growth factor (EGF; R&D systems, Minneapolis, MN, USA), 0.12 IU/ml insulin (Lilly, Saint- Cloud, France), 0.4 mg/ml hydrocortisone (UpJohn, St Quentin en Yvelelines, France) , 5 mg/ml triiodo-L- thyronine (Sigma, St Quentin Fallavier, France), 24.3 mg/ml adenine (Sigma), isoproterenol (Isuprel, Hospira France, Meudon, France) and antibiotics (20 mg/ml gentamicin (Phanpharma, Fougères, France), 100 IU/ml penicillin (Phanpharma), and 1 mg/ml amphotericin B (Phanpharma)). The medium was changed every two days. NHEK were then cultured over a period of 13 days according to the protocol currently used at the Bank of Tissues and Cells for the generation of clinical grade epidermal sheets used for the treatment of severe extended burns (Ref). When needed, cells were harvested with trypsin-EDTA 0.05% (Thermo Fisher Scientific, Waltham, MA, USA) and collected for analysis. Clonogenic assay Keratinocytes were seeded on a feeder layer of irradiated fibroblasts, at a clonal density of 10-20 cells/cm² and cultivated for 10 to 14 days. Three flasks per tested condition were fixed and colored in a single 30 mns step using rhodamine B (Sigma) diluted at 0.01 g/ml in 4% paraformaldehyde. In each tested condition, cells from 3 other flasks were numerated after detachment by trypsin treatment. -
Alterations of the Interactome of Bcl-2 Proteins in Breast Cancer at the Transcriptional, Mutational and Structural Level
RESEARCH ARTICLE Alterations of the interactome of Bcl-2 proteins in breast cancer at the transcriptional, mutational and structural level Simon Mathis Kønig1, Vendela Rissler1, Thilde Terkelsen1, Matteo Lambrughi1, 1,2 Elena PapaleoID * 1 Computational Biology Laboratory, Danish Cancer Society Research Center, Copenhagen, Denmark, a1111111111 2 Translational Disease Systems Biology, Faculty of Health and Medical Sciences, Novo Nordisk Foundation Center for Protein Research University of Copenhagen, Copenhagen, Denmark a1111111111 a1111111111 * [email protected] a1111111111 a1111111111 Abstract Apoptosis is an essential defensive mechanism against tumorigenesis. Proteins of the B- OPEN ACCESS cell lymphoma-2 (Bcl-2) family regulate programmed cell death by the mitochondrial apopto- sis pathway. In response to intracellular stress, the apoptotic balance is governed by inter- Citation: Kønig SM, Rissler V, Terkelsen T, Lambrughi M, Papaleo E (2019) Alterations of the actions of three distinct subgroups of proteins; the activator/sensitizer BH3 (Bcl-2 homology interactome of Bcl-2 proteins in breast cancer at 3)-only proteins, the pro-survival, and the pro-apoptotic executioner proteins. Changes in the transcriptional, mutational and structural level. expression levels, stability, and functional impairment of pro-survival proteins can lead to an PLoS Comput Biol 15(12): e1007485. https://doi. imbalance in tissue homeostasis. Their overexpression or hyperactivation can result in org/10.1371/journal.pcbi.1007485 oncogenic effects. Pro-survival Bcl-2 family members carry out their function by binding the Editor: Igor N. Berezovsky, A�STAR Singapore, BH3 short linear motif of pro-apoptotic proteins in a modular way, creating a complex net- SINGAPORE work of protein-protein interactions. Their dysfunction enables cancer cells to evade cell Received: July 8, 2019 death. -
Engineered Type 1 Regulatory T Cells Designed for Clinical Use Kill Primary
ARTICLE Acute Myeloid Leukemia Engineered type 1 regulatory T cells designed Ferrata Storti Foundation for clinical use kill primary pediatric acute myeloid leukemia cells Brandon Cieniewicz,1* Molly Javier Uyeda,1,2* Ping (Pauline) Chen,1 Ece Canan Sayitoglu,1 Jeffrey Mao-Hwa Liu,1 Grazia Andolfi,3 Katharine Greenthal,1 Alice Bertaina,1,4 Silvia Gregori,3 Rosa Bacchetta,1,4 Norman James Lacayo,1 Alma-Martina Cepika1,4# and Maria Grazia Roncarolo1,2,4# Haematologica 2021 Volume 106(10):2588-2597 1Department of Pediatrics, Division of Stem Cell Transplantation and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 2Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 3San Raffaele Telethon Institute for Gene Therapy, Milan, Italy and 4Center for Definitive and Curative Medicine, Stanford School of Medicine, Stanford, CA, USA *BC and MJU contributed equally as co-first authors #AMC and MGR contributed equally as co-senior authors ABSTRACT ype 1 regulatory (Tr1) T cells induced by enforced expression of interleukin-10 (LV-10) are being developed as a novel treatment for Tchemotherapy-resistant myeloid leukemias. In vivo, LV-10 cells do not cause graft-versus-host disease while mediating graft-versus-leukemia effect against adult acute myeloid leukemia (AML). Since pediatric AML (pAML) and adult AML are different on a genetic and epigenetic level, we investigate herein whether LV-10 cells also efficiently kill pAML cells. We show that the majority of primary pAML are killed by LV-10 cells, with different levels of sensitivity to killing. Transcriptionally, pAML sensitive to LV-10 killing expressed a myeloid maturation signature. -
Proteomic Signatures of Brain Regions Affected by Tau Pathology in Early and Late Stages of Alzheimer's Disease
Neurobiology of Disease 130 (2019) 104509 Contents lists available at ScienceDirect Neurobiology of Disease journal homepage: www.elsevier.com/locate/ynbdi Proteomic signatures of brain regions affected by tau pathology in early and T late stages of Alzheimer's disease Clarissa Ferolla Mendonçaa,b, Magdalena Kurasc, Fábio César Sousa Nogueiraa,d, Indira Plác, Tibor Hortobágyie,f,g, László Csibae,h, Miklós Palkovitsi, Éva Renneri, Péter Dömej,k, ⁎ ⁎ György Marko-Vargac, Gilberto B. Domonta, , Melinda Rezelic, a Proteomics Unit, Department of Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil b Gladstone Institute of Neurological Disease, San Francisco, USA c Division of Clinical Protein Science & Imaging, Department of Clinical Sciences (Lund) and Department of Biomedical Engineering, Lund University, Lund, Sweden d Laboratory of Proteomics, LADETEC, Institute of Chemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil e MTA-DE Cerebrovascular and Neurodegenerative Research Group, University of Debrecen, Debrecen, Hungary f Institute of Pathology, Faculty of Medicine, University of Szeged, Szeged, Hungary g Centre for Age-Related Medicine, SESAM, Stavanger University Hospital, Stavanger, Norway h Department of Neurology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary i SE-NAP – Human Brain Tissue Bank Microdissection Laboratory, Semmelweis University, Budapest, Hungary j Department of Psychiatry and Psychotherapy, Semmelweis University, Budapest, Hungary k National Institute of Psychiatry and Addictions, Nyírő Gyula Hospital, Budapest, Hungary ARTICLE INFO ABSTRACT Keywords: Background: Alzheimer's disease (AD) is the most common neurodegenerative disorder. Depositions of amyloid β Alzheimer's disease peptide (Aβ) and tau protein are among the major pathological hallmarks of AD. Aβ and tau burden follows Proteomics predictable spatial patterns during the progression of AD. -
Database and Bioinformatic Analysis of BCL-2 Family Proteins and BH3-Only Proteins Abdel Aouacheria, Vincent Navratil, Christophe Combet
Database and Bioinformatic Analysis of BCL-2 Family Proteins and BH3-Only Proteins Abdel Aouacheria, Vincent Navratil, Christophe Combet To cite this version: Abdel Aouacheria, Vincent Navratil, Christophe Combet. Database and Bioinformatic Analysis of BCL-2 Family Proteins and BH3-Only Proteins. Gavathiotis E. BCL-2 Family Proteins. Methods in Molecular Biology, 1877, Springer Nature, pp.23-43, 2019, Methods in Molecular Biology, 978-1-4939- 8860-0. 10.1007/978-1-4939-8861-7_2. hal-02347884 HAL Id: hal-02347884 https://hal.archives-ouvertes.fr/hal-02347884 Submitted on 5 Nov 2019 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. Copyright Database and bioinformatic analysis of BCL-2 family proteins and BH3-only proteins Abdel Aouacheria 1,*, Vincent Navratil 2 and Christophe Combet 3 1 ISEM, Institut des Sciences de l’Evolution de Montpellier, Université de Montpellier, UMR 5554, CNRS, IRD, EPHE, Place Eugène Bataillon, 34095 Montpellier, France 2 PRABI, Rhône Alpes Bioinformatics Center, UCBL, Lyon1, Université de Lyon, Lyon, France. 3 Centre de Recherche en Cancérologie de Lyon, UMR Inserm U1052, CNRS 5286, Université Claude Bernard Lyon 1, Centre Léon Bérard, Lyon, France. -
Anti-VEGF Drugs Influence Epigenetic Regulation and AMD-Specific
cells Article Anti-VEGF Drugs Influence Epigenetic Regulation and AMD-Specific Molecular Markers in ARPE-19 Cells Mohamed A. Hamid 1,2,† , M. Tarek Moustafa 1,2,† , Sonali Nashine 1, Rodrigo Donato Costa 1,3 , Kevin Schneider 1, Shari R. Atilano 1 , Baruch D. Kuppermann 1,4 and M. Cristina Kenney 1,5,* 1 Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA 92697, USA; [email protected] (M.A.H.); [email protected] (M.T.M.); [email protected] (S.N.); [email protected] (R.D.C.); [email protected] (K.S.); [email protected] (S.R.A.); [email protected] (B.D.K.) 2 Ophthalmology Department, Faculty of Medicine, Minia University, Minia 61111, Egypt 3 Instituto Donato Oftalmologia, PoVos de Caldas, MG 37701-528, Brazil 4 Department of Biomedical Engineering, University of California Irvine, Irvine, CA 92697, USA 5 Department of Pathology and Laboratory Medicine, University of California Irvine, Irvine, CA 92697, USA * Correspondence: [email protected]; Tel.: +1-949-824-7603 † Both authors contributed equally. Abstract: Our study assesses the effects of anti-VEGF (Vascular Endothelial Growth Factor) drugs and Trichostatin A (TSA), an inhibitor of histone deacetylase (HDAC) activity, on cultured ARPE-19 (Adult Retinal Pigment Epithelial-19) cells that are immortalized human retinal pigment epithelial cells. ARPE-19 cells were treated with the following anti-VEGF drugs: aflibercept, ranibizumab, or bevacizumab at 1× and 2× concentrations of the clinical intravitreal dose (12.5 µL/mL and 25 µL/mL, Citation: Hamid, M.A.; Moustafa, respectively) and analyzed for transcription profiles of genes associated with the pathogenesis M.T.; Nashine, S.; Costa, R.D.; age-related macular degeneration (AMD). -
Alterations of the Pro-Survival Bcl-2 Protein Interactome in Breast Cancer
bioRxiv preprint doi: https://doi.org/10.1101/695379; this version posted July 12, 2019. 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. 1 Alterations of the pro-survival Bcl-2 protein interactome in 2 breast cancer at the transcriptional, mutational and 3 structural level 4 5 Simon Mathis Kønig1, Vendela Rissler1, Thilde Terkelsen1, Matteo Lambrughi1, Elena 6 Papaleo1,2 * 7 1Computational Biology Laboratory, Danish Cancer Society Research Center, 8 Strandboulevarden 49, 2100, Copenhagen 9 10 2Translational Disease Systems Biology, Faculty of Health and Medical Sciences, Novo 11 Nordisk Foundation Center for Protein Research University of Copenhagen, Copenhagen, 12 Denmark 13 14 Abstract 15 16 Apoptosis is an essential defensive mechanism against tumorigenesis. Proteins of the B-cell 17 lymphoma-2 (Bcl-2) family regulates programmed cell death by the mitochondrial apoptosis 18 pathway. In response to intracellular stresses, the apoptotic balance is governed by interactions 19 of three distinct subgroups of proteins; the activator/sensitizer BH3 (Bcl-2 homology 3)-only 20 proteins, the pro-survival, and the pro-apoptotic executioner proteins. Changes in expression 21 levels, stability, and functional impairment of pro-survival proteins can lead to an imbalance 22 in tissue homeostasis. Their overexpression or hyperactivation can result in oncogenic effects. 23 Pro-survival Bcl-2 family members carry out their function by binding the BH3 short linear 24 motif of pro-apoptotic proteins in a modular way, creating a complex network of protein- 25 protein interactions. -
Asparaginase Therapy in Pediatric Acute Lymphoblastic Leukemia: a Focus on the Mode of Drug Resistance Shih-Hsiang Chen
Pediatrics and Neonatology (2015) 56, 287e293 Available online at www.sciencedirect.com ScienceDirect journal homepage: http://www.pediatr-neonatol.com REVIEW ARTICLE Asparaginase Therapy in Pediatric Acute Lymphoblastic Leukemia: A Focus on the Mode of Drug Resistance Shih-Hsiang Chen Division of Hematology/Oncology, Department of Pediatrics, Chang Gung Memorial Hospital, College of Medicine, Chang Gung University, 5 Fu-Shin Street, Kwei-Shan 333, Taoyuan, Taiwan Received Apr 24, 2014; received in revised form Aug 28, 2014; accepted Oct 6, 2014 Available online 23 December 2014 Key Words Asparaginase is one of the most important chemotherapeutic agents against pediatric acute acute lymphoblastic lymphoblastic leukemia (ALL), the most common form of childhood cancer. The therapeutic leukemia; efficacy (e.g., chemoresistance) and adverse effects of asparaginase (e.g., hypersensivity asparaginase; and pancreatitis) have been investigated over the past four decades. It was suggested early chemotherapy; on that leukemic cells are resistant to asparaginase because of their increased asparagine syn- children; thetase activity. Afterward, other mechanisms associated with asparaginase resistance were resistance reported. Not only leukemic cells but also patients themselves may play a role in causing as- paraginase resistance, which has been associated with unfavorable outcome in children with ALL. This article will briefly review asparaginase therapy in children with ALL and comprehen- sively analyze recent reports on the potential mechanisms of asparaginase resistance. Copyright ª 2015, Taiwan Pediatric Association. Published by Elsevier Taiwan LLC. All rights reserved. 1. Introduction Taiwan Childhood Cancer Foundation, there are about 130e140 newly diagnosed ALL children (younger than Acute lymphoblastic leukemia (ALL) is the most common 18 years), accounting for 25% of all childhood cancers in cancer in children. -
Down-Regulation of BCL2L13 Renders Poor Prognosis in Clear Cell And
Meng et al. Cancer Cell Int (2021) 21:332 https://doi.org/10.1186/s12935-021-02039-y Cancer Cell International PRIMARY RESEARCH Open Access Down-regulation of BCL2L13 renders poor prognosis in clear cell and papillary renal cell carcinoma Fei Meng1,2,3 , Luojin Zhang4, Mingjun Zhang5, Kaiqin Ye1,3, Wei Guo1,2, Yu Liu1,2,3, Wulin Yang1,3, Zhimin Zhai4, Hongzhi Wang1,3, Jun Xiao6* and Haiming Dai1,3* Abstract Background: BCL2L13 belongs to the BCL2 super family, with its protein product exhibits capacity of apoptosis-medi- ating in diversifed cell lines. Previous studies have shown that BCL2L13 has functional consequence in several tumor types, including ALL and GBM, however, its function in kidney cancer remains as yet unclearly. Methods: Multiple web-based portals were employed to analyze the efect of BCL2L13 in kidney cancer using the data from TCGA database. Functional enrichment analysis and hubs of BCL2L13 co-expressed genes in clear cell renal cell carcinoma (ccRCC) and papillary renal cell carcinoma (pRCC) were carried out on Cytoscape. Evaluation of BCL2L13 protein level was accomplished through immunohistochemistry on parafn embedded renal cancer tissue sections. Western blotting and fow cytometry were implemented to further analyze the pro-apoptotic function of BCL2L13 in ccRCC cell line 786-0. Results: BCL2L13 expression is signifcantly decreased in ccRCC and pRCC patients, however, mutations and copy number alterations are rarely observed. The poor prognosis of ccRCC that derived from down-regulated BCL2L13 is independent of patients’ gender or tumor grade. Furthermore, BCL2L13 only weakly correlates with the genes that mutated in kidney cancer or the genes that associated with inherited kidney cancer predisposing syndrome, while actively correlates with SLC25A4.