DOCSLIB.ORG

PIG3 (TP53I3) Rabbit Polyclonal Antibody – TA308561 | Origene

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
PIG3 (TP53I3) Rabbit Polyclonal Antibody – TA308561 | Origene OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TA308561 PIG3 (TP53I3) Rabbit Polyclonal Antibody Product data: Product Type: Primary Antibodies Applications: IF, IHC, WB Recommended Dilution: ICC/IF:1:100-1:1000; IHC:1:100-1:1000; WB:1:500-1:3000 Reactivity: Human (Predicted: Bovine) Host: Rabbit Isotype: IgG Clonality: Polyclonal Immunogen: Recombinant fragment corresponding to a region within amino acids 1 and 332 of PIG3 (Uniprot ID#Q53FA7) Formulation: 0.1M Tris, 0.1M Glycine, 10% Glycerol (pH7). 0.01% Thimerosal was added as a preservative. Purification: Purified by antigen-affinity chromatography. Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Predicted Protein Size: 36 kDa Gene Name: tumor protein p53 inducible protein 3 Database Link: NP_004872 Entrez Gene 9540 Human Q53FA7 This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 3 PIG3 (TP53I3) Rabbit Polyclonal Antibody – TA308561 Background: The protein encoded by this gene is similar to oxidoreductases, which are enzymes involved in cellular responses to oxidative stresses and irradiation. This gene is induced by the tumor suppressor p53 and is thought to be involved in p53-mediated cell death. It contains a p53 consensus binding site in its promoter region and a downstream pentanucleotide microsatellite sequence. P53 has been shown to transcriptionally activate this gene by interacting with the downstream pentanucleotide microsatellite sequence. The microsatellite is polymorphic, with a varying number of pentanucleotide repeats directly correlated with the extent of transcriptional activation by p53. It has been suggested that the microsatellite polymorphism may be associated with differential susceptibility to cancer. At least two transcript variants encoding the same protein have been found for this gene. [provided by RefSeq] Synonyms: PIG3 Note: Seq homology of immunogen across species: Bovine (88%) Protein Families: Druggable Genome Protein Pathways: p53 signaling pathway Product images: Sample (30 ug of whole cell lysate). A: Hep G2. 10% SDS PAGE. TA308561 diluted at 1:1000. This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 2 / 3 PIG3 (TP53I3) Rabbit Polyclonal Antibody – TA308561 Immunohistochemical analysis of paraffin- embedded H441 xenograft, using PIG3 (TA308561) antibody at 1:500 dilution. Immunofluorescence analysis of paraformaldehyde-fixed A549, using PIG3 (TA308561) antibody at 1:200 dilution. This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 3 / 3.
Load more

Recommended publications
  • Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene
    Hodgkin Lymphoma SUPPLEMENTARY APPENDIX Whole exome sequencing in families at high risk for Hodgkin lymphoma: identification of a predisposing mutation in the KDR gene Melissa Rotunno, 1 Mary L. McMaster, 1 Joseph Boland, 2 Sara Bass, 2 Xijun Zhang, 2 Laurie Burdett, 2 Belynda Hicks, 2 Sarangan Ravichandran, 3 Brian T. Luke, 3 Meredith Yeager, 2 Laura Fontaine, 4 Paula L. Hyland, 1 Alisa M. Goldstein, 1 NCI DCEG Cancer Sequencing Working Group, NCI DCEG Cancer Genomics Research Laboratory, Stephen J. Chanock, 5 Neil E. Caporaso, 1 Margaret A. Tucker, 6 and Lynn R. Goldin 1 1Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 2Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 3Ad - vanced Biomedical Computing Center, Leidos Biomedical Research Inc.; Frederick National Laboratory for Cancer Research, Frederick, MD; 4Westat, Inc., Rockville MD; 5Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; and 6Human Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA ©2016 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2015.135475 Received: August 19, 2015. Accepted: January 7, 2016. Pre-published: June 13, 2016. Correspondence: [email protected] Supplemental Author Information: NCI DCEG Cancer Sequencing Working Group: Mark H. Greene, Allan Hildesheim, Nan Hu, Maria Theresa Landi, Jennifer Loud, Phuong Mai, Lisa Mirabello, Lindsay Morton, Dilys Parry, Anand Pathak, Douglas R. Stewart, Philip R. Taylor, Geoffrey S. Tobias, Xiaohong R. Yang, Guoqin Yu NCI DCEG Cancer Genomics Research Laboratory: Salma Chowdhury, Michael Cullen, Casey Dagnall, Herbert Higson, Amy A.
    [Show full text]
  • Open Full Page
    Author Manuscript Published OnlineFirst on March 9, 2017; DOI: 10.1158/0008-5472.CAN-16-2339 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Title Page Title: Pancreatic cancer progression relies upon mutant p53-induced oncogenic signaling mediated by NOP14 Yongxing Du1,§, Ziwen Liu1, §, Lei You1, Pengjiao Hou2, Xiaoxia Ren1, Tao Jiao2, Wenjing Zhao1, Zongze Li1, Hong Shu1, Changzheng Liu2,*, Yupei Zhao1,* 1 Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100730, PR China 2 Department of Biochemistry and Molecular Biology, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences，School of Basic Medicine, Peking Union Medical College, Beijing 100005, PR China § Authors share co-first authorship. * To whom correspondence should be addressed: Yupei Zhao, E-mail: [email protected], Fax: 86-10-65124875; Changzheng Liu, E-mail: [email protected], Fax: 86-10-65253005. Running Title: NOP14 primes mutp53-driven cancer progression Key words: Pancreatic ductal adenocarcinoma, Mutant p53, NOP14, Cancer metastasis Abbreviations: Mutp53, Mutant p53; PDAC, Pancreatic ductal adenocarcinoma; NOP14, NOP14 nucleolar protein; rRNA, ribosomal RNA; PDGFRb, Platelet-derived 1 Downloaded from cancerres.aacrjournals.org on September 26, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on March 9,
    [Show full text]
  • Identification of Differential Expression of P53 Associated Rnas at 3 Different Treatment Timepoints, and Association with Chip- Seq Identified P53 Genes
    Rochester Institute of Technology RIT Scholar Works Theses 5-19-2017 Identification of Differential Expression of p53 associated RNAs at 3 Different Treatment Timepoints, and Association with ChIP- seq Identified p53 Genes. Julia Freewoman [email protected] Follow this and additional works at: https://scholarworks.rit.edu/theses Recommended Citation Freewoman, Julia, "Identification of Differential Expression of p53 associated RNAs at 3 Different Treatment Timepoints, and Association with ChIP-seq Identified p53 Genes." (2017). Thesis. Rochester Institute of Technology. Accessed from This Thesis is brought to you for free and open access by RIT Scholar Works. It has been accepted for inclusion in Theses by an authorized administrator of RIT Scholar Works. For more information, please contact [email protected]. R.I.T. Identification of Differential Expression of p53 associated RNAs at 3 Different Treatment Timepoints, and Association with ChIP-seq Identified p53 Genes. by Julia Freewoman A Thesis Submitted in Partial Fulfillment of the Requirements for the Degree of Master of Science in Bioinformatics. School of Thomas H. Gosnell School of Life Sciences Bioinformatics Program College of Science Rochester Institute of Technology Rochester, NY May 19, 2017 Thesis Committee Members: Feng Cui, Ph.D., thesis advisor Andre Hudson, Ph.D. Gary R. Skuse, Ph.D. ii Table of Contents Abstract ........................................................................................................................................... 1 I. Introduction
    [Show full text]
  • The Pseudo-Caspase FLIP(L) Regulates Cell Fate Following P53 Activation
    The pseudo-caspase FLIP(L) regulates cell fate following p53 activation Andrea Leesa,1, Alexander J. McIntyrea,1, Nyree T. Crawforda, Fiammetta Falconea, Christopher McCanna, Caitriona Holohana, Gerard P. Quinna, Jamie Z. Robertsa, Tamas Sesslera, Peter F. Gallaghera, Gemma M. A. Gregga, Katherine McAllistera, Kirsty M. McLaughlina, Wendy L. Allena, Laurence J. Eganb, Aideen E. Ryanb,c, Melissa J. Labonte-Wilsona, Philip D. Dunnea, Mark Wappetta, Vicky M. Coylea, Patrick G. Johnstona, Emma M. Kerra, Daniel B. Longleya,2,3, and Simon S. McDadea,2,3 aPatrick G Johnston Centre for Cancer Research, Queen’s University Belfast, Belfast, Northern Ireland BT9 7BL, United Kingdom; bDiscipline of Pharmacology & Therapeutics, Lambe Institute for Translational Research, School of Medicine, College of Medicine, Nursing and Health Sciences, National University of Ireland Galway, Galway, Ireland; and cRegenerative Medicine Institute, College of Medicine, Nursing and Health Sciences, National University of Ireland Galway, Galway, Ireland Edited by Karen H. Vousden, Francis Crick Institute, London, United Kingdom, and approved June 8, 2020 (received for review February 12, 2020) p53 is the most frequently mutated, well-studied tumor-suppressor switch from cell-cycle arrest to cell death induction remain gene, yet the molecular basis of the switch from p53-induced cell- poorly understood, although p53-mediated transcriptional up- cycle arrest to apoptosis remains poorly understood. Using a combi- regulation of PUMA has been suggested to be crucial in a nation of transcriptomics and functional genomics, we unexpectedly number of studies (10, 11). identified a nodal role for the caspase-8 paralog and only human Despite p53/TP53 being the most frequently mutated gene in pseudo-caspase, FLIP(L), in regulating this switch.
    [Show full text]
  • Downregulation of SNRPG Induces Cell Cycle Arrest and Sensitizes Human Glioblastoma Cells to Temozolomide by Targeting Myc Through a P53-Dependent Signaling Pathway
    Cancer Biol Med 2020. doi: 10.20892/j.issn.2095-3941.2019.0164 ORIGINAL ARTICLE Downregulation of SNRPG induces cell cycle arrest and sensitizes human glioblastoma cells to temozolomide by targeting Myc through a p53-dependent signaling pathway Yulong Lan1,2*, Jiacheng Lou2*, Jiliang Hu1, Zhikuan Yu1, Wen Lyu1, Bo Zhang1,2 1Department of Neurosurgery, Shenzhen People’s Hospital, Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen 518020, China;2 Department of Neurosurgery, The Second Affiliated Hospital of Dalian Medical University, Dalian 116023, China ABSTRACT Objective: Temozolomide (TMZ) is commonly used for glioblastoma multiforme (GBM) chemotherapy. However, drug resistance limits its therapeutic effect in GBM treatment. RNA-binding proteins (RBPs) have vital roles in posttranscriptional events. While disturbance of RBP-RNA network activity is potentially associated with cancer development, the precise mechanisms are not fully known. The SNRPG gene, encoding small nuclear ribonucleoprotein polypeptide G, was recently found to be related to cancer incidence, but its exact function has yet to be elucidated. Methods: SNRPG knockdown was achieved via short hairpin RNAs. Gene expression profiling and Western blot analyses were used to identify potential glioma cell growth signaling pathways affected by SNRPG. Xenograft tumors were examined to determine the carcinogenic effects of SNRPG on glioma tissues. Results: The SNRPG-mediated inhibitory effect on glioma cells might be due to the targeted prevention of Myc and p53. In addition, the effects of SNRPG loss on p53 levels and cell cycle progression were found to be Myc-dependent. Furthermore, SNRPG was increased in TMZ-resistant GBM cells, and downregulation of SNRPG potentially sensitized resistant cells to TMZ, suggesting that SNRPG deficiency decreases the chemoresistance of GBM cells to TMZ via the p53 signaling pathway.
    [Show full text]
  • Toward Understanding the Role of P53 in Cardiovascular Diseases
    J. Biomedical Science and Engineering, 2013, 6, 209-212 JBiSE http://dx.doi.org/10.4236/jbise.2013.62A025 Published Online February 2013 (http://www.scirp.org/journal/jbise/) Toward understanding the role of p53 in cardiovascular diseases Mohanalatha Chandrasekharan1, Silvia Vasquez2, Rajesh Kumar Galimudi3, Prashanth Suravajhala1 1Bioclues.org, IKP Knowledge Park, Secunderabad, India 2Instituto Peruano de Energía Nuclear, Centro Nuclear RACSO, Lima, Perú 3Department of Genetics, Osmania University, Hyderabad, India Email: [email protected], [email protected], [email protected], [email protected] Received 14 November 2012; revised 15 December 2012; accepted 22 December 2012 ABSTRACT hypertrophy to heart failure through the suppression of hypoxia inducible factor-1 (HIF-1), which regulates an- Tumour suppressor protein 53 (TP53 or simply p53) giogenesis in the hypertrophied heart. In addition, as p53 is a well known protein linked to apoptosis, cell sig- is known to promote apoptosis, which in turn is involved nalling, cascading and several myriad functions in in heart failure, p53 might be a key molecule in trigger- cells. Many diseases are linked to p53 though analysis ing the development of heart failure from multiple me- show only 216 interaction partners. Whether p53 chanisms [5,6]. While p53 can modulate the activity and plays an important role in cardiovascular diseases expression of some other proteins have been recently (CVD) remains uncertain. Through this bioinfor- studied, whether or not there are potentially beneficial matical analysis, we propose that p53 might play a effects remains to be understood. The actions of the ag- major role in CVD whilst being linked to Hypoxia ing proteins on the CVD have been well studied [7] with and Lupus.
    [Show full text]
  • Addressing the Issue of Missing Heritability: the Importance of Apoptosis in Hereditary Breast and Ovarian Cancer and Functional Assessment of Tp53i3-S252*
    Wayne State University Wayne State University Dissertations January 2020 Addressing The Issue Of Missing Heritability: The Importance Of Apoptosis In Hereditary Breast And Ovarian Cancer And Functional Assessment Of Tp53i3-S252* Sophia Chaudhry Wayne State University Follow this and additional works at: https://digitalcommons.wayne.edu/oa_dissertations Part of the Genetics Commons Recommended Citation Chaudhry, Sophia, "Addressing The Issue Of Missing Heritability: The Importance Of Apoptosis In Hereditary Breast And Ovarian Cancer And Functional Assessment Of Tp53i3-S252*" (2020). Wayne State University Dissertations. 2382. https://digitalcommons.wayne.edu/oa_dissertations/2382 This Open Access Dissertation is brought to you for free and open access by DigitalCommons@WayneState. It has been accepted for inclusion in Wayne State University Dissertations by an authorized administrator of DigitalCommons@WayneState. ADDRESSING THE ISSUE OF MISSING HERITABILITY: THE IMPORTANCE OF APOPTOSIS IN HEREDITARY BREAST AND OVARIAN CANCER AND FUNCTIONAL ASSESSMENT OF TP53I3-S252* by SOPHIA RASUL CHAUDHRY DISSERTATION Submitted to the Graduate School of Wayne State University, Detroit, Michigan in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY 2020 MAJOR: MOLECULAR GENETICS AND GENOMICS Approved By: ____________________________________ Advisor Date ____________________________________ ____________________________________ ____________________________________ DEDICATION I dedicate this work to my parents, my siblings and my nieces and nephew. All have been a positive force and motivation in becoming the scientist I am today. ii ACKNOWLEDGMENTS There are many people who deserve recognition for helping me complete my doctoral work. One of the most challenging parts of my time as a graduate student finding the right lab. I was very lucky to be accepted into the lab headed by Dr.
    [Show full text]
  • Cooperative Genetic Defects in TLX3 Rearranged Pediatric T-ALL
    Leukemia (2008) 22, 762–770 & 2008 Nature Publishing Group All rights reserved 0887-6924/08 $30.00 www.nature.com/leu ORIGINAL ARTICLE Cooperative genetic defects in TLX3 rearranged pediatric T-ALL P Van Vlierberghe1, I Homminga1, L Zuurbier1, J Gladdines-Buijs1, ER van Wering2, M Horstmann3, HB Beverloo4, R Pieters1 and JPP Meijerink1 1Department of Pediatric Oncology/Hematology, Erasmus MC/Sophia Children’s Hospital, Rotterdam, The Netherlands; 2Dutch Childhood Oncology Group (DCOG), The Hague, The Netherlands; 3German Co-operative Study Group for childhood acute lymphoblastic leukemia (COALL), Hamburg, Germany and 4Department of Clinical Genetics, Erasmus MC, Rotterdam, The Netherlands T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive for example, the del(9)(p21) that includes the CDKN2A/p15 and neoplastic disorder, in which multiple genetic abnormalities CDKN2B/p16 loci both deregulating the cell cycle.3,12 Also cooperate in the malignant transformation of thymocytes. NOTCH1 activation mutations are present in more than half About 20% of pediatric T-ALL cases are characterized by 9 TLX3 expression due to a cryptic translocation t(5;14)(q35;q32). of all T-ALL cases of all subgroups. The genetic defects as Although a number of collaborating genetic events have been identified in T-ALL so far target different cellular processes, identified in TLX3 rearranged T-ALL patients (NOTCH1 muta- including cell cycle regulation, T-cell differentiation, prolifera- tions, p15/p16 deletions, NUP214-ABL1 amplifications), further tion and survival. It is hypothesized that these genetic events elucidation of additional genetic lesions could provide a better cooperate in the leukemic transformation of thymocytes.13 understanding of the pathogenesis of this specific T-ALL subtype.
    [Show full text]
  • Effects of Distinct Drugs on Gene Transcription in an Osteosarcoma Cell Line
    4694 ONCOLOGY LETTERS 14: 4694-4700, 2017 Effects of distinct drugs on gene transcription in an osteosarcoma cell line HUI ZHOU1, XIAOFENG CUI2, HONGPING YUAN3, BOYIN ZHANG4, CHUNYANG MENG4 and DONGXU ZHAO4 Departments of 1Anesthesia and 2Gastrointestinal Colorectal and Anal Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033; 3Department of Nephrology, The Fourth Hospital of Jilin University, Changchun, Jilin 130011; 4Department of Orthopedics, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China Received May 4, 2016; Accepted May 25, 2017 DOI: 10.3892/ol.2017.6767 Abstract. Osteosarcoma (OS) is a common cancerous bone or indirectly regulate numerous further genes through several tumor which has a detrimental impact on the lives of patients hub genes including EHF and RFX through various drug and their families. The present study aimed at investigating the treatments in U2OS cells. Furthermore, p53 regulated distinct underlying molecular mechanism of various drug treatments molecular processes in various drug treatments. pertaining to OS, including dimethyl sulfoxide (DMSO), doxo- rubicin (DXP), Nutlin-3, actinomycin D (ActD) and etoposide Introduction (Eto). Microarray and p53 chromatin immunoprecipitation combined with sequencing (ChIP-seq) datasets of the OS cell Osteosarcoma (OS) is a common cancerous bone tumor most line U2OS treated with distinct drugs were acquired from prevalent in children and young adults (1). Specifically, it is a the Gene Expression Omnibus and differentially-expressed histological form of primary bone cancer derived from primi- genes (DEGs) were screened for alignment analysis. The tive transformed cells of mesenchymal origin (2). Numerous p53‑binding target genes were identified and ChIP‑seq and patients with OS also suffer from panic attacks and swelling of microarray gene expression data were combined to identify the lower femur or area directly inferior to the knee, and these directly and indirectly targeted genes.
    [Show full text]
  • Gene Set Enrichment Analysis of Alpha-Glucosidase Inhibitors from Ficus Benghalensis Pukar Khanal, B.M
    Asian Pacific Journal of Tropical Biomedicine 2019; 9(6): 263-270 263 Asian Pacific Journal of Tropical Biomedicine Original Article www.apjtb.org doi: 10.4103/2221-1691.260399 Gene set enrichment analysis of alpha-glucosidase inhibitors from Ficus benghalensis Pukar Khanal, B.M. Patil Department of Pharmacology and Toxicology, KLE College of Pharmacy Belagavi, KLE Academy of Higher Education and Research (KAHER), Belagavi-590010, India ARTICLE INFO ABSTRACT Article history: Objective: To identify alpha-glucosidase inhibitors from Ficus benghalensis and analyze gene Received 18 March 2019 set enrichment of regulated protein molecules. Revision 8 April 2019 Methods: The phytoconstituents of Ficus benghalensis were queried for inhibitors of alpha- Accepted 28 May 2019 Available online 17 June 2019 glucosidase, also identified as aldose reductase inhibitors. Druglikeness score, absorption, distribution, metabolism, excretion and toxicity profile, biological spectrum, and gene expression were predicated for each compound. Docking study was performed to predict the binding affinity with alpha-glucosidase and aldose reductase and compared with clinically Keywords: proven molecules. Kyoto Encyclopedia of Genes and Genomes pathway analysis was Ficus benghalensis performed for the regulated genes to identify the modulated pathways. Gene set enrichment Kaempferol Results: Apigenin, 3,4',5,7-tetrahydroxy-3'-methoxyflavone, and kaempferol were identified Network pharmacology as inhibitors of alpha-glucosidase and aldose reductase. Kaempferol was predicted to possess Type 2 diabetes mellitus the highest binding affinity with both targets. The p53 signaling pathway was predicted to modulate the majority of protein molecules in diabetes mellitus. All the alpha-glucosidase inhibitors were also predicted as membrane integrity agonist and anti-mutagenic compounds.
    [Show full text]
  • The Ubl-UBA Ubiquilin4 Protein Functions As a Tumor Suppressor in Gastric Cancer by P53-Dependent and P53-Independent Regulation of P21
    Cell Death & Differentiation https://doi.org/10.1038/s41418-018-0141-4 ARTICLE The UbL-UBA Ubiquilin4 protein functions as a tumor suppressor in gastric cancer by p53-dependent and p53-independent regulation of p21 1,2,3 1,2,4 5 1,2,4 6 7,8,9 10 1,2,4 Shengkai Huang ● Yan Li ● Xinghua Yuan ● Mei Zhao ● Jia Wang ● You Li ● Yuan Li ● Hong Lin ● 1,2,4 1,2,4 1,2,4 3 11 7 12 Qiao Zhang ● Wenjie Wang ● Dongdong Li ● Xin Dong ● Lanfen Li ● Min Liu ● Weiyan Huang ● Changzhi Huang1,2,4 Received: 28 November 2017 / Revised: 21 May 2018 / Accepted: 23 May 2018 © The Author(s) 2018. This article is published with open access Abstract Ubiquilin4 (Ubqln4), a member of the UbL-UBA protein family, serves as an adaptor in the degradation of specific substrates via the proteasomal pathway. However, the biological function of Ubqln4 remains largely unknown, especially in cancer. Here, we reported that Ubqln4 was downregulated in gastric cancer tissues and functioned as a tumor suppressor by inhibiting gastric cancer cell proliferation in vivo and in vitro. Overexpression of Ubqln4-induced cellular senescence 1234567890();,: 1234567890();,: and G1-S cell cycle arrest in gastric cancer cells and activated the p53/p21 axis. Moreover, Ubqln4 regulated p21 through both p53-dependent and p53-independent manners. Ubqln4 interacted with RNF114, an E3 ubiquitin ligase of p21, and negatively regulated its expression level, which in turn stabilized p21 by attenuating proteasomal degradation of p21. These effects of Ubqln4 were partly abrogated in gastric cancer cells upon silencing of p21.
    [Show full text]
  • A High-Throughput Study in Melanoma Identifies Epithelial- Mesenchymal Transition As a Major Determinant of Metastasis
    Research Article A High-Throughput Study in Melanoma Identifies Epithelial- Mesenchymal Transition as a Major Determinant of Metastasis Soledad R. Alonso,1 Lorraine Tracey,1 Pablo Ortiz,4 Beatriz Pe´rez-Go´mez,5 Jose´ Palacios,1 Marina Polla´n,5 Juan Linares,6 Salvio Serrano,7 Ana I. Sa´ez-Castillo,6 Lydia Sa´nchez,2 Raquel Pajares,2 Abel Sa´nchez-Aguilera,1 Maria J. Artiga,1 Miguel A. Piris,1 and Jose´ L. Rodrı´guez-Peralto3 1Molecular Pathology Programme and 2Histology and Immunohistochemistry Unit, Centro Nacional de Investigaciones Oncolo´gicas; Departments of 3Pathology and 4Dermatology, Hospital Universitario 12 de Octubre; 5Centro Nacional de Epidemiologı´a, Instituto de Salud Carlos III, Madrid, Spain; and Departments of 6Pathology and 7Dermatology, Hospital Universitario San Cecilio, Granada, Spain Abstract with a less favorable prognosis as potential candidates for adjuvant Metastatic disease is the primary cause of death in cutaneous or novel therapies. malignant melanoma (CMM) patients. To understand the Currently, the prognosis of primary CMM is mainly based mechanisms of CMM metastasis and identify potential on histopathologic criteria. The most important of these is the predictive markers, we analyzed gene-expression profiles of Breslow index, although it is merely a measure of tumor depth. 34 vertical growth phase melanoma cases using cDNA micro- New molecular markers that correlate with melanoma genesis and/or progression are continuously being identified but, to date, arrays. All patients had a minimum follow-up of 36 months. Twenty-one cases developed nodal metastatic disease and 13 most of them have been obtained in experimental models and did not.
    [Show full text]