Seq2pathway.Data Vignette
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
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. -
Gene Expression Polarization
Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression This information is current as of September 27, 2021. Fernando O. Martinez, Siamon Gordon, Massimo Locati and Alberto Mantovani J Immunol 2006; 177:7303-7311; ; doi: 10.4049/jimmunol.177.10.7303 http://www.jimmunol.org/content/177/10/7303 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2006/11/03/177.10.7303.DC1 Material http://www.jimmunol.org/ References This article cites 61 articles, 22 of which you can access for free at: http://www.jimmunol.org/content/177/10/7303.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 27, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression1 Fernando O. -
In Silico Analysis of Regulatory Elements of the Vitamin D Receptor
Open Access Baghdad Science Journal P-ISSN: 2078-8665 2020, 17(2):463-470 E-ISSN: 2411-7986 DOI: http://dx.doi.org/10.21123/bsj.2020.17.2.0463 In Silico Analysis of Regulatory Elements of the Vitamin D Receptor Shirin Farivar 1 Roya Amirinejad 2 Bahar Naghavi gargari 3 Seyedeh Batool Hassani 4 Zeinab Shirvani-Farsani 1* Received 26/2/2019, Accepted 5/1/2020, Published 1/6/2020 This work is licensed under a Creative Commons Attribution 4.0 International License. Abstract Vitamin D receptor (VDR) is a nuclear transcription factor that controls gene expression. Its impaired expression was found to be related to different diseases. VDR also acts as a regulator of different pathways including differentiation, inflammation, calcium and phosphate absorption, etc. but there is no sufficient knowledge about the regulation of the gene itself. Therefore, a better understanding of the genetic and epigenetic factors regulating the VDR may facilitate the improvement of strategies for the prevention and treatment of diseases associated with dysregulation of VDR. In the present investigation, a set of databases and methods were used to identify putative functional elements in the VDR locus. Histone modifications, CpG Islands, epigenetic marks at VDR locus were indicated. In addition, repeated sequences, enhancers, insulators, transcription factor binding sites and targets of the VDR gene, as well as protein- protein interactions with bioinformatics tools, were reported. Some of these genetic elements had overlapped with CpG Islands. These results revealed important new insight into the molecular mechanisms of the VDR gene regulation in human cells and tissues. Key words: CpG Islands, Epigenetics, In silico analysis, Regulation elements, VDR Introduction: Vitamin D is a steroid hormone that multiple sclerosis (10), Rheumatoid Arthritis and balances calcium and phosphate levels and is Systemic Lupus Erythematosus (11), cardiovascular crucial for bone structure. -
Genetic Variations in the PSMA6 and PSMC6 Proteasome Genes Are Associated with Multiple Sclerosis and Response to Interferon‑Β Therapy in Latvians
EXPERIMENTAL AND THERAPEUTIC MEDICINE 21: 478, 2021 Genetic variations in the PSMA6 and PSMC6 proteasome genes are associated with multiple sclerosis and response to interferon‑β therapy in Latvians NATALIA PARAMONOVA1, JOLANTA KALNINA1, KRISTINE DOKANE1, KRISTINE DISLERE1, ILVA TRAPINA1, TATJANA SJAKSTE1 and NIKOLAJS SJAKSTE1,2 1Genomics and Bioinformatics, Institute of Biology of The University of Latvia; 2Department of Medical Biochemistry of The University of Latvia, LV‑1004 Riga, Latvia Received July 8, 2020; Accepted December 8, 2020 DOI: 10.3892/etm.2021.9909 Abstract. Several polymorphisms in genes related to the Introduction ubiquitin‑proteasome system exhibit an association with pathogenesis and prognosis of various human autoimmune Multiple sclerosis (MS) is a lifelong demyelinating disease of diseases. Our previous study reported the association the central nervous system. The clinical onset of MS tends to between multiple sclerosis (MS) and the PSMA3‑rs2348071 be between the second and fourth decade of life. Similarly to polymorphism in the Latvian population. The current study other autoimmune diseases, women are affected 3‑4 times more aimed to evaluate the PSMA6 and PSMC6 genetic variations, frequently than men (1). About 10% of MS patients experience their interaction between each other and with the rs2348071, a primary progressive MS form characterized by the progres‑ on the susceptibility to MS risk and response to therapy in sion of neurological disability from the onset. In about 90% the Latvian population. PSMA6‑rs2277460, ‑rs1048990 and of MS patients, the disease undergoes the relapse‑remitting PSMC6‑rs2295826, ‑rs2295827 were genotyped in the MS MS course (RRMS); in most of these patients, the condition case/control study and analysed in terms of genotype‑protein acquires secondary progressive course (SPMS) (2). -
MAP4K4 Expression in Cardiomyocytes: Multiple Isoforms, Multiple Phosphorylations and Interactions with Striatins
MAP4K4 expression in cardiomyocytes: multiple isoforms, multiple phosphorylations and interactions with striatins Article Published Version Creative Commons: Attribution 4.0 (CC-BY) Open access Fuller, S. J., Edmunds, N. S., McGuffin, L. J. ORCID: https://orcid.org/0000-0003-4501-4767, Hardyman, M. A., Cull, J. J., Alharbi, H. O., Meijles, D. N., Sugden, P. H. and Clerk, A. ORCID: https://orcid.org/0000-0002-5658-0708 (2021) MAP4K4 expression in cardiomyocytes: multiple isoforms, multiple phosphorylations and interactions with striatins. Biochemical Journal, 478 (11). pp. 2121-2143. ISSN 0264- 6021 doi: https://doi.org/10.1042/BCJ20210003 Available at http://centaur.reading.ac.uk/98442/ It is advisable to refer to the publisher’s version if you intend to cite from the work. See Guidance on citing . Published version at: http://dx.doi.org/10.1042/BCJ20210003 To link to this article DOI: http://dx.doi.org/10.1042/BCJ20210003 Publisher: Portland Press All outputs in CentAUR are protected by Intellectual Property Rights law, including copyright law. Copyright and IPR is retained by the creators or other copyright holders. Terms and conditions for use of this material are defined in the End User Agreement . www.reading.ac.uk/centaur CentAUR Central Archive at the University of Reading Reading’s research outputs online Biochemical Journal (2021) 478 2121–2143 https://doi.org/10.1042/BCJ20210003 Research Article MAP4K4 expression in cardiomyocytes: multiple isoforms, multiple phosphorylations and interactions with striatins Stephen J. Fuller1, Nick S. Edmunds1, Liam J. McGuffin1, Michelle A. Hardyman1, Joshua J. Cull1, Hajed O. Alharbi1, Daniel N. Meijles2, Peter H. -
Supplementary Table S1. Upregulated Genes Differentially
Supplementary Table S1. Upregulated genes differentially expressed in athletes (p < 0.05 and 1.3-fold change) Gene Symbol p Value Fold Change 221051_s_at NMRK2 0.01 2.38 236518_at CCDC183 0.00 2.05 218804_at ANO1 0.00 2.05 234675_x_at 0.01 2.02 207076_s_at ASS1 0.00 1.85 209135_at ASPH 0.02 1.81 228434_at BTNL9 0.03 1.81 229985_at BTNL9 0.01 1.79 215795_at MYH7B 0.01 1.78 217979_at TSPAN13 0.01 1.77 230992_at BTNL9 0.01 1.75 226884_at LRRN1 0.03 1.74 220039_s_at CDKAL1 0.01 1.73 236520_at 0.02 1.72 219895_at TMEM255A 0.04 1.72 201030_x_at LDHB 0.00 1.69 233824_at 0.00 1.69 232257_s_at 0.05 1.67 236359_at SCN4B 0.04 1.64 242868_at 0.00 1.63 1557286_at 0.01 1.63 202780_at OXCT1 0.01 1.63 1556542_a_at 0.04 1.63 209992_at PFKFB2 0.04 1.63 205247_at NOTCH4 0.01 1.62 1554182_at TRIM73///TRIM74 0.00 1.61 232892_at MIR1-1HG 0.02 1.61 204726_at CDH13 0.01 1.6 1561167_at 0.01 1.6 1565821_at 0.01 1.6 210169_at SEC14L5 0.01 1.6 236963_at 0.02 1.6 1552880_at SEC16B 0.02 1.6 235228_at CCDC85A 0.02 1.6 1568623_a_at SLC35E4 0.00 1.59 204844_at ENPEP 0.00 1.59 1552256_a_at SCARB1 0.02 1.59 1557283_a_at ZNF519 0.02 1.59 1557293_at LINC00969 0.03 1.59 231644_at 0.01 1.58 228115_at GAREM1 0.01 1.58 223687_s_at LY6K 0.02 1.58 231779_at IRAK2 0.03 1.58 243332_at LOC105379610 0.04 1.58 232118_at 0.01 1.57 203423_at RBP1 0.02 1.57 AMY1A///AMY1B///AMY1C///AMY2A///AMY2B// 208498_s_at 0.03 1.57 /AMYP1 237154_at LOC101930114 0.00 1.56 1559691_at 0.01 1.56 243481_at RHOJ 0.03 1.56 238834_at MYLK3 0.01 1.55 213438_at NFASC 0.02 1.55 242290_at TACC1 0.04 1.55 ANKRD20A1///ANKRD20A12P///ANKRD20A2/// -
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. -
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. -
High-Throughput Discovery of Novel Developmental Phenotypes
High-throughput discovery of novel developmental phenotypes The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Dickinson, M. E., A. M. Flenniken, X. Ji, L. Teboul, M. D. Wong, J. K. White, T. F. Meehan, et al. 2016. “High-throughput discovery of novel developmental phenotypes.” Nature 537 (7621): 508-514. doi:10.1038/nature19356. http://dx.doi.org/10.1038/nature19356. Published Version doi:10.1038/nature19356 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:32071918 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Nature. Manuscript Author Author manuscript; Manuscript Author available in PMC 2017 March 14. Published in final edited form as: Nature. 2016 September 22; 537(7621): 508–514. doi:10.1038/nature19356. High-throughput discovery of novel developmental phenotypes A full list of authors and affiliations appears at the end of the article. Abstract Approximately one third of all mammalian genes are essential for life. Phenotypes resulting from mouse knockouts of these genes have provided tremendous insight into gene function and congenital disorders. As part of the International Mouse Phenotyping Consortium effort to generate and phenotypically characterize 5000 knockout mouse lines, we have identified 410 Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms #Corresponding author: [email protected]. -
NPI-0052 and Γ-Radiation Induce a Synergistic Apoptotic Effect In
Frisira et al. Cell Death and Disease (2019) 10:785 https://doi.org/10.1038/s41419-019-2026-y Cell Death & Disease ARTICLE Open Access NPI-0052 and γ-radiation induce a synergistic apoptoticeffectinmedulloblastoma Eleni Frisira1, Fatima Rashid1,SwastinaNathVarma2,SaraBadodi1, Valentine Ayodele Benjamin-Ombo1, David Michod 2 and Maria Victoria Niklison-Chirou 1 Abstract Medulloblastoma (MB) is the most common malignant solid paediatric brain tumour. The standard treatment for MB is surgical resection of the tumour, radiation and chemotherapy. This therapy is associated with high morbidity and adverse side effects. Hence, more targeted and less toxic therapies are vitally needed to improve the quality of life of survivors. NPI-0052 is a novel proteasome inhibitor that irreversibly binds the 20S proteasome subunit. This compound has anti-tumour activity in metastatic solid tumours, glioblastoma and multiple myeloma with a good safety profile. Importantly, NPI-0052 has a lipophilic structure and can penetrate the blood–brain barrier, making it a suitable treatment for brain tumours. In the present study, we performed an in silico gene expression analysis to evaluate the proteasome subunit expression in MB. To evaluate the anticancer activity of NPI-0052, we used a range of MB patient- derived MB cells and cell lines. The synergistic cell death of NPI-0052 with γ-radiation was evaluated in tumour organoids derived from patient-derived MB cells. We show that high expression of proteasome subunits is a poor prognostic factor for MB patients. Also, our preclinical work demonstrated that NPI-0052 can inhibit proteasome activity and activate apoptosis in MB cells. Moreover, we observe that NPI-0052 has a synergistic apoptotic effect with γ-radiation, a component of the current MB therapy. -
SKIP Counteracts P53-Mediated Apoptosis Via Selective Regulation of P21cip1 Mrna Splicing
Downloaded from genesdev.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press SKIP counteracts p53-mediated apoptosis via selective regulation of p21Cip1 mRNA splicing Yupeng Chen, Lirong Zhang, and Katherine A. Jones1 Regulatory Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA The Ski-interacting protein SKIP/SNW1 functions as both a splicing factor and a transcriptional coactivator for induced genes. We showed previously that transcription elongation factors such as SKIP are dispensable in cells subjected to DNA damage stress. However, we report here that SKIP is critical for both basal and stress-induced expression of the cell cycle arrest factor p21Cip1. RNAi chromatin immunoprecipitation (RNAi-ChIP) and RNA immunoprecipitation (RNA-IP) experiments indicate that SKIP is not required for transcription elongation of the gene under stress, but instead is critical for splicing and p21Cip1 protein expression. SKIP interacts with the 39 splice site recognition factor U2AF65 and recruits it to the p21Cip1 gene and mRNA. Remarkably, SKIP is not required for splicing or loading of U2AF65 at other investigated p53-induced targets, including the proapoptotic gene PUMA. Consequently, depletion of SKIP induces a rapid down-regulation of p21Cip1 and predisposes cells to undergo p53-mediated apoptosis, which is greatly enhanced by chemotherapeutic DNA damage agents. ChIP experiments reveal that SKIP is recruited to the p21Cip1, and not PUMA, gene promoters, indicating that p21Cip1 gene-specific splicing is predominantly cotranscriptional. The SKIP-associated factors DHX8 and Prp19 are also selectively required for p21Cip1 expression under stress. Together, these studies define a new step that controls cancer cell apoptosis. -
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.