Anti-POLR2L (GW22520F)

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3050 Spruce Street, Saint Louis, MO 63103 USA Tel: (800) 521-8956 (314) 771-5765 Fax: (800) 325-5052 (314) 771-5757 email: [email protected] Product Information Anti-POLR2L antibody produced in chicken, affinity isolated antibody Catalog Number GW22520F Formerly listed as GenWay Catalog Number 15-288-22520F, DNA-directed RNA polymerase II 7.6 kDa polypeptide Antibody. The product is a clear, colorless solution in phosphate – Storage Temperature Store at 20 °C buffered saline, pH 7.2, containing 0.02% sodium azide. Synonyms: DNA directed RNA polymerase II polypeptide L, Species Reactivity: Human, mouse EC 2.7.7.6; RPB10; RPB7.6; RPABC5 Tested Applications: WB Product Description Recommended Dilutions: Recommended starting dilution DNA-dependent RNA polymerase catalyzes the transcrip- for Western blot analysis is 1:500, for tissue or cell staining tion of DNA into RNA using the four ribonucleoside 1:200. triphosphates as substrates. Note: Optimal concentrations and conditions for each NCBI Accession number: NP_066951.1 application should be determined by the user. Swiss Prot Accession number: P62875 Precautions and Disclaimer Gene Information: Human .. POLR2L (5441) This product is for R&D use only, not for drug, household, or Immunogen: Recombinant protein DNA directed RNA other uses. Due to the sodium azide content a material polymerase II polypeptide L safety data sheet (MSDS) for this product has been sent to the attention of the safety officer of your institution. Please Immunogen Sequence: GI # 10863925, sequence 1 - 67 consult the Material Safety Data Sheet for information regarding hazards and safe handling practices. Storage/Stability For continuous use, store at 2–8 °C for up to one week. For extended storage, store in –20 °C freezer in working aliquots. Repeated freezing and thawing, or storage in “frostfree” freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilution samples should be discarded if not used within 12 hours. LPG,MAM12/09-1 Sigma brand products are sold through Sigma-Aldrich, Inc. Sigma-Aldrich, Inc. warrants that its products conform to the information contained in this and other Sigma-Aldrich publications. Purchaser must determine the suitability of the product(s) for their particular use. Additional terms and conditions may apply. Please see reverse side of the invoice or packing slip..

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POLR2L Antibody Cat
POLR2L Antibody Cat. No.: XW-7445 POLR2L Antibody Specifications HOST SPECIES: Chicken SPECIES REACTIVITY: Human, Mouse, Rat IMMUNOGEN: 1-67 TESTED APPLICATIONS: WB POLR2L antibody can be used for the detection of POLR2L by Western blot, may also work APPLICATIONS: for IHC and ICC. PREDICTED MOLECULAR 7.6 kDa (calculated) WEIGHT: Properties PURIFICATION: Antigen affinity-purified CLONALITY: Polyclonal CONJUGATE: Unconjugated PHYSICAL STATE: Liquid BUFFER: Phosphate-Buffered Saline. No preservatives added. CONCENTRATION: 1 mg/mL October 1, 2021 1 https://www.prosci-inc.com/polr2l-antibody-7445.html POLR2L antibody can be stored at 4˚C for short term (weeks). Long term storage should STORAGE CONDITIONS: be at -20˚C. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: POLR2L DNA-directed RNA polymerases I, II, and III subunit RPABC5, DNA-directed RNA ALTERNATE NAMES: polymerase III subunit L, RNA polymerases I, and III subunit ABC5, RBP10, RPB10, RPABC5, RPB7.6, hRPB7.6, RPB10beta, POLR2L ACCESSION NO.: NP_066951.1 PROTEIN GI NO.: 10863925 GENE ID: 5441 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References DNA directed RNA polymerase II polypeptide L; polymerase (RNA) II (DNA directed) polypeptide L (7.6kD); RNA polymerase II subunit. This protein is a subunit of RNA polymerase II, the polymerase responsible for synthesizing messenger RNA in eukaryotes. BACKGROUND: It contains four conserved cysteines characteristic of an atypical zinc-binding domain. Like its counterpart in yeast, this subunit may be shared by the other two DNA-directed RNA polymerases.
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Molecular Pharmacology of Cancer Therapy in Human Colorectal Cancer by Gene Expression Profiling1,2
[CANCER RESEARCH 63, 6855–6863, October 15, 2003] Molecular Pharmacology of Cancer Therapy in Human Colorectal Cancer by Gene Expression Profiling1,2 Paul A. Clarke,3 Mark L. George, Sandra Easdale, David Cunningham, R. Ian Swift, Mark E. Hill, Diana M. Tait, and Paul Workman Cancer Research UK Centre for Cancer Therapeutics, Institute of Cancer Research, Sutton, Surrey SM2 5NG [P. A. C., M. L. G., S. E., P. W.]; Department of Gastrointestinal Oncology, Royal Marsden Hospital, Sutton, Surrey [D. C., M. E. H., D. M. T.]; and Department of Surgery, Mayday Hospital, Croydon, Surrey [M. L. G., R. I. S.], United Kingdom ABSTRACT ment with a single dose of MMC4 and during a continuous infusion of 5FU. In this study, we report for the first time gene expression Global gene expression profiling has potential for elucidating the com- profiling in cancer patients before, and critically, during the period of plex cellular effects and mechanisms of action of novel targeted anticancer exposure to chemotherapy. We have demonstrated that the approach agents or existing chemotherapeutics for which the precise molecular is feasible, and we have detected a novel molecular response that mechanism of action may be unclear. In this study, decreased expression would not have been predicted from in vitro studies and that would of genes required for RNA and protein synthesis, and for metabolism were have otherwise been missed by conventional approaches. The results detected in rectal cancer biopsies taken from patients during a 5-fluorou- also suggest a possible new therapeutic approach. Overall our obser- racil infusion. Our observations demonstrate that this approach is feasible and can detect responses that may have otherwise been missed by con- vations suggest that gene expression profiling in response to treatment ventional methods.
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POLR2L Is Over-Expressed in Human Endometrial Cancer
Over-expression of RNA polymerase II subunit L in human endometrial cancer. Shahan Mamoor, MS1 [email protected] East Islip, NY USA Gynecologic cancers including cancers of the endometrium are a clinical problem1-4. We mined published microarray data5,6 to discover genes associated with endometrial cancers by comparing transcriptomes of the normal endometrium and endometrial tumors from humans. We identified RNA polymerase II subunit L, encoded by POLR2L, as among the most differentially expressed genes, transcriptome-wide, in cancers of the endometrium. POLR2L was expressed at significantly higher levels in endometrial tumor tissues as compared to the endometrium. Importantly, primary tumor expression of POLR2L was correlated with recurrence-free survival in patients with endometrial cancer. POLR2L may be a molecule of interest in understanding the etiology or progression of human endometrial cancer. Keywords: endometrial cancer, gynecologic cancers, endometrium, POLR2L, RNA polymerase II subunit L, systems biology of endometrial cancer, targeted therapeutics in endometrial cancer. 1 Endometrial cancer is the most common gynecologic cancer in the developed world1. Over the last three decades, the incidence of endometrial cancer has increased 21%4 and the death rate has increased 100%3. We harnessed the power of independently published microarray datasets5,6 to determine in an unbiased fashion and at the systems-level genes most differentially expressed in endometrial tumors. We report here the differential and increased expression of the RNA polymerase II subunit L (POLR2L) in human endometrial cancer. Methods We utilized datasets GSE636785 and GSE1158106 for this global differential gene expression analysis of human endometrial cancer in conjunction with GEO2R.
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Gene Duplication and Neofunctionalization: POLR3G and POLR3GL
Downloaded from genome.cshlp.org on September 27, 2021 - Published by Cold Spring Harbor Laboratory Press Research Gene duplication and neofunctionalization: POLR3G and POLR3GL Marianne Renaud,1 Viviane Praz,1,2 Erwann Vieu,1,5 Laurence Florens,3 Michael P. Washburn,3,4 Philippe l’Hoˆte,1 and Nouria Hernandez1,6 1Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland; 2Swiss Institute of Bioinformatics, 1015 Lausanne, Switzerland; 3Stowers Institute for Medical Research, Kansas City, Missouri 64110, USA; 4Department of Pathology and Laboratory Medicine, The University of Kansas Medical Center, Kansas City, Kansas 66160, USA RNA polymerase III (Pol III) occurs in two versions, one containing the POLR3G subunit and the other the closely related POLR3GL subunit. It is not clear whether these two Pol III forms have the same function, in particular whether they recognize the same target genes. We show that the POLR3G and POLR3GL genes arose from a DNA-based gene duplication, probably in a common ancestor of vertebrates. POLR3G- as well as POLR3GL-containing Pol III are present in cultured cell lines and in normal mouse liver, although the relative amounts of the two forms vary, with the POLR3G-containing Pol III relatively more abundant in dividing cells. Genome-wide chromatin immunoprecipitations followed by high-throughput sequencing (ChIP-seq) reveal that both forms of Pol III occupy the same target genes, in very constant proportions within one cell line, suggesting that the two forms of Pol III have a similar function with regard to specificity for target genes. In contrast, the POLR3G promoter—not the POLR3GL promoter—binds the transcription factor MYC, as do all other pro- moters of genes encoding Pol III subunits.
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Comprehensive Bioinformatics Analysis Identifies POLR2I As a Key
fgene-12-698570 July 30, 2021 Time: 16:49 # 1 ORIGINAL RESEARCH published: 05 August 2021 doi: 10.3389/fgene.2021.698570 Comprehensive Bioinformatics Analysis Identifies POLR2I as a Key Gene in the Pathogenesis of Hypertensive Nephropathy Shilong You, Jiaqi Xu, Boquan Wu, Shaojun Wu, Ying Zhang*, Yingxian Sun* and Naijin Zhang* Department of Cardiology, The First Hospital of China Medical University, Shenyang, China Hypertensive nephropathy (HN), mainly caused by chronic hypertension, is one of the major causes of end-stage renal disease. However, the pathogenesis of HN remains unclarified, and there is an urgent need for improved treatments. Gene expression profiles for HN and normal tissue were obtained from the Gene Expression Omnibus Edited by: database. A total of 229 differentially co-expressed genes were identified by weighted Zhi-Ping Liu, Shandong University, China gene co-expression network analysis and differential gene expression analysis. These Reviewed by: genes were used to construct protein–protein interaction networks to search for hub Mohadeseh Zarei Ghobadi, genes. Following validation in an independent external dataset and in a clinical database, University of Tehran, Iran POLR2I, one of the hub genes, was identified as a key gene related to the pathogenesis Menghui Yao, First Affiliated Hospital of Zhengzhou of HN. The expression level of POLR2I is upregulated in HN, and the up-regulation of University, China POLR2I is positively correlated with renal function in HN. Finally, we verified the protein *Correspondence: levels of POLR2I in vivo to confirm the accuracy of our analysis. In conclusion, our Naijin Zhang [email protected] study identified POLR2I as a key gene related to the pathogenesis of HN, providing new Yingxian Sun insights into the molecular mechanisms underlying HN.
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Architecture of Pol II(G) and Molecular Mechanism of Transcription Regulation by Gdown1
ARTICLES https://doi.org/10.1038/s41594-018-0118-5 Architecture of Pol II(G) and molecular mechanism of transcription regulation by Gdown1 Miki Jishage1, Xiaodi Yu2,5, Yi Shi3,6, Sai J. Ganesan 4, Wei-Yi Chen1,7, Andrej Sali4, Brian T. Chait 3, Francisco J. Asturias2,8 and Robert G. Roeder 1* Tight binding of Gdown1 represses RNA polymerase II (Pol II) function in a manner that is reversed by Mediator, but the structural basis of these processes is unclear. Although Gdown1 is intrinsically disordered, its Pol II interacting domains were localized and shown to occlude transcription factor IIF (TFIIF) and transcription factor IIB (TFIIB) binding by perfect positioning on their Pol II interaction sites. Robust binding of Gdown1 to Pol II is established by cooperative interactions of a strong Pol II binding region and two weaker binding modulatory regions, thus providing a mechanism both for tight Pol II binding and transcription inhibition and for its reversal. In support of a physiological function for Gdown1 in transcription repression, Gdown1 co-localizes with Pol II in transcriptionally silent nuclei of early Drosophila embryos but re-localizes to the cytoplasm during zygotic genome activation. Our study reveals a self-inactivation through Gdown1 binding as a unique mode of repression in Pol II function. n eukaryotes, Pol II is the central machine responsible for tran- In vitro studies also revealed that Gdown1 prevents TFIIF scription of genes that specify messenger RNAs, small nuclear from associating with Pol II, which in turns leads to inhibition RNAs, and microRNAs. In response to signals that result in of PIC assembly10.
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Synthetic Lethal Screens As a Means to Understand and Treat MYC-Driven Cancers
Downloaded from http://perspectivesinmedicine.cshlp.org/ on October 5, 2021 - Published by Cold Spring Harbor Laboratory Press Synthetic Lethal Screens as a Means to Understand and Treat MYC-Driven Cancers Silvia Cermelli1, In Sock Jang2, Brady Bernard3, and Carla Grandori1 1Human Biology Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109 2SAGE Bionetworks, Seattle, Washington 98109 3Institute for Systems Biology, Seattle, Washington 98109 Correspondence: [email protected] Although therapeutics against MYC could potentially be used against a wide range of human cancers, MYC-targeted therapies have proven difficult to develop. The convergence of break- throughs in human genomics and in gene silencing using RNA interference (RNAi) have recently allowed functional interrogation of the genome and systematic identification of synthetic lethal interactions with hyperactive MYC. Here, we focus on the pathways that have emerged through RNAi screens and present evidence that a subset of genes showing synthetic lethality with MYC are significantly interconnected and linked to chromatin and transcriptional processes, as well as to DNA repair and cell cycle checkpoints. Other syn- thetic lethal interactions with MYC point to novel pathways and potentially broaden the repertoire of targeted therapies. The elucidation of MYC synthetic lethal interactions is still in its infancy, and how these interactions may be influenced by tissue-specific programs and by concurrent genetic change will require further investigation. Nevertheless, we predict that these studies may lead the way to novel therapeutic approaches and new insights into the role of MYC in cancer. sing a synthetic lethal RNA interference ap- of MYC-SL genes has the potential to halt can- Uproach, several groups have recently iden- cers driven by aberrant MYC expression, while tified genes whose function is selectively re- sparing normal tissues.
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Analysis of Cross-Association Between Mrna Expression and Rnai Efficacy for Predictive Target Discovery in Colon Cancers
cancers Article Analysis of Cross-Association between mRNA Expression and RNAi Efficacy for Predictive Target Discovery in Colon Cancers 1, 2, 2 2 1,2, Euna Jeong y, Yejin Lee y, Youngju Kim , Jieun Lee and Sukjoon Yoon * 1 Research Institute of Women’s Health, Sookmyung Women’s University, Seoul 04310, Korea; [email protected] 2 Department of Biological Sciences, Sookmyung Women’s University, Seoul 04310, Korea; [email protected] (Y.L.); [email protected] (Y.K.); [email protected] (J.L.) * Correspondence: [email protected]; Tel.: +82-2-710-9415 These authors contributed equally to this work. y Received: 7 October 2020; Accepted: 23 October 2020; Published: 23 October 2020 Simple Summary: This study focused on finding genes for which mRNA expression was able to predict the anticancer efficacy of its RNAi treatment. Predictive target discovery is of critical importance in developing biomarker-based strategies of precision medicine. We demonstrated this carrying out cross-association analysis on collateral mRNA expression and RNAi treatment data of ~12,000 genes on a colon cell line panel. The analysis revealed several genes with significant association between mRNA expression level and the inhibitory efficacy of its RNAi treatment. The experimental validation confirm that this simple approach has general applications for studying gene association between omics data from diverse cancer lineages. Abstract: The availability of large-scale, collateral mRNA expression and RNAi data from diverse cancer cell types provides useful resources for the discovery of anticancer targets for which inhibitory efficacy can be predicted from gene expression. Here, we calculated bidirectional cross-association scores (predictivity and descriptivity) for each of approximately 18,000 genes identified from mRNA and RNAi (i.e., shRNA and sgRNA) data from colon cancer cell lines.
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Comprehensive Gene Expression Analysis of 5′-End of Mrna Identified Novel Intronic Transcripts Associated with Hepatocellular Carcinoma
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Genomics 95 (2010) 217–223 Contents lists available at ScienceDirect Genomics journal homepage: www.elsevier.com/locate/ygeno Comprehensive gene expression analysis of 5′-end of mRNA identified novel intronic transcripts associated with hepatocellular carcinoma Yuji Hodo a, Shin-ichi Hashimoto b, Masao Honda a, Taro Yamashita a, Yutaka Suzuki c, Sumio Sugano c, Shuichi Kaneko a,⁎, Kouji Matsushima b a Department of Gastroentelorogy, Kanazawa University Graduate School of Medical Science, 13-1 Takara-Machi, Kanazawa, Ishikawa 920-8641, Japan b Department of Molecular Preventive Medicine, School of Medicine, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan c Department of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 5-1-5, Kashiwanoha, Kashiwa, Chiba 277-8562, Japan article info abstract Article history: To elucidate the molecular feature of human hepatocellular carcinoma (HCC), we performed 5′-end serial Received 1 June 2009 analysis of gene expression (5′SAGE), which allows genome-wide identification of transcription start sites in Accepted 14 January 2010 addition to quantification of mRNA transcripts. Three 5′SAGE libraries were generated from normal human Available online 21 January 2010 liver (NL), non-B, non-C HCC tumor (T), and background non-tumor tissues (NT). We obtained 226,834 tags from these libraries and mapped them to the genomic sequences of a total of 8,410 genes using RefSeq Keywords: fi fi 5′-end serial analysis of gene expression database.
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Inferring Modules from Human Protein Interactome Classes Elisabetta Marras1, Antonella Travaglione1, Gautam Chaurasia2,3, Matthias Futschik2,4, Enrico Capobianco1*
Marras et al. BMC Systems Biology 2010, 4:102 http://www.biomedcentral.com/1752-0509/4/102 RESEARCH ARTICLE Open Access Inferring modules from human protein interactome classes Elisabetta Marras1, Antonella Travaglione1, Gautam Chaurasia2,3, Matthias Futschik2,4, Enrico Capobianco1* Abstract Background: The integration of protein-protein interaction networks derived from high-throughput screening approaches and complementary sources is a key topic in systems biology. Although integration of protein interaction data is conventionally performed, the effects of this procedure on the result of network analyses has not been examined yet. In particular, in order to optimize the fusion of heterogeneous interaction datasets, it is crucial to consider not only their degree of coverage and accuracy, but also their mutual dependencies and additional salient features. Results: We examined this issue based on the analysis of modules detected by network clustering methods applied to both integrated and individual (disaggregated) data sources, which we call interactome classes. Due to class diversity, we deal with variable dependencies of data features arising from structural specificities and biases, but also from possible overlaps. Since highly connected regions of the human interactome may point to potential protein complexes, we have focused on the concept of modularity, and elucidated the detection power of module extraction algorithms by independent validations based on GO, MIPS and KEGG. From the combination of protein interactions with gene expressions, a confidence scoring scheme has been proposed before proceeding via GO with further classification in permanent and transient modules. Conclusions: Disaggregated interactomes are shown to be informative for inferring modularity, thus contributing to perform an effective integrative analysis.
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Genomic Incompatibilities in the Diploid and Tetraploid Offspring of the Goldfish × Common Carp Cross
Genomic incompatibilities in the diploid and tetraploid offspring of the goldfish × common carp cross Shaojun Liua,1,2,JingLuob,c,1, Jing Chaib,c,d,e,1,LiRena,1,YiZhoua,1, Feng Huangb,c,1, Xiaochuan Liub,c,1, Yubao Chena, Chun Zhanga, Min Taoa,BinLub,c, Wei Zhouf,GuoliangLinb,c,ChaoMaif, Shuo Yuanf, Jun Wanga, Tao Lia, Qinbo Qina, Hao Fenga, Kaikun Luoa,JunXiaoa, Huan Zhonga, Rurong Zhaoa, Wei Duana, Zhenyan Songa, Yanqin Wangb,c, Jing Wangb,c,LiZhongb,c,LuWangb,c, Zhaoli Dingd, Zhenglin Dug,XuemeiLuh,YunGaod, Robert W. Murphyd,i, Yun Liua, Axel Meyerj,2, and Ya-Ping Zhangb,c,d,2 aKey Laboratory of Protein Chemistry and Fish Developmental Biology of Education Ministry of China, College of Life Sciences, Hunan Normal University, Changsha, 410081, Hunan, China; bState Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University, Kunming, 650091, Yunnan, China; cKey Laboratory for Animal Genetic Diversity and Evolution of High Education in Yunnan Province, School of Life Sciences, Yunnan University, Kunming, 650091, Yunnan, China; dState Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, Yunnan, China; eKunming College of Life Science, University of Chinese Academy of Sciences, Kunming, 650204, China; fSchool of Software, Yunnan University, Kunming, 650091, Yunnan, China; gCore Genomic Facility, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100029, China; hKey Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100101, China; iCentre for Biodiversity and Conservation Biology, Royal Ontario Museum, Toronto, ON, Canada M5S 2C6; and jDepartment of Biology, University of Konstanz, 78457 Konstanz, Germany Edited by Z.
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Genomic Incompatibilities in the Diploid and Tetraploid Offspring of the Goldfish × Common Carp Cross
Genomic incompatibilities in the diploid and tetraploid offspring of the goldfish × common carp cross Shaojun Liua,1,2,JingLuob,c,1, Jing Chaib,c,d,e,1,LiRena,1,YiZhoua,1, Feng Huangb,c,1, Xiaochuan Liub,c,1, Yubao Chena, Chun Zhanga, Min Taoa,BinLub,c, Wei Zhouf,GuoliangLinb,c,ChaoMaif, Shuo Yuanf, Jun Wanga, Tao Lia, Qinbo Qina, Hao Fenga, Kaikun Luoa,JunXiaoa, Huan Zhonga, Rurong Zhaoa, Wei Duana, Zhenyan Songa, Yanqin Wangb,c, Jing Wangb,c,LiZhongb,c,LuWangb,c, Zhaoli Dingd, Zhenglin Dug,XuemeiLuh,YunGaod, Robert W. Murphyd,i, Yun Liua, Axel Meyerj,2, and Ya-Ping Zhangb,c,d,2 aKey Laboratory of Protein Chemistry and Fish Developmental Biology of Education Ministry of China, College of Life Sciences, Hunan Normal University, Changsha, 410081, Hunan, China; bState Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University, Kunming, 650091, Yunnan, China; cKey Laboratory for Animal Genetic Diversity and Evolution of High Education in Yunnan Province, School of Life Sciences, Yunnan University, Kunming, 650091, Yunnan, China; dState Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, Yunnan, China; eKunming College of Life Science, University of Chinese Academy of Sciences, Kunming, 650204, China; fSchool of Software, Yunnan University, Kunming, 650091, Yunnan, China; gCore Genomic Facility, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100029, China; hKey Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100101, China; iCentre for Biodiversity and Conservation Biology, Royal Ontario Museum, Toronto, ON, Canada M5S 2C6; and jDepartment of Biology, University of Konstanz, 78457 Konstanz, Germany Edited by Z.
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