GPA33 Antibody

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Efficient Professional Protein and Antibody Platforms GPA33 Antibody Basic information: Catalog No.: UPA61087 Source: Rabbit Size: 50ul/100ul Clonality: polyclonal Concentration: 1mg/ml Isotype: Rabbit IgG Purification: affinity purified by Protein A Useful Information: WB:1:500-2000 Applications: IHC-P:1:400-800 Reactivity: Human, Mouse, Rat Specificity: This antibody recognizes GPA33 protein. Immunogen: KLH conjugated synthetic peptide derived from human GPA33 151-280/319 Description: May play a role in cell-cell recognition and signaling. Uniprot: Q9JKA5 Human BiowMW: 33 KDa Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Storage: Store at 4°C short term and -20°C long term. Avoid freeze-thaw cycles. Note: For research use only, not for use in diagnostic procedure. Data: Tissue/cell: human gastric carcinoma; 4% Para- formaldehyde-fixed and paraffin-embedded; An- tigen retrieval: citrate buffer at 37℃ for 20 min; Incubation: Anti-GPA33 Polyclonal Antibody, Un- conjugated 1:200, overnight at 4℃, followed by conjugation to the secondary antibody and DAB- staining Tissue/cell: human gastric carcinoma; 4% Para- formaldehyde-fixed and paraffin-embedded; An- tigen retrieval: citrate buffer at 37℃ for 20 min; Incubation: Anti-GPA33 Polyclonal Antibody, Un- conjugated 1:200, overnight at 4℃, followed by conjugation to the secondary antibody and DAB- staining Gene Universal Technology Co. Ltd www.universalbiol.com Tel: 0550-3121009 E-mail: [email protected] Efficient Professional Protein and Antibody Platforms Sample: Stomach (Rat) Lysate at 40 ug Primary: Anti-GPA33 at 1/1000 dilution Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution Predicted band size: 33 kD Observed band size: 30 kD Paraformaldehyde-fixed, paraffin embedded at 37 ℃ for 30min; Antibody incubation with (GPA33) Polyclonal Antibody, Unconjugated at 1:400 overnight at 4℃, followed by operating according to SP Kit(Rabbit) instructionsand DAB staining. Gene Universal Technology Co. Ltd www.universalbiol.com Tel: 0550-3121009 E-mail: [email protected] .

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Chromosomal Aberrations in Head and Neck Squamous Cell Carcinomas in Norwegian and Sudanese Populations by Array Comparative Genomic Hybridization
825-843 12/9/08 15:31 Page 825 ONCOLOGY REPORTS 20: 825-843, 2008 825 Chromosomal aberrations in head and neck squamous cell carcinomas in Norwegian and Sudanese populations by array comparative genomic hybridization ERIC ROMAN1,2, LEONARDO A. MEZA-ZEPEDA3, STINE H. KRESSE3, OLA MYKLEBOST3,4, ENDRE N. VASSTRAND2 and SALAH O. IBRAHIM1,2 1Department of Biomedicine, Faculty of Medicine and Dentistry, University of Bergen, Jonas Lies vei 91; 2Department of Oral Sciences - Periodontology, Faculty of Medicine and Dentistry, University of Bergen, Årstadveien 17, 5009 Bergen; 3Department of Tumor Biology, Institute for Cancer Research, Rikshospitalet-Radiumhospitalet Medical Center, Montebello, 0310 Oslo; 4Department of Molecular Biosciences, University of Oslo, Blindernveien 31, 0371 Oslo, Norway Received January 30, 2008; Accepted April 29, 2008 DOI: 10.3892/or_00000080 Abstract. We used microarray-based comparative genomic logical parameters showed little correlation, suggesting an hybridization to explore genome-wide profiles of chromosomal occurrence of gains/losses regardless of ethnic differences and aberrations in 26 samples of head and neck cancers compared clinicopathological status between the patients from the two to their pair-wise normal controls. The samples were obtained countries. Our findings indicate the existence of common from Sudanese (n=11) and Norwegian (n=15) patients. The gene-specific amplifications/deletions in these tumors, findings were correlated with clinicopathological variables. regardless of the source of the samples or attributed We identified the amplification of 41 common chromosomal carcinogenic risk factors. regions (harboring 149 candidate genes) and the deletion of 22 (28 candidate genes). Predominant chromosomal alterations Introduction that were observed included high-level amplification at 1q21 (harboring the S100A gene family) and 11q22 (including Head and neck squamous cell carcinoma (HNSCC), including several MMP family members).
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Supplementary Table 1: Adhesion Genes Data Set
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(12) Patent Application Publication (10) Pub. No.: US 2015/0072349 A1 Diamandis Et Al
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Supplemental material to this article can be found at: http://jpet.aspetjournals.org/content/suppl/2018/04/13/jpet.118.249292.DC1 1521-0103/366/1/220–236$35.00 https://doi.org/10.1124/jpet.118.249292 THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS J Pharmacol Exp Ther 366:220–236, July 2018 Copyright ª 2018 by The American Society for Pharmacology and Experimental Therapeutics Analysis of the Indacaterol-Regulated Transcriptome in Human Airway Epithelial Cells Implicates Gene Expression Changes in the s Adverse and Therapeutic Effects of b2-Adrenoceptor Agonists Dong Yan, Omar Hamed, Taruna Joshi,1 Mahmoud M. Mostafa, Kyla C. Jamieson, Radhika Joshi, Robert Newton, and Mark A. Giembycz Departments of Physiology and Pharmacology (D.Y., O.H., T.J., K.C.J., R.J., M.A.G.) and Cell Biology and Anatomy (M.M.M., R.N.), Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada Received March 22, 2018; accepted April 11, 2018 Downloaded from ABSTRACT The contribution of gene expression changes to the adverse and activity, and positive regulation of neutrophil chemotaxis. The therapeutic effects of b2-adrenoceptor agonists in asthma was general enriched GO term extracellular space was also associ- investigated using human airway epithelial cells as a therapeu- ated with indacaterol-induced genes, and many of those, in- tically relevant target. Operational model-fitting established that cluding CRISPLD2, DMBT1, GAS1, and SOCS3, have putative jpet.aspetjournals.org the long-acting b2-adrenoceptor agonists (LABA) indacaterol, anti-inflammatory, antibacterial, and/or antiviral activity. Numer- salmeterol, formoterol, and picumeterol were full agonists on ous indacaterol-regulated genes were also induced or repressed BEAS-2B cells transfected with a cAMP-response element in BEAS-2B cells and human primary bronchial epithelial cells by reporter but differed in efficacy (indacaterol $ formoterol .
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PMC6851141.Pdf
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Rna-Sequencing Applications: Gene Expression Quantification and Methylator Phenotype Identification
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Published online 4 May 2017 Nucleic Acids Research, 2017, Vol. 45, No. 13 e123 doi: 10.1093/nar/gkx371 Precise integration of inducible transcriptional elements (PrIITE) enables absolute control of gene expression Rita Pinto1,2,3,4, Lars Hansen4, John Hintze4, Raquel Almeida1,2,3,5, Sylvester Larsen6,7, Mehmet Coskun8,9, Johanne Davidsen6, Cathy Mitchelmore6, Leonor David1,2,3, Jesper Thorvald Troelsen6 and Eric Paul Bennett4,* 1i3S, Instituto de Investigac¸ao˜ e Inovac¸ao˜ em Saude,´ Universidade do Porto, Porto, Portugal, 2Ipatimup, Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal, 3Faculty of Medicine of the University of Porto, Porto, Portugal, 4Copenhagen Center for Glycomics, Departments of Cellular and Molecular Medicine and Odontology, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark, 5Department of Biology, Faculty of Sciences of the University of Porto, Porto, Portugal, 6Department of Science and Environment, Roskilde University, Roskilde, Denmark, 7Department of Clinical Immunology, Naestved Hospital, Naestved, Denmark, 8Department of Gastroenterology, Medical Section, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark and 9The Bioinformatics Centre, Department of Biology & Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark Received October 03, 2016; Revised March 30, 2017; Editorial Decision April 10, 2017; Accepted April 27, 2017 ABSTRACT INTRODUCTION Tetracycline-based inducible systems provide pow- Historically, analysis of the molecular genetic mechanisms erful methods for functional studies where gene ex- underlying cell fate and animal phenotypes has been studied pression can be controlled. However, the lack of tight by abrogating gene function in cellular and animal model control of the inducible system, leading to leakiness systems.
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Anti-GPA33 Antibody
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393LN V 393P 344SQ V 393P Probe Set Entrez Gene
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Published OnlineFirst February 2, 2016; DOI: 10.1158/0008-5472.CAN-15-3089 Cancer Molecular and Cellular Pathobiology Research Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model Stefan Thiem1, Moritz F. Eissmann1, Joachim Elzer1, Anna Jonas2, Tracy L. Putoczki3, Ashleigh Poh1,3, Paul Nguyen1,3, Adele Preaudet3, Dustin Flanagan4, Elizabeth Vincan4, Paul Waring5, Michael Buchert1, Andrew Jarnicki1,6, and Matthias Ernst1 Abstract About 5% to 10% of human gastric tumors harbor oncogenic terized by excessive STAT3 activity. To assess the contribution of mutations in the KRAS pathway, but their presence alone is often STAT3 to the spontaneously developing gastric adenomas in insufficient for inducing gastric tumorigenesis, suggesting a gp130F/F mice, which carry a knockin mutation in the Il6 requirement for additional mutagenic events or microenviron- signal transducer (Il6st), we generated Tg(Tff1-CreERT2); fl fl mental stimuli, including inflammation. Assessing the contribu- Stat3 / ;gp130F/F mice that also harbor a conditional Stat3 knock- tion of such events in preclinical mouse models requires Cre out allele and found that tamoxifen administration conferred a recombinase–mediated conditional gene expression in stem or significant reduction in their tumor burden. Conversely, excessive þ progenitor cells of normal and transformed gastric epithelium. Kras activity in Tg(Tff1-CreERT2);KrasLSL-G12D/ ;gp130F/F mice We therefore constructed a bacterial artificial chromosome con- promoted more extensive gastric inflammation, metaplastic taining transgene (Tg), comprising the regulatory elements of the transformation, and tumorigenesis than observed in Tg(Tff1- þ trefoil factor 1 (Tff1) gene and the tamoxifen-inducible Cre CreERT2);KrasLSL-G12D/ mice.
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Genome-Wide Association Study of Endo-Parasite Phenotypes Using
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