13207 PSMB7 (E1L5H) Rabbit Mab
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The Effect of Temperature Adaptation on the Ubiquitin–Proteasome Pathway in Notothenioid Fishes Anne E
© 2017. Published by The Company of Biologists Ltd | Journal of Experimental Biology (2017) 220, 369-378 doi:10.1242/jeb.145946 RESEARCH ARTICLE The effect of temperature adaptation on the ubiquitin–proteasome pathway in notothenioid fishes Anne E. Todgham1,*, Timothy A. Crombie2 and Gretchen E. Hofmann3 ABSTRACT proliferation to compensate for the effects of low temperature on ’ There is an accumulating body of evidence suggesting that the sub- aerobic metabolism (Johnston, 1989; O Brien et al., 2003; zero Antarctic marine environment places physiological constraints Guderley, 2004). Recently, there has been an accumulating body – on protein homeostasis. Levels of ubiquitin (Ub)-conjugated proteins, of literature to suggest that protein homeostasis the maintenance of – 20S proteasome activity and mRNA expression of many proteins a functional protein pool has been highly impacted by evolution involved in both the Ub tagging of damaged proteins as well as the under these cold and stable conditions. different complexes of the 26S proteasome were measured to Maintaining protein homeostasis is a fundamental physiological examine whether there is thermal compensation of the Ub– process, reflecting a dynamic balance in synthetic and degradation proteasome pathway in Antarctic fishes to better understand the processes. There are numerous lines of evidence to suggest efficiency of the protein degradation machinery in polar species. Both temperature compensation of protein synthesis in Antarctic Antarctic (Trematomus bernacchii, Pagothenia borchgrevinki)and invertebrates (Whiteley et al., 1996; Marsh et al., 2001; Robertson non-Antarctic (Notothenia angustata, Bovichtus variegatus) et al., 2001; Fraser et al., 2002) and fish (Storch et al., 2005). In notothenioids were included in this study to investigate the zoarcid fishes, it has been demonstrated that Antarctic eelpouts mechanisms of cold adaptation of this pathway in polar species. -
Inhibition of the Nrf2 Transcription Factor by the Alkaloid
Oncogene (2013) 32, 4825–4835 & 2013 Macmillan Publishers Limited All rights reserved 0950-9232/13 www.nature.com/onc ORIGINAL ARTICLE Inhibition of the Nrf2 transcription factor by the alkaloid trigonelline renders pancreatic cancer cells more susceptible to apoptosis through decreased proteasomal gene expression and proteasome activity A Arlt1,4, S Sebens2,4, S Krebs1, C Geismann1, M Grossmann1, M-L Kruse1, S Schreiber1,3 and H Scha¨fer1 Evidence accumulates that the transcription factor nuclear factor E2-related factor 2 (Nrf2) has an essential role in cancer development and chemoresistance, thus pointing to its potential as an anticancer target and undermining its suitability in chemoprevention. Through the induction of cytoprotective and proteasomal genes, Nrf2 confers apoptosis protection in tumor cells, and inhibiting Nrf2 would therefore be an efficient strategy in anticancer therapy. In the present study, pancreatic carcinoma cell lines (Panc1, Colo357 and MiaPaca2) and H6c7 pancreatic duct cells were analyzed for the Nrf2-inhibitory effect of the coffee alkaloid trigonelline (trig), as well as for its impact on Nrf2-dependent proteasome activity and resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and anticancer drug-induced apoptosis. Chemoresistant Panc1 and Colo357 cells exhibit high constitutive Nrf2 activity, whereas chemosensitive MiaPaca2 and H6c7 cells display little basal but strong tert-butylhydroquinone (tBHQ)-inducible Nrf2 activity and drug resistance. Trig efficiently decreased basal and tBHQ-induced Nrf2 activity in all cell lines, an effect relying on a reduced nuclear accumulation of the Nrf2 protein. Along with Nrf2 inhibition, trig blocked the Nrf2-dependent expression of proteasomal genes (for example, s5a/psmd4 and a5/psma5) and reduced proteasome activity in all cell lines tested. -
CD226 T Cells Expressing the Receptors TIGIT and Divergent Phenotypes of Human Regulatory
The Journal of Immunology Divergent Phenotypes of Human Regulatory T Cells Expressing the Receptors TIGIT and CD226 Christopher A. Fuhrman,*,1 Wen-I Yeh,*,1 Howard R. Seay,* Priya Saikumar Lakshmi,* Gaurav Chopra,† Lin Zhang,* Daniel J. Perry,* Stephanie A. McClymont,† Mahesh Yadav,† Maria-Cecilia Lopez,‡ Henry V. Baker,‡ Ying Zhang,x Yizheng Li,{ Maryann Whitley,{ David von Schack,x Mark A. Atkinson,* Jeffrey A. Bluestone,‡ and Todd M. Brusko* Regulatory T cells (Tregs) play a central role in counteracting inflammation and autoimmunity. A more complete understanding of cellular heterogeneity and the potential for lineage plasticity in human Treg subsets may identify markers of disease pathogenesis and facilitate the development of optimized cellular therapeutics. To better elucidate human Treg subsets, we conducted direct transcriptional profiling of CD4+FOXP3+Helios+ thymic-derived Tregs and CD4+FOXP3+Helios2 T cells, followed by comparison with CD4+FOXP32Helios2 T conventional cells. These analyses revealed that the coinhibitory receptor T cell Ig and ITIM domain (TIGIT) was highly expressed on thymic-derived Tregs. TIGIT and the costimulatory factor CD226 bind the common ligand CD155. Thus, we analyzed the cellular distribution and suppressive activity of isolated subsets of CD4+CD25+CD127lo/2 T cells expressing CD226 and/or TIGIT. We observed TIGIT is highly expressed and upregulated on Tregs after activation and in vitro expansion, and is associated with lineage stability and suppressive capacity. Conversely, the CD226+TIGIT2 population was associated with reduced Treg purity and suppressive capacity after expansion, along with a marked increase in IL-10 and effector cytokine production. These studies provide additional markers to delineate functionally distinct Treg subsets that may help direct cellular therapies and provide important phenotypic markers for assessing the role of Tregs in health and disease. -
Isolation and Characterization of Lymphocyte-Like Cells from a Lamprey
Isolation and characterization of lymphocyte-like cells from a lamprey Werner E. Mayer*, Tatiana Uinuk-ool*, Herbert Tichy*, Lanier A. Gartland†, Jan Klein*, and Max D. Cooper†‡ *Max-Planck-Institut fu¨r Biologie, Abteilung Immungenetik, Corrensstrasse 42, D-72076 Tu¨bingen, Germany; and †Howard Hughes Medical Institute, University of Alabama, 378 Wallace Tumor Institute, Birmingham, AL 35294 Contributed by Max D. Cooper, August 30, 2002 Lymphocyte-like cells in the intestine of the sea lamprey, Petro- existence of the adaptive immune system in jawless fishes, myzon marinus, were isolated by flow cytometry under light- the identity of these cells has remained in doubt. The aim of the scatter conditions used for the purification of mouse intestinal present study was to exploit contemporary methods of cell lymphocytes. The purified lamprey cells were morphologically separation to isolate the agnathan lymphocyte-like cells to indistinguishable from mammalian lymphocytes. A cDNA library characterize them morphologically and by the genes they was prepared from the lamprey lymphocyte-like cells, and more express. than 8,000 randomly selected clones were sequenced. Homology searches comparing these ESTs with sequences deposited in the Materials and Methods databases led to the identification of numerous genes homologous Source and Preparation of Cell Suspension. Ammocoete larvae to those predominantly or characteristically expressed in mamma- (8–13 cm long) of the sea lamprey, Petromyzon marinus (from lian lymphocytes, which included genes controlling lymphopoiesis, Lake Huron, MI) were dissected along the ventral side to extract intracellular signaling, proliferation, migration, and involvement the intestine and the associated typhlosole (spiral valve). Cells of lymphocytes in innate immune responses. -
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. -
Original Article PSMB4 Promotes Glioma Proliferation Via NF-Κb Signaling
Int J Clin Exp Med 2016;9(10):19164-19174 www.ijcem.com /ISSN:1940-5901/IJCEM0027183 Original Article PSMB4 promotes glioma proliferation via NF-κB signaling Xing Su1,2, Qi Yao2, Zhikai Gu2, Jianhong Shen2, Zhongyong Wang1, Jian Chen2, Qin Lan1 1Department of Neurosurgery, Second Affiliated Hospital of Suzhou University, 1055 Sanxiang Road, Suzhou 215004, People’s Republic of China; 2Department of Neurosurgery, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong 226001, People’s Republic of China Received March 3, 2016; Accepted September 10, 2016; Epub October 15, 2016; Published October 30, 2016 Abstract: Proteasomal subunit PSMB4 plays a dominant role in maintaining genomic stability and promoting tu- morigenesis. However, the regulatory mechanism of PSMB4 on carcinogenesis process remains unclear. In this study, we identified the expression and role of PSMB4 in glioma. We found a significant upregulation of PSMB4 both in glioma plasma and cell lines. Higher frequency of PSMB4 positive cells was detected in tumor tissues of gliomas compared to non-tumor tissues. Meanwhile the high frequency of PSMB4 expression was also remarkably associated with poor prognosis of glioma patients. Furthermore, ectopic overexpression of PSMB4 promoted the cell growth and colony forming ability of glioma cells, whereas inhibition of PSMB4 led to a decrease in such events. Our results demonstrated that the upregulation of PSMB4 enhanced cell proliferation of U251 cell line using a BrdU incorporation assay, whereas knockdown of PSMB4 markedly suppressed the cell proliferation and clone-formation. Additionally, while enforced expression of PSMB4 profoundly increased NF-κB activity and the level of PCNA and CyclinD1, PSMB4 knockdown or NF-κB inhibition restrained colony forming ability in glioma cells. -
Intratumoral Injection of SYNB1891, a Synthetic Biotic Medicine Designed
Intratumoral injection of SYNB1891 A Synthetic Biotic medicine designed to activate the innate immune system. Therapy demonstrates target engagement in humans including intratumoral STING activation. Janku F, MD Anderson Cancer Center; Luke JJ, UPMC Hillman Cancer Center; Brennan AM, Synlogic; Riese RJ, Synlogic; Varterasian M, Pharmaceutical Consultant; Kuhn K, Synlogic; Sokolovska A, Synlogic; Strauss J, Mary Crowley Cancer Research Presented by Filip Janku, MD, PhD Study supported by Synlogic, Inc American Association for Cancer Research (AACR) April 2021 Introduction and Methods SYNB1891 Strain Phase 1 First-in-Human Clinical Trial • Live, modified strain of the probiotic E. coli • Enrolling patients with refractory advanced solid Nissle engineered to produce cyclic tumors or lymphoma dinucleotides (CDN) under hypoxia leading to stimulator of interferon genes (STING)- • Intratumoral (IT) injection of SYNB1891 on Days activation 1, 8 and 15 of the first 21-day cycle and then on Day 1 of each subsequent cycle. • Preferentially taken up by phagocytic antigen- presenting cells in tumors, activating • Dose escalation planned across 7 cohorts (1x106 complementary innate immune pathways – 1x109 live cells) with Arm 1 consisting of (direct CDN STING activation; cGAS-mediated SYNB1891 as monotherapy, and Arm 2 in STING activation and TLR4/MyD88 activation by combination with atezolizumab the bacterial chassis) SYNB1891 was safe and well-tolerated in heterogenous population Nov 2020: Interim Analysis IA Updated through 15 Mar 2021 15 Mar 2021: -
Functional Gene Clusters in Global Pathogenesis of Clear Cell Carcinoma of the Ovary Discovered by Integrated Analysis of Transcriptomes
International Journal of Environmental Research and Public Health Article Functional Gene Clusters in Global Pathogenesis of Clear Cell Carcinoma of the Ovary Discovered by Integrated Analysis of Transcriptomes Yueh-Han Hsu 1,2, Peng-Hui Wang 1,2,3,4,5 and Chia-Ming Chang 1,2,* 1 Department of Obstetrics and Gynecology, Taipei Veterans General Hospital, Taipei 112, Taiwan; [email protected] (Y.-H.H.); [email protected] (P.-H.W.) 2 School of Medicine, National Yang-Ming University, Taipei 112, Taiwan 3 Institute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan 4 Department of Medical Research, China Medical University Hospital, Taichung 440, Taiwan 5 Female Cancer Foundation, Taipei 104, Taiwan * Correspondence: [email protected]; Tel.: +886-2-2875-7826; Fax: +886-2-5570-2788 Received: 27 April 2020; Accepted: 31 May 2020; Published: 2 June 2020 Abstract: Clear cell carcinoma of the ovary (ovarian clear cell carcinoma (OCCC)) is one epithelial ovarian carcinoma that is known to have a poor prognosis and a tendency for being refractory to treatment due to unclear pathogenesis. Published investigations of OCCC have mainly focused only on individual genes and lack of systematic integrated research to analyze the pathogenesis of OCCC in a genome-wide perspective. Thus, we conducted an integrated analysis using transcriptome datasets from a public domain database to determine genes that may be implicated in the pathogenesis involved in OCCC carcinogenesis. We used the data obtained from the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) DataSets. We found six interactive functional gene clusters in the pathogenesis network of OCCC, including ribosomal protein, eukaryotic translation initiation factors, lactate, prostaglandin, proteasome, and insulin-like growth factor. -
Open Data for Differential Network Analysis in Glioma
International Journal of Molecular Sciences Article Open Data for Differential Network Analysis in Glioma , Claire Jean-Quartier * y , Fleur Jeanquartier y and Andreas Holzinger Holzinger Group HCI-KDD, Institute for Medical Informatics, Statistics and Documentation, Medical University Graz, Auenbruggerplatz 2/V, 8036 Graz, Austria; [email protected] (F.J.); [email protected] (A.H.) * Correspondence: [email protected] These authors contributed equally to this work. y Received: 27 October 2019; Accepted: 3 January 2020; Published: 15 January 2020 Abstract: The complexity of cancer diseases demands bioinformatic techniques and translational research based on big data and personalized medicine. Open data enables researchers to accelerate cancer studies, save resources and foster collaboration. Several tools and programming approaches are available for analyzing data, including annotation, clustering, comparison and extrapolation, merging, enrichment, functional association and statistics. We exploit openly available data via cancer gene expression analysis, we apply refinement as well as enrichment analysis via gene ontology and conclude with graph-based visualization of involved protein interaction networks as a basis for signaling. The different databases allowed for the construction of huge networks or specified ones consisting of high-confidence interactions only. Several genes associated to glioma were isolated via a network analysis from top hub nodes as well as from an outlier analysis. The latter approach highlights a mitogen-activated protein kinase next to a member of histondeacetylases and a protein phosphatase as genes uncommonly associated with glioma. Cluster analysis from top hub nodes lists several identified glioma-associated gene products to function within protein complexes, including epidermal growth factors as well as cell cycle proteins or RAS proto-oncogenes. -
PSMB6 Polyclonal Antibody Catalog Number:11684-2-AP 1 Publications
For Research Use Only PSMB6 Polyclonal antibody Catalog Number:11684-2-AP 1 Publications www.ptglab.com Catalog Number: GenBank Accession Number: Purification Method: Basic Information 11684-2-AP BC000835 Antigen affinity purification Size: GeneID (NCBI): Recommended Dilutions: 150UL , Concentration: 450 μg/ml by 5694 WB 1:500-1:2000 Nanodrop and 227 μg/ml by Bradford Full Name: IHC 1:50-1:500 method using BSA as the standard; proteasome (prosome, macropain) IF 1:50-1:500 Source: subunit, beta type, 6 Rabbit Calculated MW: Isotype: 239 aa, 25 kDa IgG Observed MW: Immunogen Catalog Number: 25 kDa AG2296 Applications Tested Applications: Positive Controls: IF, IHC, WB,ELISA WB : HeLa cells, Caco-2 cells, fetal human brain tissue, Cited Applications: human liver tissue, mouse brain tissue, rat brain tissue WB IHC : human colon cancer tissue, human gliomas tissue Species Specificity: IF : HeLa cells, human, mouse, rat Cited Species: rat Note-IHC: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0 PSMB6(Proteasome subunit beta type-6) is also named as LMPY, Y and belongs to the peptidase T1B family.The Background Information proteasome is a multicatalytic proteinase complex which is characterized by its ability to cleave peptides with Arg, Phe, Tyr, Leu, and Glu adjacent to the leaving group at neutral or slightly basic pH.It may also catalyzes basal processing of intracellular antigens.It can be up-regulated in anaplastic thyroid cancer cell lines and down- regulated by IFNG/IFN-gamma (at protein level)(PMID:8066462;15613457). -
Selection and Evaluation of Potential Reference Genes for Quantitative Real-Time PCR in Agaricus Blazei Based on Transcriptome Sequencing Data
Hindawi BioMed Research International Volume 2021, Article ID 6661842, 13 pages https://doi.org/10.1155/2021/6661842 Research Article Selection and Evaluation of Potential Reference Genes for Quantitative Real-Time PCR in Agaricus blazei Based on Transcriptome Sequencing Data Yuan-Ping Lu, Jian-Hua Liao , Zhong-Jie Guo, Hui-Qing Zheng, Ling-Fang Lu, Zhi-Xin Cai, Zhi-Heng Zeng, Zheng-He Ying, and Mei-Yuan Chen Institute of Edible Fungi, Fujian Academy of Agricultural Sciences, Fuzhou, 350014 Fujian Province, China Correspondence should be addressed to Jian-Hua Liao; [email protected] and Mei-Yuan Chen; [email protected] Received 9 November 2020; Accepted 3 February 2021; Published 9 April 2021 Academic Editor: Giuliana Banche Copyright © 2021 Yuan-Ping Lu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Quantitative real-time PCR (qRT-PCR) is widely used to detect gene expression due to its high sensitivity, high throughput, and convenience. The accurate choice of reference genes is required for normalization of gene expression in qRT-PCR analysis. In order to identify the optimal candidates for gene expression analysis using qRT-PCR in Agaricus blazei, we studied the potential reference genes in this economically important edible fungus. In this study, transcriptome datasets were used as source for identification of candidate reference genes. And 27 potential reference genes including 21 newly stable genes, three classical housekeeping genes, and homologous genes of three ideal reference genes in Volvariella volvacea, were screened based on transcriptome datasets of A. -
Exosome-Transmitted PSMA3 and PSMA3-AS1 Promote Proteasome Inhibitor Resistance in Multiple Myeloma
Published OnlineFirst January 4, 2019; DOI: 10.1158/1078-0432.CCR-18-2363 Translational Cancer Mechanisms and Therapy Clinical Cancer Research Exosome-Transmitted PSMA3 and PSMA3-AS1 Promote Proteasome Inhibitor Resistance in Multiple Myeloma Hongxia Xu1,2, Huiying Han1, Sha Song1, Nengjun Yi3, Chen'ao Qian4, Yingchun Qiu1, Wenqi Zhou1, Yating Hong5, Wenyue Zhuang6, Zhengyi Li7, Bingzong Li5, and Wenzhuo Zhuang1 Abstract Purpose: How exosomal RNAs released within the bone Results: We identified that PSMA3 and PSMA3-AS1 in MSCs marrow microenvironment affect proteasome inhibitors' (PI) could be packaged into exosomes and transferred to myeloma sensitivity of multiple myeloma is currently unknown. This cells, thus promoting PI resistance. PSMA3-AS1 could form an study aims to evaluate which exosomal RNAs are involved and RNA duplex with pre-PSMA3, which transcriptionally promot- by which molecular mechanisms they exert this function. ed PSMA3 expression by increasing its stability. In xenograft Experimental Design: Exosomes were characterized by models, intravenously administered siPSMA3-AS1 was found dynamic light scattering, transmission electron microscopy, and to be effective in increasing carfilzomib sensitivity. Moreover, Western blot analysis. Coculture experiments were performed to plasma circulating exosomal PSMA3 and PSMA3-AS1 derived assess exosomal RNAs transferring from mesenchymal stem from patients with multiple myeloma were significantly asso- cells (MSC) to multiple myeloma cells. The role of PSMA3-AS1 ciated with PFS and OS. in PI sensitivity was further evaluated in vivo. To determine the Conclusions: This study suggested a unique role of exoso- prognostic significance of circulating exosomal PSMA3 and mal PSMA3 and PSMA3-AS1 in transmitting PI resistance from PSMA3-AS1, a cohort of patients with newly diagnosed multiple MSCs to multiple myeloma cells, through a novel exosomal myeloma was enrolled to study.