Genomic Profiling of Short- and Long-Term Caloric Restriction Effects in the Liver of Aging Mice
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Cystatins in Immune System
Journal of Cancer 2013, Vol. 4 45 Ivyspring International Publisher Journal of Cancer 2013; 4(1): 45-56. doi: 10.7150/jca.5044 Review Cystatins in Immune System Špela Magister1 and Janko Kos1,2 1. Jožef Stefan Institute, Department of Biotechnology, Ljubljana, Slovenia; 2. University of Ljubljana, Faculty of Pharmacy, Ljubljana, Slovenia. Corresponding author: Janko Kos, Ph. D., Department of Biotechnology, Jožef Stefan Institute, &Faculty of Pharmacy, University of Ljubljana, Slovenia; [email protected]; Phone+386 1 4769 604, Fax +3861 4258 031. © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/ licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. Received: 2012.10.22; Accepted: 2012.12.01; Published: 2012.12.20 Abstract Cystatins comprise a large superfamily of related proteins with diverse biological activities. They were initially characterised as inhibitors of lysosomal cysteine proteases, however, in recent years some alternative functions for cystatins have been proposed. Cystatins pos- sessing inhibitory function are members of three families, family I (stefins), family II (cystatins) and family III (kininogens). Stefin A is often linked to neoplastic changes in epithelium while another family I cystatin, stefin B is supposed to have a specific role in neuredegenerative diseases. Cystatin C, a typical type II cystatin, is expressed in a variety of human tissues and cells. On the other hand, expression of other type II cystatins is more specific. Cystatin F is an endo/lysosome targeted protease inhibitor, selectively expressed in immune cells, suggesting its role in processes related to immune response. -
Anti-Cystatin B / Stefin B Antibody (ARG56897)
Product datasheet [email protected] ARG56897 Package: 100 μl anti-Cystatin B / Stefin B antibody Store at: -20°C Summary Product Description Rabbit Polyclonal antibody recognizes Cystatin B / Stefin B Tested Reactivity Hu Tested Application ICC/IF, IHC-P, WB Host Rabbit Clonality Polyclonal Isotype IgG Target Name Cystatin B / Stefin B Antigen Species Human Immunogen Recombinant fusion protein corresponding to aa. 1-98 of Human Cystatin B / Stefin B (NP_000091.1). Conjugation Un-conjugated Alternate Names Liver thiol proteinase inhibitor; EPM1; CPI-B; EPM1A; Cystatin-B; Stefin-B; PME; CST6; ULD; STFB Application Instructions Application table Application Dilution ICC/IF 1:50 - 1:200 IHC-P 1:50 - 1:200 WB 1:500 - 1:2000 Application Note * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist. Positive Control MCF7 and DU145 Calculated Mw 11 kDa Observed Size 14 kDa Properties Form Liquid Purification Affinity purified. Buffer PBS (pH 7.3), 0.02% Sodium azide and 50% Glycerol. Preservative 0.02% Sodium azide Stabilizer 50% Glycerol Storage instruction For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use. www.arigobio.com 1/3 Note For laboratory research only, not for drug, diagnostic or other use. Bioinformation Gene Symbol CSTB Gene Full Name cystatin B (stefin B) Background The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. -
FABP2 Ala54thr Polymorphism and Post-Training Changes of Body Composition and Biochemical Parameters in Caucasian Women
G C A T T A C G G C A T genes Article FABP2 Ala54Thr Polymorphism and Post-Training Changes of Body Composition and Biochemical Parameters in Caucasian Women Agata Leo ´nska-Duniec 1,*, Katarzyna Switała´ 1, Ildus I. Ahmetov 2,3 , Craig Pickering 4 , Myosotis Massidda 5 , Maciej Buryta 6, Andrzej Mastalerz 7 and Ewelina Maculewicz 7 1 Faculty of Physical Education, Gdansk University of Physical Education and Sport, 80-336 Gdansk, Poland; [email protected] 2 Laboratory of Molecular Genetics, Kazan State Medical University, 420012 Kazan, Russia; [email protected] 3 Department of Physical Education, Plekhanov Russian University of Economics, 117997 Moscow, Russia 4 Institute of Coaching and Performance, School of Sport and Wellbeing, University of Central Lancashire, Preston PR1 2HE, UK; [email protected] 5 Department of Life and Environmental Sciences, University of Cagliari, 09124 Cagliari, Italy; [email protected] 6 Institute of Physical Culture Sciences, University of Szczecin, 70-453 Szczecin, Poland; [email protected] 7 Faculty of Physical Education, Jozef Pilsudski University of Physical Education in Warsaw, 00-968 Warsaw, Poland; [email protected] (A.M.); [email protected] (E.M.) * Correspondence: [email protected] Abstract: The functional FABP2 Ala54Thr polymorphism (rs1799883) is strongly associated with lipid Citation: Leo´nska-Duniec,A.; Switała,´ K.; Ahmetov, I.I.; Pickering, and carbohydrate metabolism, although the function of its potential modifying effect on training- C.; Massidda, M.; Buryta, M.; induced changes in obesity-related parameters is still unknown. The aim of the present study was Mastalerz, A.; Maculewicz, E. -
Architecture of a Lymphomyeloid Developmental Switch Controlled by PU.1, Notch and Gata3 Marissa Morales Del Real and Ellen V
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Caltech Authors DEVELOPMENT AND STEM CELLS RESEARCH ARTICLE 1207 Development 140, 1207-1219 (2013) doi:10.1242/dev.088559 © 2013. Published by The Company of Biologists Ltd Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3 Marissa Morales Del Real and Ellen V. Rothenberg* SUMMARY Hematopoiesis is a classic system with which to study developmental potentials and to investigate gene regulatory networks that control choices among alternate lineages. T-cell progenitors seeding the thymus retain several lineage potentials. The transcription factor PU.1 is involved in the decision to become a T cell or a myeloid cell, and the developmental outcome of expressing PU.1 is dependent on exposure to Notch signaling. PU.1-expressing T-cell progenitors without Notch signaling often adopt a myeloid program, whereas those exposed to Notch signals remain in a T-lineage pathway. Here, we show that Notch signaling does not alter PU.1 transcriptional activity by degradation/alteration of PU.1 protein. Instead, Notch signaling protects against the downregulation of T-cell factors so that a T-cell transcriptional network is maintained. Using an early T-cell line, we describe two branches of this network. The first involves inhibition of E-proteins by PU.1 and the resulting inhibition of Notch signaling target genes. Effects of E- protein inhibition can be reversed by exposure to Notch signaling. The second network is dependent on the ability of PU.1 to inhibit important T-cell transcription factor genes such as Myb, Tcf7 and Gata3 in the absence of Notch signaling. -
Supplementary Figure 1. Qrt-PCR Analyses for Measuring the Knockdown Efficiency of Transcription Factors. A549 and U937 Cells Kn
Supplementary Figure 1. qRT-PCR analyses for measuring the knockdown efficiency of transcription factors. A549 and U937 cells knocking down or overexpressing different transcription factors including NF-κB subunits p65 and p50 (A), HIF1 (B), TCF4 (C), AP-1 subunits c-Jun and c-FOS (D), or FOXP3 (E) were subjected to RNA isolation, followed by qRT-PCR analyses to examine the expression of these transcription factors. **P<0.01 and ***P<0.001. 1 Supplementary Figure 2. Effects of FOXP3 downregulation and overexpression on the expression of NLRP1, IL1B and IL18. A549 and U937 cells were transfected with si-FOXP3 or pCDNA3-2×Flag-FOXP3. After 24 h, cells were subjected to RNA isolation, followed by qRT-PCR analyses to examine the expression of NLRP1 (A), IL1B (B) and IL18 (C). ***P<0.001. 2 Supplementary Figure 3. Effects of CtBP2 downregulation and overexpression on the expression of miR-199a-3p, NLRP1, IL1B and IL18. A549 and U937 cells were transfected with si-CtBP2 or pCDNA3-2×Flag-CtBP2. After 24 h, cells were subjected to RNA isolation, followed by qRT-PCR analyses to examine the expression of miR-199a-3p (A), NLRP1 (B), IL1B (C) and IL18 (D). ***P<0.001. 3 Supplementary Figure 4. CHFTC specifically bond to the promoter of miR-199a-3p. (A and B) Effects of CtBP2 knockdown and overexpression on HDAC1 and FOXP3 protein levels. A549 cells were transfected with two CtBP2-specific shRNAs and pCDNA3-2×Flag-CtBP2 to obtain two CtBP2-knockdown cell lines (KD-1 and KD-2) (A) and two CtBP2-overexpression cells lines (OE-1 and OE-2) (B), respectively. -
Stefin B (CSTB) Mouse Monoclonal Antibody [Clone ID: OTI1E8] Product Data
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 TA813046 Stefin B (CSTB) Mouse Monoclonal Antibody [Clone ID: OTI1E8] Product data: Product Type: Primary Antibodies Clone Name: OTI1E8 Applications: IHC, WB Recommended Dilution: WB 1:500, IHC 1:500 Reactivity: Human Host: Mouse Isotype: IgG1 Clonality: Monoclonal Immunogen: Human recombinant protein fragment corresponding to amino acids 1-98 of human CSTB (NP_000091) produced in E.coli. Formulation: PBS (PH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide. Concentration: 1 mg/ml Purification: Purified from mouse ascites fluids or tissue culture supernatant by affinity chromatography (protein A/G) Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Predicted Protein Size: 11 kDa Gene Name: cystatin B Database Link: NP_000091 Entrez Gene 1476 Human P04080 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 / 2 Stefin B (CSTB) Mouse Monoclonal Antibody [Clone ID: OTI1E8] – TA813046 Background: The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. Some of the members are active cysteine protease inhibitors, while others have lost or perhaps never acquired this inhibitory activity. There are three inhibitory families in the superfamily, including the type 1 cystatins (stefins), type 2 cystatins and kininogens. This gene encodes a stefin that functions as an intracellular thiol protease inhibitor. -
ACE2 Interaction Networks in COVID-19: a Physiological Framework for Prediction of Outcome in Patients with Cardiovascular Risk Factors
Journal of Clinical Medicine Article ACE2 Interaction Networks in COVID-19: A Physiological Framework for Prediction of Outcome in Patients with Cardiovascular Risk Factors Zofia Wicik 1,2 , Ceren Eyileten 2, Daniel Jakubik 2,Sérgio N. Simões 3, David C. Martins Jr. 1, Rodrigo Pavão 1, Jolanta M. Siller-Matula 2,4,* and Marek Postula 2 1 Centro de Matemática, Computação e Cognição, Universidade Federal do ABC, Santo Andre 09606-045, Brazil; zofi[email protected] (Z.W.); [email protected] (D.C.M.J.); [email protected] (R.P.) 2 Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, Center for Preclinical Research and Technology CEPT, 02-091 Warsaw, Poland; [email protected] (C.E.); [email protected] (D.J.); [email protected] (M.P.) 3 Federal Institute of Education, Science and Technology of Espírito Santo, Serra, Espírito Santo 29056-264, Brazil; [email protected] 4 Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, 1090 Vienna, Austria * Correspondence: [email protected]; Tel.: +43-1-40400-46140; Fax: +43-1-40400-42160 Received: 9 October 2020; Accepted: 17 November 2020; Published: 21 November 2020 Abstract: Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (coronavirus disease 2019; COVID-19) is associated with adverse outcomes in patients with cardiovascular disease (CVD). The aim of the study was to characterize the interaction between SARS-CoV-2 and Angiotensin-Converting Enzyme 2 (ACE2) functional networks with a focus on CVD. Methods: Using the network medicine approach and publicly available datasets, we investigated ACE2 tissue expression and described ACE2 interaction networks that could be affected by SARS-CoV-2 infection in the heart, lungs and nervous system. -
Insulin-Like Growth Factor 1 Treatment Extends Longevity in a Mouse Model of Human Premature Aging by Restoring Somatotroph Axis Function
Insulin-like growth factor 1 treatment extends longevity in a mouse model of human premature aging by restoring somatotroph axis function Guillermo Mariñoa,1, Alejandro P. Ugaldea,1, Álvaro F. Fernándeza, Fernando G. Osorioa, Antonio Fueyob, José M. P. Freijea, and Carlos López-Otína,2 aDepartamento de Bioquímica y Biología Molecular and bBiología Funcional, Facultad de Medicina, Instituto Universitario de Oncología, Universidad de Oviedo, 33006 Oviedo, Spain Edited by Cynthia Kenyon, University of California, San Francisco, CA, and approved August 4, 2010 (received for review March 2, 2010) − − Zmpste24 (also called FACE-1) is a metalloproteinase involved in the Zmpste24 / mice, which constitute an appropriate murine model maturation of lamin A, an essential component of the nuclear of Hutchinson–Gilford progeria, demonstrate a clear dysregula- envelope. Zmpste24-deficient mice exhibit multiple defects that tion of somatotroph axis signaling. In addition, we show that this − − phenocopy human accelerated aging processes such as Hutchinson– alteration is detrimental, given that Zmpste24 / mice treated with Gilford progeria syndrome. In this work, we report that progeroid recombinant IGF-1 show a clear amelioration of progeroid fea- Zmpste24-/− mice present profound transcriptional alterations in tures and significantly extended longevity compared with un- − − genes that regulate the somatotroph axis, together with extremely treated Zmpste24 / mice. high circulating levels of growth hormone (GH) and a drastic reduc- tion in plasma insulin-like growth factor 1 (IGF-1). We also show that Results recombinant IGF-1 treatment restores the proper balance between To gain insight into the alterations associated with the premature aging -/− − − IGF-1 and GH in Zmpste24 mice, delays the onset of many proge- phenotypeobservedinZmpste24 / mice, and considering the increasing roid features, and significantly extends the lifespan of these proge- evidence for the importance of somatotroph axis regulation in longevity, roid animals. -
Meta-Analysis of Nasopharyngeal Carcinoma
BMC Genomics BioMed Central Research article Open Access Meta-analysis of nasopharyngeal carcinoma microarray data explores mechanism of EBV-regulated neoplastic transformation Xia Chen†1,2, Shuang Liang†1, WenLing Zheng1,3, ZhiJun Liao1, Tao Shang1 and WenLi Ma*1 Address: 1Institute of Genetic Engineering, Southern Medical University, Guangzhou, PR China, 2Xiangya Pingkuang associated hospital, Pingxiang, Jiangxi, PR China and 3Southern Genomics Research Center, Guangzhou, Guangdong, PR China Email: Xia Chen - [email protected]; Shuang Liang - [email protected]; WenLing Zheng - [email protected]; ZhiJun Liao - [email protected]; Tao Shang - [email protected]; WenLi Ma* - [email protected] * Corresponding author †Equal contributors Published: 7 July 2008 Received: 16 February 2008 Accepted: 7 July 2008 BMC Genomics 2008, 9:322 doi:10.1186/1471-2164-9-322 This article is available from: http://www.biomedcentral.com/1471-2164/9/322 © 2008 Chen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Epstein-Barr virus (EBV) presumably plays an important role in the pathogenesis of nasopharyngeal carcinoma (NPC), but the molecular mechanism of EBV-dependent neoplastic transformation is not well understood. The combination of bioinformatics with evidences from biological experiments paved a new way to gain more insights into the molecular mechanism of cancer. Results: We profiled gene expression using a meta-analysis approach. Two sets of meta-genes were obtained. Meta-A genes were identified by finding those commonly activated/deactivated upon EBV infection/reactivation. -
Bioinformatics Identification of Potential Genes and Pathways in Preeclampsia Based on Functional Gene Set Enrichment Analyses
EXPERIMENTAL AND THERAPEUTIC MEDICINE 18: 1837-1844, 2019 Bioinformatics identification of potential genes and pathways in preeclampsia based on functional gene set enrichment analyses XUE LI and YANNING FANG Department of Obstetrics, The First People's Hospital of Jining, Jining, Shandong 272000, P.R. China Received October 24, 2018; Accepted May 2, 2019 DOI: 10.3892/etm.2019.7749 Abstract. Preeclampsia is a complication of pregnancy the sample into four distinct groups based on different incu- characterized by new-onset hypertension and proteinuria of bation time. The top 3 candidates were Toll-like receptor 2 gestation, with serious consequences for mother and infant. (TLR2), glutathione S-transferase omega 1 (GSTO1) and Although a vast amount of research has been performed on mitogen-activated protein kinase 13 (MAPK13). TLR2 and the pathogenesis of preeclampsia, the underlying mechanisms associated pathways are known to be closely associated with of this multisystemic disease have remained to be fully eluci- preeclampsia, indirectly demonstrating the applicability of dated. Data were retrieved from Gene Expression Omnibus the analytic process applied. However, the role of GSTO1 and database GSE40182 dataset. After data preprocessing, differ- MAPK13 in preeclampsia has remained poorly investigated, entially expressed genes of placental cells cultured in vitro and elucidation thereof may be a worthwhile endeavor. The from preeclampsia and normal pregnancy were determined present study may provide a basis for exploring potential novel and subjected to Kyoto Encyclopedia of Genes and Genomes genes and pathways as therapeutic targets for preeclampsia. (KEGG) enrichment analysis to identify the associated path- ways. Furthermore, functional principal component analysis Introduction (FPCA) was used to calculate the corresponding F-value of each gene. -
The Analysis of Regulatory Sequences Required for High Level Induction of Rat Á2u-Globulin Gene Expression by Dexamethasone
129 The analysis of regulatory sequences required for high level induction of rat á2u-globulin gene expression by dexamethasone K S Wang and R B Hodgetts Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2E9, Canada (Requests for offprints should be addressed to R B Hodgetts) (K S Wang is now at Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA) ABSTRACT The á2u-globulins are the major urinary proteins in response element 5*-AGAACAnnnTGTACC-3*,is adult male rats. They are encoded by a gene family, situated 513 bp upstream of the transcription start the expression of which is under multihormonal site. We infer that this element or its left half site is control in the liver. Glucocorticoids are positive necessary for the dexamethasone-induced expres- regulatory hormones and we have analyzed the sion of clone 91 from the observation that a second contribution of 5*-upstream sequences to the gene, clone 2, that contained a base substitution at induction by dexamethasone of two cloned position 5 in the left half site was not inducible. It members of the family transfected into mouse now appears that at least three distinct cis-acting L-cells. The results demonstrate that sequences regulatory regions, all of which bind to the from "762 bp to "226 bp of clone 91 are required glucocorticoid receptor in vitro, may contribute to for the 24-fold level of induction that was observed. the full induction of clone 91 by dexamethasone. Addition of 5·5 kb of upstream sequence beyond These are: the distal upstream region identified by "762 bp did not alter the level of induction this study, a proximal upstream region that binds significantly, whereas deletion of the DNA between not only the receptor but also á2uNF1, a "762 bp and "226 bp reduced inducibility to constitutively expressed nuclear protein required about 4-fold. -
A Private 16Q24.2Q24.3 Microduplication in a Boy with Intellectual Disability, Speech Delay and Mild Dysmorphic Features
G C A T T A C G G C A T genes Article A Private 16q24.2q24.3 Microduplication in a Boy with Intellectual Disability, Speech Delay and Mild Dysmorphic Features Orazio Palumbo * , Pietro Palumbo , Ester Di Muro, Luigia Cinque, Antonio Petracca, Massimo Carella and Marco Castori Division of Medical Genetics, Fondazione IRCCS-Casa Sollievo della Sofferenza, San Giovanni Rotondo, 71013 Foggia, Italy; [email protected] (P.P.); [email protected] (E.D.M.); [email protected] (L.C.); [email protected] (A.P.); [email protected] (M.C.); [email protected] (M.C.) * Correspondence: [email protected]; Tel.: +39-088-241-6350 Received: 5 June 2020; Accepted: 24 June 2020; Published: 26 June 2020 Abstract: No data on interstitial microduplications of the 16q24.2q24.3 chromosome region are available in the medical literature and remain extraordinarily rare in public databases. Here, we describe a boy with a de novo 16q24.2q24.3 microduplication at the Single Nucleotide Polymorphism (SNP)-array analysis spanning ~2.2 Mb and encompassing 38 genes. The patient showed mild-to-moderate intellectual disability, speech delay and mild dysmorphic features. In DECIPHER, we found six individuals carrying a “pure” overlapping microduplication. Although available data are very limited, genomic and phenotype comparison of our and previously annotated patients suggested a potential clinical relevance for 16q24.2q24.3 microduplication with a variable and not (yet) recognizable phenotype predominantly affecting cognition. Comparing the cytogenomic data of available individuals allowed us to delineate the smallest region of overlap involving 14 genes. Accordingly, we propose ANKRD11, CDH15, and CTU2 as candidate genes for explaining the related neurodevelopmental manifestations shared by these patients.