Cancer Vulnerabilities Unveiled by Genomic Loss
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The Potential Role of Necroptosis in Clinical Diseases (Review)
INTERNATIONAL JOURNAL OF MOleCular meDICine 47: 89, 2021 The potential role of necroptosis in clinical diseases (Review) WENLI DAI1*, JIN CHENG1*, XI LENG2, XIAOQING HU1 and YINGFANG AO1 1Institute of Sports Medicine, Beijing Key Laboratory of Sports Injuries, Peking University Third Hospital, Beijing 100191; 2Medical Imaging Center, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, P.R. China Received November 19, 2020; Accepted March 8, 2021 DOI: 10.3892/ijmm.2021.4922 Abstract. As an important type of programmed cell death in 1. Introduction addition to apoptosis, necroptosis occurs in a variety of patho‑ physiological processes, including infections, liver diseases, Necroptosis, an emerging field closely related to apoptosis, is a kidney injury, neurodegenerative diseases, cardiovascular non‑caspase‑dependent cell death that has been implicated in diseases, and human tumors. It can be triggered by a variety the pathological processes of various diseases. It is regulated of factors, such as tumor necrosis factor receptor and Toll‑like by various genes that cause regular and ordered cell death. receptor families, intracellular DNA and RNA sensors, and Through activating specific death signaling pathways, it shares interferon, and is mainly mediated by receptor‑interacting typical characteristics of necrosis, including loss of metabolic protein kinase 1 (RIP1), RIP3, and mixed lineage kinase function and subcellular changes (1,2). Receptor‑interacting domain‑like protein. A better understanding of the mechanism protein kinase 1 (RIP1) was the first signaling molecule of necroptosis may be useful in the development of novel drugs identified in the necrosome (3). RIP1 and RIP3 interact for necroptosis‑related diseases. -
A Minimal Set of Internal Control Genes for Gene Expression Studies in Head
bioRxiv preprint doi: https://doi.org/10.1101/108381; this version posted February 14, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.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 A minimal set of internal control genes for gene expression studies in head 2 and neck squamous cell carcinoma. 1 1 1 2 3 Vinayak Palve , Manisha Pareek , Neeraja M Krishnan , Gangotri Siddappa , 2 2 1,3* 4 Amritha Suresh , Moni Abraham Kuriakose and Binay Panda 5 1 6 Ganit Labs, Bio-IT Centre, Institute of Bioinformatics and Applied Biotechnology, 7 Bangalore 560100 2 8 Mazumdar Shaw Cancer Centre and Mazumdar Shaw Centre for Translational 9 Research, Bangalore 560096 3 10 Strand Life Sciences, Bangalore 560024 11 * Corresponding author: [email protected] 12 13 Abstract: 14 Background: Selection of the right reference gene(s) is crucial in the analysis and 15 interpretation of gene expression data. In head and neck cancer, studies evaluating 16 the efficacy of internal reference genes are rare. Here, we present data for a minimal 17 set of candidates as internal control genes for gene expression studies in head and 18 neck cancer. 19 Methods: We analyzed data from multiple sources (in house whole-genome gene 20 expression microarrays, n=21; TCGA RNA-seq, n=42, and published gene 21 expression studies in head and neck tumors from literature) to come up with a set of 22 genes (discovery set) for their stable expression across tumor and normal tissues. -
Selective Androgen Receptor Modulators (Sarms) And
(19) TZZ ¥6B_T (11) EP 2 222 636 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: C07D 207/08 (2006.01) C07D 207/09 (2006.01) 10.04.2013 Bulletin 2013/15 C07D 498/04 (2006.01) A61K 31/402 (2006.01) A61P 5/26 (2006.01) (21) Application number: 08865188.0 (86) International application number: (22) Date of filing: 12.12.2008 PCT/US2008/013657 (87) International publication number: WO 2009/082437 (02.07.2009 Gazette 2009/27) (54) SELECTIVE ANDROGEN RECEPTOR MODULATORS (SARMS) AND USES THEREOF SELEKTIVE ANDROGENREZEPTORMODULATOREN (SARMS) UND IHRE VERWENDUNG MODULATEURS SÉLECTIFS DU RÉCEPTEUR ANDROGÈNE (SARM) ET LEURS UTILISATIONS (84) Designated Contracting States: (74) Representative: Baldock, Sharon Claire AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Boult Wade Tennant HR HU IE IS IT LI LT LU LV MC MT NL NO PL PT Verulam Gardens RO SE SI SK TR 70 Gray’s Inn Road Designated Extension States: London WC1X 8BT (GB) AL BA MK RS (56) References cited: (30) Priority: 21.12.2007 US 8731 P WO-A-02/068427 WO-A-03/090672 WO-A-2005/090282 WO-A-2006/124447 (43) Date of publication of application: WO-A-2007/015567 01.09.2010 Bulletin 2010/35 • HIGUCHI ET AL: "Potent, nonsteroidal selective (60) Divisional application: androgen receptor modulators (SARMs) based 12168231.4 / 2 489 656 on 8H-[1,4]oxazino[2,3-f]quinolin-8-ones" BIOORGANIC & MEDICINAL CHEMISTRY (73) Proprietor: Ligand Pharmaceuticals Inc. -
Protein Expression Analysis of an in Vitro Murine Model of Prostate Cancer Progression: Towards Identification of High-Potential Therapeutic Targets
Journal of Personalized Medicine Article Protein Expression Analysis of an In Vitro Murine Model of Prostate Cancer Progression: Towards Identification of High-Potential Therapeutic Targets Hisham F. Bahmad 1,2,3 , Wenjing Peng 4, Rui Zhu 4, Farah Ballout 1, Alissar Monzer 1, 1,5 6, , 1, , 4, , Mohamad K. Elajami , Firas Kobeissy * y , Wassim Abou-Kheir * y and Yehia Mechref * y 1 Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut 1107-2020, Lebanon; [email protected] (H.F.B.); [email protected] (F.B.); [email protected] (A.M.); [email protected] (M.K.E.) 2 Arkadi M. Rywlin M.D. Department of Pathology and Laboratory Medicine, Mount Sinai Medical Center, Miami Beach, FL 33140, USA 3 Herbert Wertheim College of Medicine, Florida International University, Miami, FL 33199, USA 4 Department of Chemistry and Biochemistry, Texas Tech University, Lubbock, TX 79409, USA; [email protected] (W.P.); [email protected] (R.Z.) 5 Department of Internal Medicine, Mount Sinai Medical Center, Miami Beach, FL 33140, USA 6 Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut 1107-2020, Lebanon * Correspondence: [email protected] (F.K.); [email protected] (W.A.-K.); [email protected] (Y.M.); Tel.: +961-1-350000 (ext. 4805) (F.K.); +961-1-350000 (ext. 4778) (W.A.K.); +1-806-834-8246 (Y.M.); Fax: +1-806-742-1289 (Y.M.); 961-1-744464 (W.A.K.) These authors have contributed equally to this work as joint senior authors. -
Role of Phytochemicals in Colon Cancer Prevention: a Nutrigenomics Approach
Role of phytochemicals in colon cancer prevention: a nutrigenomics approach Marjan J van Erk Promotor: Prof. Dr. P.J. van Bladeren Hoogleraar in de Toxicokinetiek en Biotransformatie Wageningen Universiteit Co-promotoren: Dr. Ir. J.M.M.J.G. Aarts Universitair Docent, Sectie Toxicologie Wageningen Universiteit Dr. Ir. B. van Ommen Senior Research Fellow Nutritional Systems Biology TNO Voeding, Zeist Promotiecommissie: Prof. Dr. P. Dolara University of Florence, Italy Prof. Dr. J.A.M. Leunissen Wageningen Universiteit Prof. Dr. J.C. Mathers University of Newcastle, United Kingdom Prof. Dr. M. Müller Wageningen Universiteit Dit onderzoek is uitgevoerd binnen de onderzoekschool VLAG Role of phytochemicals in colon cancer prevention: a nutrigenomics approach Marjan Jolanda van Erk Proefschrift ter verkrijging van graad van doctor op gezag van de rector magnificus van Wageningen Universiteit, Prof.Dr.Ir. L. Speelman, in het openbaar te verdedigen op vrijdag 1 oktober 2004 des namiddags te vier uur in de Aula Title Role of phytochemicals in colon cancer prevention: a nutrigenomics approach Author Marjan Jolanda van Erk Thesis Wageningen University, Wageningen, the Netherlands (2004) with abstract, with references, with summary in Dutch ISBN 90-8504-085-X ABSTRACT Role of phytochemicals in colon cancer prevention: a nutrigenomics approach Specific food compounds, especially from fruits and vegetables, may protect against development of colon cancer. In this thesis effects and mechanisms of various phytochemicals in relation to colon cancer prevention were studied through application of large-scale gene expression profiling. Expression measurement of thousands of genes can yield a more complete and in-depth insight into the mode of action of the compounds. -
Anti-Inflammatory Role of Curcumin in LPS Treated A549 Cells at Global Proteome Level and on Mycobacterial Infection
Anti-inflammatory Role of Curcumin in LPS Treated A549 cells at Global Proteome level and on Mycobacterial infection. Suchita Singh1,+, Rakesh Arya2,3,+, Rhishikesh R Bargaje1, Mrinal Kumar Das2,4, Subia Akram2, Hossain Md. Faruquee2,5, Rajendra Kumar Behera3, Ranjan Kumar Nanda2,*, Anurag Agrawal1 1Center of Excellence for Translational Research in Asthma and Lung Disease, CSIR- Institute of Genomics and Integrative Biology, New Delhi, 110025, India. 2Translational Health Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, 110067, India. 3School of Life Sciences, Sambalpur University, Jyoti Vihar, Sambalpur, Orissa, 768019, India. 4Department of Respiratory Sciences, #211, Maurice Shock Building, University of Leicester, LE1 9HN 5Department of Biotechnology and Genetic Engineering, Islamic University, Kushtia- 7003, Bangladesh. +Contributed equally for this work. S-1 70 G1 S 60 G2/M 50 40 30 % of cells 20 10 0 CURI LPSI LPSCUR Figure S1: Effect of curcumin and/or LPS treatment on A549 cell viability A549 cells were treated with curcumin (10 µM) and/or LPS or 1 µg/ml for the indicated times and after fixation were stained with propidium iodide and Annexin V-FITC. The DNA contents were determined by flow cytometry to calculate percentage of cells present in each phase of the cell cycle (G1, S and G2/M) using Flowing analysis software. S-2 Figure S2: Total proteins identified in all the three experiments and their distribution betwee curcumin and/or LPS treated conditions. The proteins showing differential expressions (log2 fold change≥2) in these experiments were presented in the venn diagram and certain number of proteins are common in all three experiments. -
Nuclear Factor-Erythroid-2 Related Transcription Factor-1 (Nrf1) Is Regulated MARK by O-Glcnac Transferase
Free Radical Biology and Medicine 110 (2017) 196–205 Contents lists available at ScienceDirect Free Radical Biology and Medicine journal homepage: www.elsevier.com/locate/freeradbiomed Original article Nuclear factor-erythroid-2 related transcription factor-1 (Nrf1) is regulated MARK by O-GlcNAc transferase Jeong Woo Hana,1, Joshua L. Valdeza,1, Daniel V. Hoa, Candy S. Leea, Hyun Min Kima, ⁎ Xiaorong Wangb, Lan Huangb,Jefferson Y. Chana, a Department of Laboratory Medicine and Pathology, University of California, Irvine, D440 Medical Sciences, Irvine, CA 92697, USA b Departments of Physiology and Biophysics, University of California, Irvine, D440 Medical Sciences, Irvine, CA 92697, USA ARTICLE INFO ABSTRACT Keywords: The Nrf1 (Nuclear factor E2-related factor 1) transcription factor performs a critical role in regulating cellular Oxidative stress homeostasis. Using a proteomic approach, we identified Host Cell Factor-1 (HCF1), a co-regulator of tran- O-GlcNAcylation scription, and O-GlcNAc transferase (OGT), the enzyme that mediates protein O-GlcNAcylation, as cellular OGT partners of Nrf1a, an isoform of Nrf1. Nrf1a directly interacts with HCF1 through the HCF1 binding motif Transcription factor (HBM), while interaction with OGT is mediated through HCF1. Overexpression of HCF1 and OGT leads to Protein stability increased Nrf1a protein stability. Addition of O-GlcNAc decreases ubiquitination and degradation of Nrf1a. Transcriptional activation by Nrf1a is increased by OGT overexpression and treatment with PUGNAc. Together, these data suggest that OGT can act as a regulator of Nrf1a. 1. Introduction recognized as an essential co-factor for various transcription factors, and it is involved in regulating a plethora of cellular processes including O-GlcNAc transferase (OGT) is a highly conserved enzyme that cell-cycle progression and gene expression [18–21]. -
Supplementary Table S1. Correlation Between the Mutant P53-Interacting Partners and PTTG3P, PTTG1 and PTTG2, Based on Data from Starbase V3.0 Database
Supplementary Table S1. Correlation between the mutant p53-interacting partners and PTTG3P, PTTG1 and PTTG2, based on data from StarBase v3.0 database. PTTG3P PTTG1 PTTG2 Gene ID Coefficient-R p-value Coefficient-R p-value Coefficient-R p-value NF-YA ENSG00000001167 −0.077 8.59e-2 −0.210 2.09e-6 −0.122 6.23e-3 NF-YB ENSG00000120837 0.176 7.12e-5 0.227 2.82e-7 0.094 3.59e-2 NF-YC ENSG00000066136 0.124 5.45e-3 0.124 5.40e-3 0.051 2.51e-1 Sp1 ENSG00000185591 −0.014 7.50e-1 −0.201 5.82e-6 −0.072 1.07e-1 Ets-1 ENSG00000134954 −0.096 3.14e-2 −0.257 4.83e-9 0.034 4.46e-1 VDR ENSG00000111424 −0.091 4.10e-2 −0.216 1.03e-6 0.014 7.48e-1 SREBP-2 ENSG00000198911 −0.064 1.53e-1 −0.147 9.27e-4 −0.073 1.01e-1 TopBP1 ENSG00000163781 0.067 1.36e-1 0.051 2.57e-1 −0.020 6.57e-1 Pin1 ENSG00000127445 0.250 1.40e-8 0.571 9.56e-45 0.187 2.52e-5 MRE11 ENSG00000020922 0.063 1.56e-1 −0.007 8.81e-1 −0.024 5.93e-1 PML ENSG00000140464 0.072 1.05e-1 0.217 9.36e-7 0.166 1.85e-4 p63 ENSG00000073282 −0.120 7.04e-3 −0.283 1.08e-10 −0.198 7.71e-6 p73 ENSG00000078900 0.104 2.03e-2 0.258 4.67e-9 0.097 3.02e-2 Supplementary Table S2. -
Produktinformation
Produktinformation Diagnostik & molekulare Diagnostik Laborgeräte & Service Zellkultur & Verbrauchsmaterial Forschungsprodukte & Biochemikalien Weitere Information auf den folgenden Seiten! See the following pages for more information! Lieferung & Zahlungsart Lieferung: frei Haus Bestellung auf Rechnung SZABO-SCANDIC Lieferung: € 10,- HandelsgmbH & Co KG Erstbestellung Vorauskassa Quellenstraße 110, A-1100 Wien T. +43(0)1 489 3961-0 Zuschläge F. +43(0)1 489 3961-7 [email protected] • Mindermengenzuschlag www.szabo-scandic.com • Trockeneiszuschlag • Gefahrgutzuschlag linkedin.com/company/szaboscandic • Expressversand facebook.com/szaboscandic PSMD10 Antibody, Biotin conjugated Product Code CSB-PA018899LD01HU Abbreviation 26S proteasome non-ATPase regulatory subunit 10 Storage Upon receipt, store at -20°C or -80°C. Avoid repeated freeze. Uniprot No. O75832 Immunogen Recombinant Human 26S proteasome non-ATPase regulatory subunit 10 protein (1-226AA) Raised In Rabbit Species Reactivity Human Tested Applications ELISA Relevance Acts as a chaperone during the assembly of the 26S proteasome, specifically of the PA700/19S regulatory complex (RC). In the initial step of the base subcomplex assembly is part of an intermediate PSMD10:PSMC4:PSMC5:PAAF1 module which probably assembles with a PSMD5:PSMC2:PSMC1:PSMD2 module. Independently of the proteasome, regulates EGF-induced AKT activation through inhibition of the RHOA/ROCK/PTEN pahway, leading to prolonged AKT activation. Plays an important role in RAS-induced tumorigenesis. Acts as an proto-oncoprotein by being involved in negative regulation of tumor suppressors RB1 and p53/TP53. Overexpression is leading to phosphorylation of RB1 and proteasomal degradation of RB1. Regulates CDK4-mediated phosphorylation of RB1 by competing with CDKN2A for binding with CDK4. Facilitates binding of MDM2 to p53/TP53 and the mono- and polyubiquitination of p53/TP53 by MDM2 suggesting a function in targeting the TP53:MDM2 complex to the 26S proteasome. -
Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement. -
PSMD10 Antibody (Center) Purified Rabbit Polyclonal Antibody (Pab) Catalog # AW5126
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 PSMD10 Antibody (Center) Purified Rabbit Polyclonal Antibody (Pab) Catalog # AW5126 Specification PSMD10 Antibody (Center) - Product Information Application IF, WB, IHC-P,E Primary Accession O75832 Other Accession Q9Z2X2 Reactivity Human Predicted Mouse Host Rabbit Clonality Polyclonal Calculated MW H=24,16;M=25;Ra t=25 KDa Isotype Rabbit Ig Antigen Source HUMAN PSMD10 Antibody (Center) - Additional Information Gene ID 5716 Fluorescent image of Hela cells stained with PSMD10 Antibody (Center)(Cat#AW5126). Antigen Region AW5126 was diluted at 1:25 dilution. An 43-76 Alexa Fluor 488-conjugated goat anti-rabbit lgG at 1:400 dilution was used as the Other Names secondary antibody (green). Cytoplasmic 26S proteasome non-ATPase regulatory subunit 10, 26S proteasome regulatory actin was counterstained with Alexa Fluor® subunit p28, Gankyrin, p28(GANK), PSMD10 555 conjugated with Phalloidin (red). Dilution IF~~1:25 WB~~ 1:1000 IHC-P~~1:25 Target/Specificity This PSMD10 antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 43-76 amino acids from the Central region of human PSMD10. Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. Western blot analysis of lysates from MCF-7, PC-3, K562 cell line (from left to right), using Storage PSMD10 Antibody (Center)(Cat. #AW5126). Page 1/3 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 Maintain refrigerated at 2-8°C for up to 2 AW5126 was diluted at 1:1000 at each lane. -
Inactive USP14 and Inactive UCHL5 Cause Accumulation of Distinct Ubiquitinated Proteins In
bioRxiv preprint doi: https://doi.org/10.1101/479758; this version posted November 26, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Inactive USP14 and inactive UCHL5 cause accumulation of distinct ubiquitinated proteins in mammalian cells Jayashree Chadchankar, Victoria Korboukh, Peter Doig, Steve J. Jacobsen, Nicholas J. Brandon, Stephen J. Moss, Qi Wang AstraZeneca Tufts Laboratory for Basic and Translational Neuroscience, Tufts University, Boston, MA (J.C., S.J.M.) Neuroscience, IMED Biotech Unit, AstraZeneca, Boston, MA (S.J.J., N.J.B., Q.W.) Discovery Sciences, IMED Biotech Unit, AstraZeneca, Boston, MA (V.K., P.D.) Department of Neuroscience, Tufts University School of Medicine, Boston, MA (S.J.M.) Department of Neuroscience, Physiology and Pharmacology, University College, London, WC1E, 6BT, UK (S.J.M.) 1 bioRxiv preprint doi: https://doi.org/10.1101/479758; this version posted November 26, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Running title: Effects of inactive USP14 and UCHL5 in mammalian cells Keywords: USP14, UCHL5, deubiquitinase, proteasome, ubiquitin, β‐catenin Corresponding author: Qi Wang Address: Neuroscience, IMED Biotech Unit, AstraZeneca, Boston, MA 02451 Email address: [email protected] 2 bioRxiv preprint doi: https://doi.org/10.1101/479758; this version posted November 26, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission.