Human MED19 Peptide (DAG-P0675) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

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Human MED19 peptide (DAG-P0675) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description MED19 is a component of the Mediator complex, which is a coactivator for DNA-binding factors that activate transcription via RNA polymerase II (Sato et al., 2003 [PubMed 12584197]).[supplied by OMIM, Oct 2008] Nature Synthetic Expression System N/A Conjugate Unconjugated Sequence Similarities Belongs to the Mediator complex subunit 19 family. Cellular Localization Nucleus. Procedure None Format Liquid Preservative None Storage Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles. Information available upon request. ANTIGEN GENE INFORMATION Gene Name MED19 mediator complex subunit 19 [ Homo sapiens (human) ] Official Symbol MED19 Synonyms MED19; mediator complex subunit 19; LCMR1; DT2P1G7; mediator of RNA polymerase II transcription subunit 19; lung cancer metastasis-related protein 1; mediator of RNA polymerase II transcription, subunit 19 homolog; Entrez Gene ID 219541 mRNA Refseq NM_153450.1 Protein Refseq NP_703151.1 UniProt ID A0JLT2 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved Chromosome Location 11q12.1 Pathway Developmental Biology, organism-specific biosystem; Fatty acid, triacylglycerol, and ketone body metabolism, organism-specific biosystem; Metabolism, organism-specific biosystem; Metabolism of lipids and lipoproteins, organism-specific biosystem; PPARA Activates Gene Expression, organism-specific biosystem; Regulation of Lipid Metabolism by Peroxisome proliferator- activated receptor alpha (PPARalpha), organism-specific biosystem; Transcriptional Regulation of White Adipocyte Differentiation, org Function RNA polymerase II transcription cofactor activity; 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 2 © Creative Diagnostics All Rights Reserved.

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Supplementary Data
Figure 2S 4 7 A - C 080125 CSCs 080418 CSCs - + IFN-a 48 h + IFN-a 48 h + IFN-a 72 h 6 + IFN-a 72 h 3 5 MRFI 4 2 3 2 1 1 0 0 MHC I MHC II MICA MICB ULBP-1 ULBP-2 ULBP-3 ULBP-4 MHC I MHC II MICA MICB ULBP-1 ULBP-2 ULBP-3 ULBP-4 7 B 13 080125 FBS - D 080418 FBS - + IFN-a 48 h 12 + IFN-a 48 h + IFN-a 72 h + IFN-a 72 h 6 080125 FBS 11 10 5 9 8 4 7 6 3 MRFI 5 4 2 3 2 1 1 0 0 MHC I MHC II MICA MICB ULBP-1 ULBP-2 ULBP-3 ULBP-4 MHC I MHC II MICA MICB ULBP-1 ULBP-2 ULBP-3 ULBP-4 Molecule Molecule FIGURE 4S FIGURE 5S Panel A Panel B FIGURE 6S A B C D Supplemental Results Table 1S. Modulation by IFN-α of APM in GBM CSC and FBS tumor cell lines. Molecule * Cell line IFN-α‡ HLA β2-m# HLA LMP TAP1 TAP2 class II A A HC§ 2 7 10 080125 CSCs - 1∞ (1) 3 (65) 2 (91) 1 (2) 6 (47) 2 (61) 1 (3) 1 (2) 1 (3) + 2 (81) 11 (80) 13 (99) 1 (3) 8 (88) 4 (91) 1 (2) 1 (3) 2 (68) 080125 FBS - 2 (81) 4 (63) 4 (83) 1 (3) 6 (80) 3 (67) 2 (86) 1 (3) 2 (75) + 2 (99) 14 (90) 7 (97) 5 (75) 7 (100) 6 (98) 2 (90) 1 (4) 3 (87) 080418 CSCs - 2 (51) 1 (1) 1 (3) 2 (47) 2 (83) 2 (54) 1 (4) 1 (2) 1 (3) + 2 (81) 3 (76) 5 (75) 2 (50) 2 (83) 3 (71) 1 (3) 2 (87) 1 (2) 080418 FBS - 1 (3) 3 (70) 2 (88) 1 (4) 3 (87) 2 (76) 1 (3) 1 (3) 1 (2) + 2 (78) 7 (98) 5 (99) 2 (94) 5 (100) 3 (100) 1 (4) 2 (100) 1 (2) 070104 CSCs - 1 (2) 1 (3) 1 (3) 2 (78) 1 (3) 1 (2) 1 (3) 1 (3) 1 (2) + 2 (98) 8 (100) 10 (88) 4 (89) 3 (98) 3 (94) 1 (4) 2 (86) 2 (79) * expression of APM molecules was evaluated by intracellular staining and cytofluorimetric analysis; ‡ cells were treatead or not (+/-) for 72 h with 1000 IU/ml of IFN-α; # β-2 microglobulin; § β-2 microglobulin-free HLA-A heavy chain; ∞ values are indicated as ratio between the mean of fluorescence intensity of cells stained with the selected mAb and that of the negative control; bold values indicate significant MRFI (≥ 2).
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Genomic Signatures of Recent Adaptive Divergence in the Swamp Sparrow (Melospiza Georgiana)
GENOMIC SIGNATURES OF RECENT ADAPTIVE DIVERGENCE IN THE SWAMP SPARROW (MELOSPIZA GEORGIANA) A Dissertation Presented to the Faculty of the Graduate School of Cornell University In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy by Petra Elizabeth Deane December 2017 © 2017 Petra Elizabeth Deane GENOMIC SIGNATURES OF RECENT ADAPTIVE DIVERGENCE IN THE SWAMP SPARROW (MELOSPIZA GEORGIANA) Petra Elizabeth Deane, Ph. D. Cornell University 2017 Populations that have recently diverged across sharp environmental gradients provide an opportunity to study the mechanisms by which natural selection drives adaptive divergence. Inland and coastal populations of the North American swamp sparrow (Melospiza georgiana) have become an emerging model system for studies of natural selection because they are morphologically and behaviorally distinct despite a very recent divergence time (<15,000 years), yet common garden experiments have demonstrated a genetic basis for their differences. I characterized genomic patterns of variation within and between inland and coastal swamp sparrows via reduced representation sequencing and demonstrated that background genomic differentiation (FST=0.02) and divergence (ΦST=0.05) between these populations is very low, rendering signatures of natural selection highly detectable (max FST=0.8). I then sequenced and assembled a de novo reference genome for the species and conducted a scan for genes involved in coastal adaptation, particularly the evolution of a deeper bill, darker plumage, and tolerance for salinity. I recovered a multigenic snapshot of adaptation via robust signatures of selection at 31 genes. As in Darwin’s finches, bone morphogenetic protein (BMP) signaling appears responsible for changes in bill depth, a putative magic trait for ecological speciation.
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Structure and Mechanism of the RNA Polymerase II Transcription Machinery
Downloaded from genesdev.cshlp.org on October 9, 2021 - Published by Cold Spring Harbor Laboratory Press REVIEW Structure and mechanism of the RNA polymerase II transcription machinery Allison C. Schier and Dylan J. Taatjes Department of Biochemistry, University of Colorado, Boulder, Colorado 80303, USA RNA polymerase II (Pol II) transcribes all protein-coding ingly high resolution, which has rapidly advanced under- genes and many noncoding RNAs in eukaryotic genomes. standing of the molecular basis of Pol II transcription. Although Pol II is a complex, 12-subunit enzyme, it lacks Structural biology continues to transform our under- the ability to initiate transcription and cannot consistent- standing of complex biological processes because it allows ly transcribe through long DNA sequences. To execute visualization of proteins and protein complexes at or near these essential functions, an array of proteins and protein atomic-level resolution. Combined with mutagenesis and complexes interact with Pol II to regulate its activity. In functional assays, structural data can at once establish this review, we detail the structure and mechanism of how enzymes function, justify genetic links to human dis- over a dozen factors that govern Pol II initiation (e.g., ease, and drive drug discovery. In the past few decades, TFIID, TFIIH, and Mediator), pausing, and elongation workhorse techniques such as NMR and X-ray crystallog- (e.g., DSIF, NELF, PAF, and P-TEFb). The structural basis raphy have been complemented by cryoEM, cross-linking for Pol II transcription regulation has advanced rapidly mass spectrometry (CXMS), and other methods. Recent in the past decade, largely due to technological innova- improvements in data collection and imaging technolo- tions in cryoelectron microscopy.
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1 a Genome-Wide RNA Interference Screen Identifies New Regulators Of
Downloaded from genome.cshlp.org on September 30, 2021 - Published by Cold Spring Harbor Laboratory Press A genome-wide RNA interference screen identifies new regulators of androgen receptor function in prostate cancer cells Keren Imberg-Kazdan1 Susan Ha1,2 Alex Greenfield3 Christopher S. Poultney3^ Richard Bonneau3 Susan K. Logan1,2,4 Michael J. Garabedian2, 3,4 Departments of Biochemistry and Molecular Pharmacology1, Urology2, Microbiology4, and NYU Cancer Institute5, New York University School of Medicine, 550 First Avenue, New York, NY 10016; 3Center for Genomics and Systems Biology, New York University, New York, New York 10003 ^ present address: Seaver Autism Center for Research and Treatment, Department of Psychiatry, Mount Sinai Medical Center, New York, New York 10029 Corresponding Author: Michael J. Garabedian Department of Microbiology NYU School of Medicine 550 First Avenue, New York, NY 10016 Phone 212 263-7662 Fax 212 263-8276 Email: [email protected] Running Title: Genome-wide RNAi screen for AR regulators Keywords: Androgen receptor, RNAi screen, transcriptional regulation, HIPK2, MED19, Mediator complex, prostate cancer 1 Downloaded from genome.cshlp.org on September 30, 2021 - Published by Cold Spring Harbor Laboratory Press Abstract The androgen receptor (AR) is a mediator of both androgen-dependent and castration- resistant prostate cancers. Identification of cellular factors affecting AR transcriptional activity could in principle yield new targets that reduce AR activity and combat prostate cancer, yet a comprehensive analysis of the genes required for AR-dependent transcriptional activity has not been determined. Using an unbiased genetic approach that takes advantage of the evolutionary conservation of AR signaling, we have conducted a genome-wide RNAi screen in Drosophila cells for genes required for AR transcriptional activity and applied the results to human prostate cancer cells.
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(Med19) Induces Apoptosis in Human Laryngocarcinoma Hep2 Cells in an Apaf-1-Dependent Pathway
Am J Transl Res 2017;9(2):755-761 www.ajtr.org /ISSN:1943-8141/AJTR0038848 Original Article Down-regulation of mediator complex subunit 19 (Med19) induces apoptosis in human laryngocarcinoma HEp2 cells in an Apaf-1-dependent pathway Yan Zhao1*, Qingfeng Meng2*, Xu Gao3, Lihua Zhang1, Lixin An1 Departments of 1Allergy, 2Ophthalmology, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang Province, China; 3Department of Biochemistry, Harbin Medical University, Harbin 150001, Heilongjiang Province, China. *Equal contributors. Received February 29, 2016; Accepted December 21, 2016; Epub February 15, 2017; Published February 28, 2017 Abstract: Mediator 19 (Med19) is a component of the mediator complex which is a co-activator for DNA-binding factors that activate transcription via RNA polymerase II. Accumulating evidence has shown that Med19 plays im- portant roles in cancer cell proliferation and tumorigenesis. The physiological mechanism by which Med19 exerts its promoting effects in laryngocarcinoma is not yet fully understood. Here, we found that the expression of Med19 was increased in laryngocarcinoma samples from patients compared to normal bone tissues. Med19 knockdown significantly induced growth inhibition and suppressed migration in the HEp2 cell lines. Med19 knockdown also induced apoptosis in HEp2 cells via activation of caspase-3, 9 and Apaf-1. In addition, The tumorigenicity of Med19 short hairpin RNA (shRNA)-expressing cells were decreased after inoculating into nude mice. Taken together, our data suggest that Med19 acts as an oncogene in laryngocarcinoma via a possible caspase modulation pathway. Keywords: Apoptosis, laryngocarcinoma, proliferation, Med19, caspase Introduction strated to be a component of the Mediator com- plex [8] and is essential for mediator binding laryngocarcinoma is among the most common and its activation of RNA Pol II [9, 10].
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PCQAP Monoclonal Antibody (M02), ARC/DRIP and May Function As a Transcriptional Clone 4A4 Coactivator in RNA Polymerase II Transcription
PCQAP monoclonal antibody (M02), ARC/DRIP and may function as a transcriptional clone 4A4 coactivator in RNA polymerase II transcription. This gene contains stretches of trinucleotide repeats and is Catalog Number: H00051586-M02 located in the chromosome 22 region which is deleted in DiGeorge syndrome. Two transcript variants encoding Regulation Status: For research use only (RUO) different isoforms have been found for this gene. [provided by RefSeq] Product Description: Mouse monoclonal antibody raised against a partial recombinant PCQAP. References: 1. MED19 and MED26 are synergistic functional targets Clone Name: 4A4 of the RE1 silencing transcription factor in epigenetic silencing of neuronal gene expression. Ding N, Immunogen: PCQAP (NP_056973, 1 a.a. ~ 88 a.a) Tomomori-Sato C, Sato S, Conaway RC, Conaway JW, partial recombinant protein with GST tag. MW of the Boyer TG. J Biol Chem. 2009 Jan 30;284(5):2648-56. GST tag alone is 26 KDa. Epub 2008 Dec 2. 2. TAZ controls Smad nucleocytoplasmic shuttling and Sequence: regulates human embryonic stem-cell self-renewal. MDVSGQETDWRSTAFRQKLVSQIEDAMRKAGVAHSK Varelas X, Sakuma R, Samavarchi-Tehrani P, Peerani SSKDMESHVFLKAKTRDEYLSLVARLIIHFRDIHNKKSQ R, Rao BM, Dembowy J, Yaffe MB, Zandstra PW, ASVSDPMNALQSL Wrana JL. Nat Cell Biol. 2008 Jul;10(7):837-48. Epub 2008 Jun 22. Host: Mouse Reactivity: Human Applications: ELISA, IF, S-ELISA, WB-Re (See our web site product page for detailed applications information) Protocols: See our web site at http://www.abnova.com/support/protocols.asp or product page for detailed protocols Isotype: IgG2a Kappa Storage Buffer: In 1x PBS, pH 7.4 Storage Instruction: Store at -20°C or lower.
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Using an Atlas of Gene Regulation Across 44 Human Tissues to Inform Complex Disease- and Trait-Associated Variation
Using an atlas of gene regulation across 44 human tissues to inform complex disease- and trait-associated variation The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Gamazon, Eric R. "Using an atlas of gene regulation across 44 human tissues to inform complex disease- and trait-associated variation." Nature Genetics 50, 7 (July 2018): 956–967 © 2018 The Author(s) As Published http://dx.doi.org/10.1038/S41588-018-0154-4 Publisher Springer Nature Version Author's final manuscript Citable link https://hdl.handle.net/1721.1/121227 Terms of Use Creative Commons Attribution-Noncommercial-Share Alike Detailed Terms http://creativecommons.org/licenses/by-nc-sa/4.0/ Europe PMC Funders Group Author Manuscript Nat Genet. Author manuscript; available in PMC 2018 December 28. Published in final edited form as: Nat Genet. 2018 July ; 50(7): 956–967. doi:10.1038/s41588-018-0154-4. Europe PMC Funders Author Manuscripts Using an atlas of gene regulation across 44 human tissues to inform complex disease- and trait-associated variation Eric R. Gamazon1,2,§,*, Ayellet V. Segrè3,4,§,*, Martijn van de Bunt5,6,§, Xiaoquan Wen7, Hualin S. Xi8, Farhad Hormozdiari9,10, Halit Ongen11,12,13, Anuar Konkashbaev1, Eske M. Derks14, François Aguet3, Jie Quan8, GTEx Consortium15, Dan L. Nicolae16,17,18, Eleazar Eskin9, Manolis Kellis3,19, Gad Getz3,20, Mark I. McCarthy5,6, Emmanouil T. Dermitzakis11,12,13, Nancy J. Cox1, and Kristin G. Ardlie3 1Division of Genetic Medicine, Department of Medicine,
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Mrna Expression in Human Leiomyoma and Eker Rats As Measured by Microarray Analysis
Table 3S: mRNA Expression in Human Leiomyoma and Eker Rats as Measured by Microarray Analysis Human_avg Rat_avg_ PENG_ Entrez. Human_ log2_ log2_ RAPAMYCIN Gene.Symbol Gene.ID Gene Description avg_tstat Human_FDR foldChange Rat_avg_tstat Rat_FDR foldChange _DN A1BG 1 alpha-1-B glycoprotein 4.982 9.52E-05 0.68 -0.8346 0.4639 -0.38 A1CF 29974 APOBEC1 complementation factor -0.08024 0.9541 -0.02 0.9141 0.421 0.10 A2BP1 54715 ataxin 2-binding protein 1 2.811 0.01093 0.65 0.07114 0.954 -0.01 A2LD1 87769 AIG2-like domain 1 -0.3033 0.8056 -0.09 -3.365 0.005704 -0.42 A2M 2 alpha-2-macroglobulin -0.8113 0.4691 -0.03 6.02 0 1.75 A4GALT 53947 alpha 1,4-galactosyltransferase 0.4383 0.7128 0.11 6.304 0 2.30 AACS 65985 acetoacetyl-CoA synthetase 0.3595 0.7664 0.03 3.534 0.00388 0.38 AADAC 13 arylacetamide deacetylase (esterase) 0.569 0.6216 0.16 0.005588 0.9968 0.00 AADAT 51166 aminoadipate aminotransferase -0.9577 0.3876 -0.11 0.8123 0.4752 0.24 AAK1 22848 AP2 associated kinase 1 -1.261 0.2505 -0.25 0.8232 0.4689 0.12 AAMP 14 angio-associated, migratory cell protein 0.873 0.4351 0.07 1.656 0.1476 0.06 AANAT 15 arylalkylamine N-acetyltransferase -0.3998 0.7394 -0.08 0.8486 0.456 0.18 AARS 16 alanyl-tRNA synthetase 5.517 0 0.34 8.616 0 0.69 AARS2 57505 alanyl-tRNA synthetase 2, mitochondrial (putative) 1.701 0.1158 0.35 0.5011 0.6622 0.07 AARSD1 80755 alanyl-tRNA synthetase domain containing 1 4.403 9.52E-05 0.52 1.279 0.2609 0.13 AASDH 132949 aminoadipate-semialdehyde dehydrogenase -0.8921 0.4247 -0.12 -2.564 0.02993 -0.32 AASDHPPT 60496 aminoadipate-semialdehyde
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Identification of Putative Regulatory Regions and Transcription Factors Associated with Intramuscular Fat Content Traits Aline S
Cesar et al. BMC Genomics (2018) 19:499 https://doi.org/10.1186/s12864-018-4871-y RESEARCHARTICLE Open Access Identification of putative regulatory regions and transcription factors associated with intramuscular fat content traits Aline S. M. Cesar1,2, Luciana C. A. Regitano3, James M. Reecy2, Mirele D. Poleti1, Priscila S. N. Oliveira3, Gabriella B. de Oliveira1, Gabriel C. M. Moreira1, Maurício A. Mudadu4, Polyana C. Tizioto1, James E. Koltes2, Elyn Fritz-Waters2, Luke Kramer2, Dorian Garrick5, Hamid Beiki2, Ludwig Geistlinger3, Gerson B. Mourão1, Adhemar Zerlotini4 and Luiz L. Coutinho1* Abstract Background: Integration of high throughput DNA genotyping and RNA-sequencing data allows for the identification of genomic regions that control gene expression, known as expression quantitative trait loci (eQTL), on a whole genome scale. Intramuscular fat (IMF) content and carcass composition play important roles in metabolic and physiological processes in mammals because they influence insulin sensitivity and consequently prevalence of metabolic diseases such as obesity and type 2 diabetes. However, limited information is available on the genetic variants and mechanisms associated with IMF deposition in mammals. Thus, our hypothesis was that eQTL analyses could identify putative regulatory regions and transcription factors (TFs) associated with intramuscular fat (IMF) content traits. Results: We performed an integrative eQTL study in skeletal muscle to identify putative regulatory regions and factors associated with intramuscular fat content traits. Data obtained from skeletal muscle samples of 192 animals was used for association analysis between 461,466 SNPs and the transcription level of 11,808 genes. This yielded 1268 cis- and 10,334 trans-eQTLs, among which we identified nine hotspot regions that each affected the expression of > 119 genes.
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MED19 Alters AR Occupancy and Gene Expression in Prostate Cancer Cells, Driving MAOA Expression and Growth Under Low Androgen
bioRxiv preprint doi: https://doi.org/10.1101/857235; this version posted November 27, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 2 3 4 MED19 alters AR occupancy and gene expression in prostate cancer cells, driving MAOA 5 expression and growth under low androgen 6 7 8 Hannah Weber1, Rachel Ruoff1, and Michael J. Garabedian1* 9 10 11 1Departments of Microbiology and Urology, NYU School of Medicine, New York, NY, USA 12 13 14 *Michael J. Garabedian 15 Email: [email protected] (MJG) 16 17 18 19 20 21 22 23 Short title: MED19 promotes androgen-independent prostate cancer growth through MAOA 1 bioRxiv preprint doi: https://doi.org/10.1101/857235; this version posted November 27, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 24 Abstract 25 Androgen deprivation therapy (ADT) is a mainstay of prostate cancer treatment, given 26 the dependence of prostate cells on androgen and the androgen receptor (AR). However, tumors 27 become ADT-resistant, and there is a need to understand the mechanism. One possible 28 mechanism is the upregulation of AR co-regulators, although only a handful have been 29 definitively linked to disease. We previously identified the Mediator subunit MED19 as an AR 30 co-regulator, and reported that MED19 depletion inhibits AR transcriptional activity and growth 31 of androgen-insensitive LNCaP-abl cells.
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Enriched Genes FLX07
enriched genes FLX07 Entrez Symbols Name TermID TermDesc 24950 MGC156498,S5AR 1,Srd5a1 steroid-5-alpha-reductase, alpha polypeptide 1 (3-oxo-5 alpha-steroid delta 4-dehydrogenase alpha 1) GO:0003865 3-oxo-5-alpha-steroid 4-dehydrogenase activity 361191 Nsun2,RGD1311954 NOL1/NOP2/Sun domain family, member 2 GO:0003865 3-oxo-5-alpha-steroid 4-dehydrogenase activity 305291 RGD1308828,S5AR 3,Srd5a3 steroid 5 alpha-reductase 3 GO:0003865 3-oxo-5-alpha-steroid 4-dehydrogenase activity 311569 Acas2,Acss2 acyl-CoA synthetase short-chain family member 2 GO:0003987 acetate-CoA ligase activity 296259 Acas2l,Acss1 acyl-CoA synthetase short-chain family member 1 GO:0003987 acetate-CoA ligase activity 25288 ACS,Acas,Acsl1,COAA,Facl2 acyl-CoA synthetase long-chain family member 1 GO:0003987 acetate-CoA ligase activity 114024 Acs3,Acsl3,Facl3 acyl-CoA synthetase long-chain family member 3 GO:0003987 acetate-CoA ligase activity 299002 G2e3,RGD1310263 G2/M-phase specific E3 ubiquitin ligase GO:0016881 acid-amino acid ligase activity 361866 Hace1 HECT domain and ankyrin repeat containing, E3 ubiquitin protein ligase 1 GO:0016881 acid-amino acid ligase activity 316395 Hecw2 HECT, C2 and WW domain containing E3 ubiquitin protein ligase 2 GO:0016881 acid-amino acid ligase activity 309758 Herc4 hect domain and RLD 4 GO:0016881 acid-amino acid ligase activity 361815 MGC116114,Rnf8 ring finger protein 8 GO:0016881 acid-amino acid ligase activity 298576 Mul1,RGD1309944 mitochondrial ubiquitin ligase activator of NFKB 1 GO:0016881 acid-amino acid ligase activity
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Gene Expression Profiling in Hepatocellular Carcinoma: Upregulation of Genes in Amplified Chromosome Regions
Modern Pathology (2008) 21, 505–516 & 2008 USCAP, Inc All rights reserved 0893-3952/08 $30.00 www.modernpathology.org Gene expression profiling in hepatocellular carcinoma: upregulation of genes in amplified chromosome regions Britta Skawran1, Doris Steinemann1, Anja Weigmann1, Peer Flemming2, Thomas Becker3, Jakobus Flik4, Hans Kreipe2, Brigitte Schlegelberger1 and Ludwig Wilkens1,2 1Institute of Cell and Molecular Pathology, Hannover Medical School, Hannover, Germany; 2Institute of Pathology, Hannover Medical School, Hannover, Germany; 3Department of Visceral and Transplantation Surgery, Hannover Medical School, Hannover, Germany and 4Institute of Virology, Hannover Medical School, Hannover, Germany Cytogenetics of hepatocellular carcinoma and adenoma have revealed gains of chromosome 1q as a significant differentiating factor. However, no studies are available comparing these amplification events with gene expression. Therefore, gene expression profiling was performed on tumours cytogenetically well characterized by array-based comparative genomic hybridisation. For this approach analysis was carried out on 24 hepatocellular carcinoma and 8 hepatocellular adenoma cytogenetically characterised by array-based comparative genomic hybridisation. Expression profiles of mRNA were determined using a genome-wide microarray containing 43 000 spots. Hierarchical clustering analysis branched all hepatocellular adenoma from hepatocellular carcinoma. Significance analysis of microarray demonstrated 722 dysregulated genes in hepatocellular carcinoma. Gene set enrichment analysis detected groups of upregulated genes located in chromosome bands 1q22–42 seen also as the most frequently gained regions by comparative genomic hybridisation. Comparison of significance analysis of microarray and gene set enrichment analysis narrowed down the number of dysregulated genes to 18, with 7 genes localised on 1q22 (SCAMP3, IQGAP3, PYGO2, GPATC4, ASH1L, APOA1BP, and CCT3). In hepatocellular adenoma 26 genes in bands 11p15, 11q12, and 12p13 were upregulated.
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