DDT HEK293 Cell Transient Overexpression Lysate(Non-Denatured)

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DDT HEK293 Cell Transient Overexpression Lysate(Non-Denatured) Catalog # : L066T6 規格 : [ 100 ug ] List All Specification Application Image Transfected HEK293 Western Blot Cell Line: Immunoprecipitation Plasmid: pCMV-DDT full length Host: Human Theoretical MW 13 (kDa): Lysis Buffer: Modified RIPA Lysis Buffer:50 mM Tris-HCl pH 7.4, 150 mM NaCl, 1mM EDTA, 1% Triton X-100, 0.1% SDS, 1% Sodium deoxycholate, 1mM PMSF. Concentration: 2 mg/ml Quality Control Transient overexpression cell lysate was tested with Anti-DDT antibody Testing: () by Western Blots. SDS-PAGE Gel DDT transfected lysate Western Blot Lane 1: DDT transfected lysate ( 13 KDa). Lane 2: Non-transfected lysate. Recommend Use it directly for immuno-precipitation, or heat lysate with SDS gel Usage: loading buffer to 95°C for 5 minutes followed by rapid cooling for western blot application. If dissociating conditions are required, add reducing agent prior to heating. Page 1 of 2 2016/7/25 Storage Buffer: In modified RIPA Lysis Buffer. Storage Store at -80°C. Aliquot to avoid repeated freezing and thawing. Instruction: Applications Western Blot Immunoprecipitation Protocol Download Gene Information Entrez GeneID: 1652 GeneBank BC005971 Accession#: Protein AAH05971 Accession#: Gene Name: DDT Gene Alias: DDCT Gene D-dopachrome tautomerase Description: Omim ID: 602750 Gene Ontology: Hyperlink Gene Summary: D-dopachrome tautomerase converts D-dopachrome into 5,6- dihydroxyindole. The DDT gene is related to the migration inhibitory factor (MIF) in terms of sequence, enzyme activity, and gene structure. DDT and MIF are closely linked on chromosome 22. [provided by RefSeq Other D-dopachrome decarboxylase Designations: Related Disease Cardiovascular Diseases Diabetes Mellitus, Type 2 Edema 服務條款 | 隱私權政策 | 著作及商標 | 網站地圖 ©2016 亞諾法生技股份有限公司 Abnova Corporation. 版權所有. Page 2 of 2 2016/7/25.

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Research Article Human Environmental Disease Network: a Computational Model to Assess Toxicology of Contaminants1
ALTEX Online first published October 21, 2016 https://doi.org/10.14573/altex.1607201 Research Article Human Environmental Disease Network: A computational model to assess toxicology of contaminants1 Olivier Taboureau1,2,3and Karine Audouze1,2 1INSERM UMR-S973, Molécules Thérapeutiques in silico, Paris, France; 2 University of Paris Diderot, Paris, France; 3Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark Summary During the past decades, many epidemiological, toxicological and biological studies have been performed to assess the role of environmental chemicals as potential toxicants for diverse human disorders. However, the relationships between diseases based on chemical exposure have been rarely studied by computational biology. We developed a human environmental disease network (EDN) to explore and suggest novel disease-disease and chemical-disease relationships. The presented scored EDN model is built upon the integration on systems biology and chemical toxicology using chemical contaminants information and their disease relationships from the reported TDDB database. The resulting human EDN takes into consideration the level of evidence of the toxicant-disease relationships allowing including some degrees of significance in the disease-disease associations. Such network can be used to identify uncharacterized connections between diseases. Examples are discussed with type 2 diabetes (T2D). Additionally, this computational model allows to confirm already know chemical-disease links (e.g. bisphenol A and behavioral disorders) and also to reveal unexpected associations between chemicals and diseases (e.g. chlordane and olfactory alteration), thus predicting which chemicals may be risk factors to human health. With the proposed human EDN model, it is possible to explore common biological mechanism between two diseases through chemical exposure helping us to gain insight into disease etiology and comorbidity.
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University of Copenhagen, Copenhagen, Denmark
Human Environmental Disease Network A computational model to assess toxicology of contaminants Taboureau, Olivier; Audouze, Karine Published in: Altex DOI: 10.14573/altex.1607201 Publication date: 2017 Document version Publisher's PDF, also known as Version of record Document license: CC BY Citation for published version (APA): Taboureau, O., & Audouze, K. (2017). Human Environmental Disease Network: A computational model to assess toxicology of contaminants. Altex, 17(2), 289-300. https://doi.org/10.14573/altex.1607201 Download date: 01. Oct. 2021 Research Article Human Environmental Disease Network: A Computational Model to Assess Toxicology of Contaminants Olivier Taboureau 1,2,3 and Karine Audouze 1,2 1 INSERM UMR-S973, Molécules Thérapeutiques in silico, Paris, France; 2University of Paris Diderot, Paris, France; 3Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark Summary During the past decades, many epidemiological, toxicological and biological studies have been performed to assess the role of environmental chemicals as potential toxicants associated with diverse human disorders. However, the relationships between diseases based on chemical exposure rarely have been studied by computational biology. We developed a human environmental disease network (EDN) to explore and suggest novel disease-disease and chemical-disease relationships. The presented scored EDN model is built upon the integration of systems biology and chemical toxicology using information on chemical contaminants and their disease relationships reported in the TDDB database. The resulting human EDN takes into consideration the level of evidence of the toxicant-disease relationships, allowing inclusion of some degrees of significance in the disease-disease associations.
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