Anti-GPA33 Antibody

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D220703 Anti-GPA33 antibody Cat. No. D220703 Package 25 μl/100 μl/200 μl Storage -20°C, pH7.4 PBS, 0.05% NaN3, 40% Glycerol Product overview Description A n ti-GPA33 rabbit polyclonal antibody Applications ELISA, WB, IHC Immunogen Fusion protein of human GPA33 Reactivity Human Content 0 .2 mg/ml Host species Rabbit Ig class Immunogen-specific rabbit IgG Purification Antigen affinity purification Target information Symbol GPA33 Full name glycoprotein A33 (transmembrane) Synonyms A33 Swissprot Q99795 Target Background The glycoprotein encoded by this gene is a cell surface antigen that is expressed in greater than 95% of human colon cancers. The open reading frame encodes a 319-amino acid polypeptide having a putative secretory signal sequence and 3 potential glycosylation sites. The predicted mature protein has a 213-amino acid extracellular region, a single transmembrane domain, and a 62-amino acid intracellular tail. The sequence of the extracellular region contains 2 domains characteristic of the CD2 subgroup of the immunoglobulin (Ig) superfamily. Sangon Biotech Applications Immunohistochemistry Predicted cell location: Cytoplasm and membrane Predicted cell location: Cytoplasm and membrane Positive control: Human colon cancer Positive control: Human thyroid cancer Recommended dilution: 50-200 Recommended dilution: 50-200 The image on the left is immunohistochemistry of paraffin-embedded The image on the left is immunohistochemistry of paraffin-embedded Human colon cancer tissue using D220703(GPA33 Antibody) at Human thyroid cancer tissue using D220703(GPA33 Antibody) at dilution 1/30, on the right is treated with fusion protein. (Original dilution 1/30, on the right is treated with fusion protein. (Original magnification: ×200) magnification: ×200) Western blotting Predicted band size:36 kDa Positive control:293T and human colon cancer tissue, 231 cells Recommended dilution: 500-2000 Gel: 15%SDS-PAGE Lysate: 40 μg Lane 1-3: 293T cells, human colon cancer tissue, 231 cells Primary antibody: D220703(GPA33 Antibody) at dilution 1/600 Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution Exposure time: 5 seconds ELISA Sangon Biotech Recommended dilution: 2000-5000 .

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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
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like,
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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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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.
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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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