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Produktinformation Diagnostik & molekulare Diagnostik Laborgeräte & Service Zellkultur & Verbrauchsmaterial Forschungsprodukte & Biochemikalien Weitere Information auf den folgenden Seiten! See the following pages for more information! Lieferung & Zahlungsart Lieferung: frei Haus Bestellung auf Rechnung SZABO-SCANDIC Lieferung: € 10,- HandelsgmbH & Co KG Erstbestellung Vorauskassa Quellenstraße 110, A-1100 Wien T. +43(0)1 489 3961-0 Zuschläge F. +43(0)1 489 3961-7 [email protected] • Mindermengenzuschlag www.szabo-scandic.com • Trockeneiszuschlag • Gefahrgutzuschlag linkedin.com/company/szaboscandic • Expressversand facebook.com/szaboscandic PDLIM2 purified MaxPab mouse polyclonal antibody (B01P) Catalog # : H00064236-B01P 規格 : [ 50 ug ] List All Specification Application Image Product Mouse polyclonal antibody raised against a full-length human PDLIM2 Western Blot (Tissue lysate) Description: protein. Immunogen: PDLIM2 (NP_067643.2, 1 a.a. ~ 352 a.a) full-length human protein. Sequence: MALTVDVAGPAPWGFRITGGRDFHTPIMVTKVAERGKAKDADLRPGDIIV AINGESAEGMLHAEAQSKIRQSPSPLRLQLDRSQATSPGQTNGDSSLEV enlarge LATRFQGSVRTYTESQSSLRSSYSSPTSLSPRAGSPFSPPPSSSSLTGE AAISRSFQSLACSPGLPAADRLSYSGRPGSRQAGLGRAGDSAVLVLPPS Western Blot (Transfected PGPRSSRPSMDSEGGSLLLDEDSEVFKMLQENREGRAAPRQSSSFRLL lysate) QEALEAEERGGTPAFLPSSLSPQSSLPASRALATPPKLHTCEKCSTSIAN QAVRIQEGRYRHPGCYTCADCGLNLKMRGHFWVGDELYCEKHARQRY SAPATLSSRA Host: Mouse Reactivity: Human enlarge Quality Control Antibody reactive against mammalian transfected lysate. Testing: Storage Buffer: In 1x PBS, pH 7.4 Storage Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. Instruction: MSDS: Download Datasheet: Download Publication Reference 1. Human T-cell leukemia virus type 1 bZIP factor selectively suppresses the classical pathway of NF-{kappa}B. Zhao T, Yasunaga JI, Satou Y, Nakao M, Takahashi M, Fujii M, Matsuoka M.Blood. 2009 Mar 19;113(12):2755-64. Epub 2008 Dec 8. Applications Western Blot (Tissue lysate) PDLIM2 MaxPab polyclonal antibody. Western Blot analysis of PDLIM2 expression in Page 1 of 2 2020/6/26 human liver. Protocol Download Western Blot (Transfected lysate) Western Blot analysis of PDLIM2 expression in transfected 293T cell line (H00064236-T01) by PDLIM2 MaxPab polyclonal antibody. Lane 1: PDLIM2 transfected lysate(38.72 KDa). Lane 2: Non-transfected lysate. Protocol Download Gene Information Entrez GeneID: 64236 GeneBank NM_021630.4 Accession#: Protein NP_067643.2 Accession#: Gene Name: PDLIM2 Gene Alias: FLJ34715,MYSTIQUE,SLIM Gene PDZ and LIM domain 2 (mystique) Description: Omim ID: 609722 Gene Ontology: Hyperlink Other PDZ and LIM domain 2 Designations: 服務條款 | 隱私權政策 | 著作及商標 | 網站地圖 ©2020 亞諾法生技股份有限公司 Abnova Corporation. 版權所有. Page 2 of 2 2020/6/26.

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Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-Like Mouse Models: Tracking the Role of the Hairless Gene
University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Doctoral Dissertations Graduate School 5-2006 Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene Yutao Liu University of Tennessee - Knoxville Follow this and additional works at: https://trace.tennessee.edu/utk_graddiss Part of the Life Sciences Commons Recommended Citation Liu, Yutao, "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino- like Mouse Models: Tracking the Role of the Hairless Gene. " PhD diss., University of Tennessee, 2006. https://trace.tennessee.edu/utk_graddiss/1824 This Dissertation is brought to you for free and open access by the Graduate School at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Doctoral Dissertations by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. To the Graduate Council: I am submitting herewith a dissertation written by Yutao Liu entitled "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene." I have examined the final electronic copy of this dissertation for form and content and recommend that it be accepted in partial fulfillment of the requirements for the degree of Doctor of Philosophy, with a major in Life Sciences. Brynn H. Voy, Major Professor We have read this dissertation and recommend its acceptance: Naima Moustaid-Moussa, Yisong Wang, Rogert Hettich Accepted for the Council: Carolyn R.
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Inactivation of the Putative Ubiquitin-E3 Ligase PDLIM2 in Classical Hodgkin and Anaplastic Large Cell Lymphoma
OPEN Leukemia (2016), 1–12 www.nature.com/leu ORIGINAL ARTICLE Inactivation of the putative ubiquitin-E3 ligase PDLIM2 in classical Hodgkin and anaplastic large cell lymphoma KD Wurster1,2, F Hummel1,2, J Richter3, M Giefing3,4, S Hartmann5, M-L Hansmann5, S Kreher2, K Köchert1,2, D Krappmann6, W Klapper7, M Hummel8, S-S Wenzel2, G Lenz9, M Janz1,2, B Dörken1,2,10, R Siebert3,11 and S Mathas1,2,10 Apart from its unique histopathological appearance with rare tumor cells embedded in an inflammatory background of bystander cells, classical Hodgkin lymphoma (cHL) is characterized by an unusual activation of a broad range of signaling pathways involved in cellular activation. This includes constitutive high-level activity of nuclear factor-κB (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), activator protein-1 (AP-1) and interferon regulatory factor (IRF) transcription factors (TFs) that are physiologically only transiently activated. Here, we demonstrate that inactivation of the putative ubiquitin E3-ligase PDLIM2 contributes to this TF activation. PDLIM2 expression is lost at the mRNA and protein levels in the majority of cHL cell lines and Hodgkin and Reed–Sternberg (HRS) cells of nearly all cHL primary samples. This loss is associated with PDLIM2 genomic alterations, promoter methylation and altered splicing. Reconstitution of PDLIM2 in HRS cell lines inhibits proliferation, blocks NF-κB transcriptional activity and contributes to cHL-specific gene expression. In non-Hodgkin B-cell lines, small interfering RNA-mediated PDLIM2 knockdown results in superactivation of TFs NF-κB and AP-1 following phorbol 12-myristate 13-acetate (PMA) stimulation.
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Molecular and Epigenetic Features of Melanomas and Tumor Immune
Seremet et al. J Transl Med (2016) 14:232 DOI 10.1186/s12967-016-0990-x Journal of Translational Medicine RESEARCH Open Access Molecular and epigenetic features of melanomas and tumor immune microenvironment linked to durable remission to ipilimumab‑based immunotherapy in metastatic patients Teofila Seremet1,3*† , Alexander Koch2†, Yanina Jansen1, Max Schreuer1, Sofie Wilgenhof1, Véronique Del Marmol3, Danielle Liènard3, Kris Thielemans4, Kelly Schats5, Mark Kockx5, Wim Van Criekinge2, Pierre G. Coulie6, Tim De Meyer2, Nicolas van Baren6,7 and Bart Neyns1 Abstract Background: Ipilimumab (Ipi) improves the survival of advanced melanoma patients with an incremental long-term benefit in 10–15 % of patients. A tumor signature that correlates with this survival benefit could help optimizing indi- vidualized treatment strategies. Methods: Freshly frozen melanoma metastases were collected from patients treated with either Ipi alone (n: 7) or Ipi combined with a dendritic cell vaccine (TriMixDC-MEL) (n: 11). Samples were profiled by immunohistochemistry (IHC), whole transcriptome (RNA-seq) and methyl-DNA sequencing (MBD-seq). Results: Patients were divided in two groups according to clinical evolution: durable benefit (DB; 5 patients) and no clinical benefit (NB; 13 patients). 20 metastases were profiled by IHC and 12 were profiled by RNA- and MBD-seq. 325 genes were identified as differentially expressed between DB and NB. Many of these genes reflected a humoral and cellular immune response. MBD-seq revealed differences between DB and NB patients in the methylation of genes linked to nervous system development and neuron differentiation. DB tumors were more infiltrated by CD8+ and PD-L1+ cells than NB tumors.
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PDLIM2 Antibody A
Revision 1 C 0 2 - t PDLIM2 Antibody a e r o t S Orders: 877-616-CELL (2355) [email protected] Support: 877-678-TECH (8324) 4 4 Web: [email protected] 1 www.cellsignal.com 8 # 3 Trask Lane Danvers Massachusetts 01923 USA For Research Use Only. Not For Use In Diagnostic Procedures. Applications: Reactivity: Sensitivity: MW (kDa): Source: UniProt ID: Entrez-Gene Id: WB H M Endogenous 38 Rabbit Q96JY6 64236 Product Usage Information Application Dilution Western Blotting 1:1000 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody. Specificity / Sensitivity PDLIM2 Antibody recognizes endogenous levels of total PDLIM2 protein. Species Reactivity: Human, Mouse Source / Purification Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly255 of human PDLIM2 protein. Antibodies are purified by protein A and peptide affinity chromatography. Background PDLIM2, also known as Mystique, contains an amino-terminal PDZ domain and a carboxy-terminal LIM domain. PDLIM2 was orginally found to be associated with cytoskeletal proteins in epithelial cells to promote cell attachment and migration (1,2). Subsequent studies have shown that PDLIM2 can also inhibit NF-κB activity by acting as a nuclear ubiquitin E3 ligase for p65 (3). PDLIM2 is suppressed in cancer cell lines by DNA methylation (4,5). Expression of PDLIM2 can inhibit anchorage-independent growth and tumor formation. 1. Torrado, M. et al. (2004) Invest Ophthalmol Vis Sci 45, 3955-63. 2. Loughran, G.
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BASIC RESEARCH www.jasn.org Phosphoproteomic Analysis Reveals Regulatory Mechanisms at the Kidney Filtration Barrier †‡ †| Markus M. Rinschen,* Xiongwu Wu,§ Tim König, Trairak Pisitkun,¶ Henning Hagmann,* † † † Caroline Pahmeyer,* Tobias Lamkemeyer, Priyanka Kohli,* Nicole Schnell, †‡ †† ‡‡ Bernhard Schermer,* Stuart Dryer,** Bernard R. Brooks,§ Pedro Beltrao, †‡ Marcus Krueger,§§ Paul T. Brinkkoetter,* and Thomas Benzing* *Department of Internal Medicine II, Center for Molecular Medicine, †Cologne Excellence Cluster on Cellular Stress | Responses in Aging-Associated Diseases, ‡Systems Biology of Ageing Cologne, Institute for Genetics, University of Cologne, Cologne, Germany; §Laboratory of Computational Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; ¶Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand; **Department of Biology and Biochemistry, University of Houston, Houston, Texas; ††Division of Nephrology, Baylor College of Medicine, Houston, Texas; ‡‡European Molecular Biology Laboratory–European Bioinformatics Institute, Hinxton, Cambridge, United Kingdom; and §§Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany ABSTRACT Diseases of the kidney ﬁltration barrier are a leading cause of ESRD. Most disorders affect the podocytes, polarized cells with a limited capacity for self-renewal that require tightly controlled signaling to maintain their integrity, viability, and function. Here, we provide an atlas of in vivo phosphorylated, glomerulus- expressed
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Downloaded, Each with Over 20 Samples for AD-Specific Pathways, Biological Processes, and Driver Each Specific Brain Region in Each Condition
Xiang et al. BMC Medical Genomics 2018, 11(Suppl 6):115 https://doi.org/10.1186/s12920-018-0431-1 RESEARCH Open Access Condition-specific gene co-expression network mining identifies key pathways and regulators in the brain tissue of Alzheimer’s disease patients Shunian Xiang1,2, Zhi Huang4, Wang Tianfu1, Zhi Han3, Christina Y. Yu3,5, Dong Ni1*, Kun Huang3* and Jie Zhang2* From 29th International Conference on Genome Informatics Yunnan, China. 3-5 December 2018 Abstract Background: Gene co-expression network (GCN) mining is a systematic approach to efficiently identify novel disease pathways, predict novel gene functions and search for potential disease biomarkers. However, few studies have systematically identified GCNs in multiple brain transcriptomic data of Alzheimer’s disease (AD) patients and looked for their specific functions. Methods: In this study, we first mined GCN modules from AD and normal brain samples in multiple datasets respectively; then identified gene modules that are specific to AD or normal samples; lastly, condition-specific modules with similar functional enrichments were merged and enriched differentially expressed upstream transcription factors were further examined for the AD/normal-specific modules. Results: We obtained 30 AD-specific modules which showed gain of correlation in AD samples and 31 normal- specific modules with loss of correlation in AD samples compared to normal ones, using the network mining tool lmQCM. Functional and pathway enrichment analysis not only confirmed known gene functional categories related to AD, but also identified novel regulatory factors and pathways. Remarkably, pathway analysis suggested that a variety of viral, bacteria, and parasitic infection pathways are activated in AD samples.
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Transdifferentiation of Human Mesenchymal Stem Cells
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Supplementary Methods Microarray Experiments (Single Color Mode) The Microarray utilized in this study represents a refined version of the Whole Human Genome Oligo Microarray 4 × 44K v2 (Design ID 026652, Agilent Technologies, (Santa Clara, CA, USA), called ‘054261On1M’ (Design ID 066335) developed at the Research Core Unit Transcriptomics (RCUT) of Hannover Medical School (Hannover, Germany). The microarray design was created in Agilent’s eArray portal using a 1 × 1 M design format for mRNA expression as template. All non-control probes of design ID 026652 have been printed five times within a region comprising a total of 181,560 Features (170 columns × 1068 rows). Four of such regions were placed within one 1 M region giving rise to four microarray fields per slide to be hybridized individually (Customer Specified Feature Layout). Control probes required for proper Feature Extraction software operation were determined and placed automatically by eArray using recommended default settings. An amount of 250 ng of total RNA were used for synthesis of aminoallyl-UTP-modified (aaUTP) cRNA with the ‘Quick Amp Labeling kit, no dye’ (#5190-0447, Agilent Technologies) according to the manufacturer’s recommendations, except that reaction volumes were quartered and contained NTP- mix was exchanged by NTP Set (ATP, CTP, GTP, UTP) and aminoallyl-UTP (Fermentas, Thermo Fisher Scientific; Waltham, MA, USA); order numbers R1091, R0481, respectively). Final NTP concentrations used for in-vitro transcription were 2.5 mM (ATP, CTP, GTP), 1.88 mM UTP, and 0.62 mM aaUTP. The labeling of aaUTP-cRNA was performed by use of Alexa Fluor 555 Reactive Dye (#A32756; LifeTechnologies) as described in the Amino Allyl MessageAmp™ II Kit Manual (#AM1753; Life Technologies, Carlsbad, CA, USA) except that reaction volumes were quartered.
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Downloaded Per Proteome Cohort Via the Web- Site Links of Table 1, Also Providing Information on the Deposited Spectral Datasets
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Survival Analysis of Infected Mice Reveals Pathogenic Variations in The
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Supporting Information Extendend Materials and Methods Animals A
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