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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 Tel:240-252-7368(USA) Fax:240-252-7376(USA) www.elabscience.com ® E-mail:[email protected] Elabscience Elabscience Biotechnology Inc. CRMP1 Polyclonal Antibody Catalog No. E-AB-12333 Reactivity H,M,R Storage Store at -20℃. Avoid freeze / thaw cycles. Host Rabbit Applications WB,ELISA ElabscienceIsotype IgG Note: Centrifuge before opening to ensure complete recovery of vial contents. Images Immunogen Information Elabscience Immunogen Synthetic peptide of human CRMP1 Gene Accession NP_001304 Swissprot Q14194 Synonyms DRP1,DRP-1,CRMP-1,DPYSL1,ULIP-3 Western Blot analysis of Mouse brain Product Information tissue using CRMP1 Polyclonal Calculated MW 62kDa Antibody at dilution of 1:500 Buffer PBS with 0.05% sodium azide and 50% glycerol, PH7.4 Purify Affinity purification Dilution WB 1:500-1:1000 Elabscience Background Collapsin response mediator protein 1, encoded by the CRMP1 gene, is a human protein of the CRMP family. This gene encodes a member of a family of cytosolic phosphoproteins expressed exclusively in the nervous system. The encoded protein is thought to be a part of the semaphorin signal transduction pathway implicated in semaphorin-induced growth cone collapse during neural development. Alternative splicing results in multiple transcript variants. CRMP1 mediates reelin signaling in cortical neuronalElabscience migration. Mice deficient in CRMP1 exhibit impaired long-term potentiation and impaired spatial learning and memory. CRMP1 gene overlaps with another gene called EVC. CRMP1 has been shown to interact with DPYSL2. Elabscience For Research Use Only Focus on your research Thank you for your recent purchase. If you would like to learn more about antibodies,please visit www.elabscience.com. Service for life science Applications:WB-Western Blot IHC-Immunohistochemistry IF-Immunofluorescence IP-Immunoprecipitation FC-Flow cytometry ChIP- Chromatin Immunoprecipitation Reactivity: H-HumanElabscience R-Rat M-Mouse Mk-Monkey Dg-Dog Ch-Chicken Hm-Hamster Rb-Rabbit Sh- Sheep Pg-Pig Z-Zebrafish X-Xenopus C-Cow. Powered by TCPDF (www.tcpdf.org).

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Deregulated Gene Expression Pathways in Myelodysplastic Syndrome Hematopoietic Stem Cells
Leukemia (2010) 24, 756–764 & 2010 Macmillan Publishers Limited All rights reserved 0887-6924/10 $32.00 www.nature.com/leu ORIGINAL ARTICLE Deregulated gene expression pathways in myelodysplastic syndrome hematopoietic stem cells A Pellagatti1, M Cazzola2, A Giagounidis3, J Perry1, L Malcovati2, MG Della Porta2,MJa¨dersten4, S Killick5, A Verma6, CJ Norbury7, E Hellstro¨m-Lindberg4, JS Wainscoat1 and J Boultwood1 1LRF Molecular Haematology Unit, NDCLS, John Radcliffe Hospital, Oxford, UK; 2Department of Hematology Oncology, University of Pavia Medical School, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy; 3Medizinische Klinik II, St Johannes Hospital, Duisburg, Germany; 4Division of Hematology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; 5Department of Haematology, Royal Bournemouth Hospital, Bournemouth, UK; 6Albert Einstein College of Medicine, Bronx, NY, USA and 7Sir William Dunn School of Pathology, University of Oxford, Oxford, UK To gain insight into the molecular pathogenesis of the the World Health Organization.6,7 Patients with refractory myelodysplastic syndromes (MDS), we performed global gene anemia (RA) with or without ringed sideroblasts, according to expression profiling and pathway analysis on the hemato- poietic stem cells (HSC) of 183 MDS patients as compared with the the French–American–British classification, were subdivided HSC of 17 healthy controls. The most significantly deregulated based on the presence or absence of multilineage dysplasia. In pathways in MDS include interferon signaling, thrombopoietin addition, patients with RA with excess blasts (RAEB) were signaling and the Wnt pathways. Among the most signifi- subdivided into two categories, RAEB1 and RAEB2, based on the cantly deregulated gene pathways in early MDS are immuno- percentage of bone marrow blasts.
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Integrative Analysis Identifies Candidate Tumor Microenvironment and Intracellular Signaling Pathways That Define Tumor Heterogeneity in NF1
bioRxiv preprint doi: https://doi.org/10.1101/2020.01.13.904771; this version posted January 15, 2020. 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. Integrative analysis identifies candidate tumor microenvironment and intracellular signaling pathways that define tumor heterogeneity in NF1 Jineta Banerjee1#, Robert J Allaway1#, Jaclyn N Taroni2, Aaron Baker1,4, Xiaochun Zhang5, Chang In Moon5, Jaishri O Blakeley6, Justin Guinney1, Angela Hirbe5, Casey S Greene2,3, Sara JC Gosline1* 1 Computational Oncology, Sage Bionetworks, Seattle, WA, 98121 2 Childhood Cancer Data LaB, Alex's Lemonade Stand Foundation, Philadelphia, PA, 19102 3 Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104 4 University of Wisconsin-Madison, Madison, WI, 53715 5 Division of Oncology, Washington University Medical School, St. Louis, MO 63110 6 Neurology, Neurosurgery and Oncology, Johns Hopkins University, Baltimore, MD 21287 # Equal ContriBution * Correspondence: [email protected] Abstract: NeurofiBromatosis type 1 is a monogenic syndrome that gives rise to numerous symptoms including cognitive impairment, skeletal aBnormalities, and growth of Benign nerve sheath tumors. Nearly all NF1 patients develop cutaneous neurofiBromas (cNFs), which occur on the skin surface, while 40-60% of patients develop plexiform neurofibromas (pNFs) which are deeply embedded in the peripheral nerves. Patients with pNFs have a ~10% lifetime chance of these tumors Becoming malignant peripheral nerve sheath tumors (MPNSTs). These tumors have a severe prognosis and few treatment options other than surgery.
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Genome-Wide Analysis of Thyroid Hormone Receptors Shared and Specific Functions in Neural Cells
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249 A Di Domenico et al. Genetics and epigenetics 24:9 R315–R334 Review of NET Genetic and epigenetic drivers of neuroendocrine tumours (NET) Correspondence Annunziata Di Domenico1,2, Tabea Wiedmer1,2, Ilaria Marinoni1,* and Aurel Perren1,* should be addressed to I Marinoni or A Perren 1 Institute of Pathology, University of Bern, Bern, Switzerland Email 2 Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland ilaria.marinoni@pathology. *(I Marinoni and A Perren contributed equally to this work) unibe.ch or aurel.perren@ pathology.unibe.ch Abstract Neuroendocrine tumours (NET) of the gastrointestinal tract and the lung are a rare Key Words and heterogeneous group of tumours. The molecular characterization and the clinical f genetic classification of these tumours have been evolving slowly and show differences according f genomic to organs of origin. Novel technologies such as next-generation sequencing revealed new f epigenetic molecular aspects of NET over the last years. Notably, whole-exome/genome sequencing f pancreatic NET (WES/WGS) approaches underlined the very low mutation rate of well-differentiated f lung NET and small NET of all organs compared to other malignancies, while the engagement of epigenetic intestinal NET changes in driving NET evolution is emerging. Indeed, mutations in genes encoding f DNA methylation for proteins directly involved in chromatin remodelling, such as DAXX and ATRX are f chromatin a frequent event in NET. Epigenetic changes are reversible and targetable; therefore, f histone modification an attractive target for treatment. The discovery of the mechanisms underlying the epigenetic changes and the implication on gene and miRNA expression in the different Endocrine-Related Cancer Endocrine-Related subgroups of NET may represent a crucial change in the diagnosis of this disease, reveal new therapy targets and identify predictive markers.
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Published OnlineFirst November 10, 2009; DOI: 10.1158/0008-5472.CAN-09-1778 Cell, Tumor, and Stem Cell Biology Loss of Collapsin Response Mediator Protein1, as Detected by iTRAQ Analysis, Promotes Invasion of Human Gliomas Expressing Mutant EGFRvIII Joydeep Mukherjee,1 Leroi V. DeSouza,2 Johann Micallef,1 Zia Karim,1 Sid Croul,3 K.W. Michael Siu,2 and Abhijit Guha1,4 1Arthur and Sonia Labatts Brain Tumor Research Center, Hospital for Sick Children's Research Institute, University of Toronto, 2Department of Chemistry and Centre for Research in Mass Spectrometry, York University, 3Division of Neuropathology, Department of Pathology, Toronto Western Hospital, University of Toronto, and 4Division of Neurosurgery, Department of Surgery, Toronto Western Hospital, University of Toronto, Toronto, Canada Abstract cellular domain of the 180-kDa wtEGFR. This mutant EGFR, Δ – Glioblastoma multiforme (GBM) is the most common and le- termed EGFR, de2-7 EGFR, or most commonly EGFRvIII (4 7), ∼ thal primary human brain tumor. GBMs are characterized by results in a truncated 140-kDa constitutively activated EGFRvIII, a variety of genetic alterations, among which oncogenic muta- with an identical intracellular domain to wtEGFR (3, 4, 8). Preclin- tions of epidermal growth factor receptor (EGFRvIII) is most ical studies have shown that GBMs that harbor EGFRvIII have an in vitro in vivo common. GBMs harboring EGFRvIII have increased prolifera- and growth advantage, compared with GBMs that tion and invasive characteristics versus those expressing wild- just overexpress wtEGFR (9). Clinical studies suggest that the ∼ type (wt) EGFR. To identify the molecular basis of this 25% of all GBM patients whose tumors express both EGFRvIII increased tumorgenic phenotype, we used iTRAQ-labeling dif- and wtEGFR have a shorter interval to relapse and decreased sur- ferential proteomic analysis.
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Robles JTO Supplemental Digital Content 1
Supplementary Materials An Integrated Prognostic Classifier for Stage I Lung Adenocarcinoma based on mRNA, microRNA and DNA Methylation Biomarkers Ana I. Robles1, Eri Arai2, Ewy A. Mathé1, Hirokazu Okayama1, Aaron Schetter1, Derek Brown1, David Petersen3, Elise D. Bowman1, Rintaro Noro1, Judith A. Welsh1, Daniel C. Edelman3, Holly S. Stevenson3, Yonghong Wang3, Naoto Tsuchiya4, Takashi Kohno4, Vidar Skaug5, Steen Mollerup5, Aage Haugen5, Paul S. Meltzer3, Jun Yokota6, Yae Kanai2 and Curtis C. Harris1 Affiliations: 1Laboratory of Human Carcinogenesis, NCI-CCR, National Institutes of Health, Bethesda, MD 20892, USA. 2Division of Molecular Pathology, National Cancer Center Research Institute, Tokyo 104-0045, Japan. 3Genetics Branch, NCI-CCR, National Institutes of Health, Bethesda, MD 20892, USA. 4Division of Genome Biology, National Cancer Center Research Institute, Tokyo 104-0045, Japan. 5Department of Chemical and Biological Working Environment, National Institute of Occupational Health, NO-0033 Oslo, Norway. 6Genomics and Epigenomics of Cancer Prediction Program, Institute of Predictive and Personalized Medicine of Cancer (IMPPC), 08916 Badalona (Barcelona), Spain. List of Supplementary Materials Supplementary Materials and Methods Fig. S1. Hierarchical clustering of based on CpG sites differentially-methylated in Stage I ADC compared to non-tumor adjacent tissues. Fig. S2. Confirmatory pyrosequencing analysis of DNA methylation at the HOXA9 locus in Stage I ADC from a subset of the NCI microarray cohort. 1 Fig. S3. Methylation Beta-values for HOXA9 probe cg26521404 in Stage I ADC samples from Japan. Fig. S4. Kaplan-Meier analysis of HOXA9 promoter methylation in a published cohort of Stage I lung ADC (J Clin Oncol 2013;31(32):4140-7). Fig. S5. Kaplan-Meier analysis of a combined prognostic biomarker in Stage I lung ADC.
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Differentially Expressed Proteins in Glioblastoma Multiforme Identified
www.impactjournals.com/oncotarget/ Oncotarget, 2017, Vol. 8, (No. 27), pp: 44141-44158 Research Paper Differentially expressed proteins in glioblastoma multiforme identified with a nanobody-based anti-proteome approach and confirmed by OncoFinder as possible tumor-class predictive biomarker candidates Ivana Jovčevska1, Neja Zupanec1, Žiga Urlep2, Andrej Vranič3, Boštjan Matos4, Clara Limbaeck Stokin5, Serge Muyldermans6, Michael P. Myers7, Anton A. Buzdin8,9, Ivan Petrov10,11 and Radovan Komel1 1Medical Center for Molecular Biology, Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia 2Center for Functional Genomics and Bio-Chips, Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia 3Department of Neurosurgery, Foundation Rothschild, Paris, France 4Department of Neurosurgery, University Clinical Center, Ljubljana, Slovenia 5Institute of Histopathology, Charing Cross Hospital, London, United Kingdom 6Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium 7International Center for Genetic Engineering and Biotechnology, Trieste, Italy 8First Oncology Research and Advisory Center, Moscow, Russia 9National Research Center 'Kurchatov Institute', Center of Convergence of Nano-, Bio-, Information and Cognitive Sciences and Technologies, Moscow, Russia 10Center for Biogerontology and Regenerative Medicine, IC Skolkovo, Moscow, Russia 11Moscow Institute of Physics and Technology, Moscow, Russia Correspondence to: Radovan Komel, email: [email protected] Ivana Jovčevska, email: [email protected] Keywords: glioblastoma multiforme, biomarkers, nanobodies, cancer biology, OncoFinder Received: September 14, 2016 Accepted: April 10, 2017 Published: April 24, 2017 Copyright: Jovčevska et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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A Radiation Hybrid Map of Chicken Chromosome 4
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Underexpression of HOXA11 Is Associated with Treatment Resistance and Poor Prognosis in Glioblastoma
pISSN 1598-2998, eISSN 2005-9256 Cancer Res Treat. 2017;49(2):387-398 https://doi.org/10.4143/crt.2016.106 Original Article Open Access Underexpression of HOXA11 Is Associated with Treatment Resistance and Poor Prognosis in Glioblastoma Young-Bem Se, MD1 Purpose Seung Hyun Kim, MD2 Homeobox (HOX) genes are essential developmental regulators that should normally be in the silenced state in an adult brain. The aberrant expression of HOX genes has been asso- Ji Young Kim, MS1 ciated with the prognosis of many cancer types, including glioblastoma (GBM). This study PhD1 Ja Eun Kim, examined the identity and role of HOX genes affecting GBM prognosis and treatment 1 Yun-Sik Dho, MD resistance. Jin Wook Kim, MD, PhD1 Yong Hwy Kim, MD1 Materials and Methods The full series of HOX genes of five pairs of initial and recurrent human GBM samples were Hyun Goo Woo, MD, PhD3 screened by microarray analysis to determine the most plausible candidate responsible for MD, PhD4 Se-Hyuk Kim, GBM prognosis. Another 20 newly diagnosed GBM samples were used for prognostic vali- 5 Shin-Hyuk Kang, MD, PhD dation. In vitro experiments were performed to confirm the role of HOX in treatment resist- 6 Hak Jae Kim, MD, PhD ance. Mediators involved in HOX gene regulation were searched using differentially Tae Min Kim, MD, PhD7 expressed gene analysis, gene set enrichment tests, and network analysis. Soon-Tae Lee, MD, PhD8 Results MD, PhD9 Seung Hong Choi, The underexpression of HOXA11 was identified as a consistent signature for a poor prog- 10 Sung-Hye Park, MD, PhD nosis among the HOX genes.
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