Monoclonal Antibody to TFE3

Total Page：16

File Type：pdf, Size：1020Kb

AM10141SU-N OriGene Technologies Inc. OriGene EU Acris Antibodies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-858-888-7900 Phone: +49-5221-34606-0 Fax: +1-858-888-7904 Fax: +49-5221-34606-11 [email protected] [email protected] Monoclonal Antibody to TFE3 - Supernatant Alternate names: Transcription factor E3 Catalog No.: AM10141SU-N Quantity: 1 ml Background: Xp11 translocation renal cell carcinomas (RCC) are a recently recognized subset of RCC, characterized by chromosome translocations involving the Xp11.2 break point and resulting in gene fusions involving the TFE3 transcription factor gene that maps to this locus. Xp11 translocation RCC represents the most common type of RCC in children. The most sensitive and specific immunohistochemical marker for the Xp11 translocation RCC is nuclear labeling of TFE3 protein, which reflects over-expression of the resulting fusion proteins relative to native TFE3. The hallmark of Alveolar soft part sarcoma (ASPS) is a chromosomal rearrangement at 17q25 and Xp11.2 engendering an ASPSCR1-TFE3 fusion gene responsible for an aberrant transcription factor presumably enabling pathogenesis. The presence of this 'super-activated' transcription factor may induce the expression of numerous molecules contributing to ASPS diagnosis, progression, and metastasis. Uniprot ID: P19532 NCBI: NP_000526 GeneID: 7030 Host / Isotype: Rabbit / IgG Clone: MRQ-37 Immunogen: TFE3 peptide. Format: State: Liquid purified Ig fraction with 0.2% BSA and 15mM Sodium Azide. Applications: Immunohistochemistry on Formalin-Fixed and Paraffin-Embedded Sections: 1/25-1/100 Pretreatment of deperaffinized tissue with heat-induced epitope retrieval is recommended. Use Polymer anti Mouse/Rabbit IgG as a detection system. Positive Control: Testis (germ cells) or Xp11 translocation renal cell carcinoma. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user. Specificity: Recognizes TFE3 Cellular Localization: Nuclear. Species Reactivity: Tested: Human. Storage: Store the antibody undiluted at 2-8°C. Shelf life: one year from despatch. For research and in vitro use only. Not for diagnostic or therapeutic work. RS/20150424 Material Safety Datasheets are available at www.acris-antibodies.com or on request. Acris Antibodies is now part of the OriGene family. Learn more at www.origene.com 1 / 2 AM10141SU-N: Monoclonal Antibody to TFE3 - Supernatant Pictures: Formalin-Fixed, Paraffin-Embedded Human renal cell carcinoma stained with TFE3 antibody Cat.-No. AM10141SU-N using peroxidase conjugate and DAB chromogen. Note nuclear staining of tumor cells. For research and in vitro use only. Not for diagnostic or therapeutic work. RS/20150424 Material Safety Datasheets are available at www.acris-antibodies.com or on request. Acris Antibodies is now part of the OriGene family. Learn more at www.origene.com 2 / 2 Powered by TCPDF (www.tcpdf.org).

Copy Link

Recommended publications

Molecular Cytogenetic Analysis for TFE3 Rearrangement In
Modern Pathology (2014) 27, 113–127 & 2014 USCAP, Inc. All rights reserved 0893-3952/14 $32.00 113 Molecular cytogenetic analysis for TFE3 rearrangement in Xp11.2 renal cell carcinoma and alveolar soft part sarcoma: validation and clinical experience with 75 cases Jennelle C Hodge, Kathryn E Pearce, Xiaoke Wang, Anne E Wiktor, Andre M Oliveira and Patricia T Greipp Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA Renal cell carcinoma with TFE3 rearrangement at Xp11.2 is a distinct subtype manifesting an indolent clinical course in children, with recent reports suggesting a more aggressive entity in adults. This subtype is morphologically heterogeneous and can be misclassified as clear cell or papillary renal cell carcinoma. TFE3 is also rearranged in alveolar soft part sarcoma. To aid in diagnosis, a break-apart strategy fluorescence in situ hybridization (FISH) probe set specific for TFE3 rearrangement and a reflex dual-color, single-fusion strategy probe set involving the most common TFE3 partner gene, ASPSCR1, were validated on formalin-fixed, paraffin- embedded tissues from nine alveolar soft part sarcoma, two suspected Xp11.2 renal cell carcinoma, and nine tumors in the differential diagnosis. The impact of tissue cut artifact was reduced through inclusion of a chromosome X centromere control probe. Analysis of the UOK-109 renal carcinoma cell line confirmed the break-apart TFE3 probe set can distinguish the subtle TFE3/NONO fusion-associated inversion of chromosome X. Subsequent extensive clinical experience was gained through analysis of 75 cases with an indication of Xp11.2 renal cell carcinoma (n ¼ 54), alveolar soft part sarcoma (n ¼ 13), perivascular epithelioid cell neoplasms (n ¼ 2), chordoma (n ¼ 1), or unspecified (n ¼ 5).
[Show full text]
Rap-3971 Alveolar Soft Part Sarcoma Chromosome
DATA SHEET Alveolar Soft Part Sarcoma Chromosome Region, Candidate 1 Human Item Number rAP-3971 Synonyms ASPCR1, ASPL, ASPS, RCC17, TUG, UBXD9, UBXN9, Tether containing UBX domain for GLUT4, Alveo- lar soft part sarcoma chromosomal region candidate gene 1 protein, Alveolar soft part sarcoma locus, Re- nal papillary cell carcinoma protein 17, UBX domain-containin Description ASPSCR1 Human Recombinant produced in E. coli is a single polypeptide chain containing 576 amino acids (1-553) and having a molecular mass of 62.6kDa. ASPSCR1 is fused to a 23 amino acid His-tag at N- terminus & purified by proprietary chromatographic techniques. Uniprot Accesion Number Q9BZE9 Amino Acid Sequence MGSSHHHHHH SSGLVPRGSH MGSMAAPAGG GGSAVSVLAP NGRRHTVKVT PSTVLLQVLE DTCRRQDFNP CEYDLKFQRS VLDLSLQWRF ANLPNNAKLE MVPASRSREG PENMVRIALQ LDDGS- RLQDS FCSGQTLWEL LSHFPQIREC LQHPGGATPV CVYTRDEVTG EAALRGTTLQ SLGLTGGSAT IRFVMKCYDP VGKTPGSLGS SASAGQAAAS APLPLESGEL SRGDLSRPED ADTSGPCCEH TQEKQSTRAP AAAPFVPFSG GGQRLGGPPG PTRPLTSSSA KLPKSLSSPG GPSKPKKSKS GQDPQQEQEQ ERERDPQQEQ ERERPVDREP VDREPVVCHP DLEERLQAWP AELPDEFFEL Source Escherichia Coli. Physical Appearance Sterile Filtered clear solution. Store at 4°C if entire vial will be used within 2-4 weeks. Store, frozen at -20°C and Stability for longer periods of time. For long term storage it is recommended to add a carrier protein (0.1% HSA or BSA).Avoid multiple freeze-thaw cycles. Formulation and Purity The ASPSCR1 solution (0.25mg/ml) contains 20mM Tris-HCl buffer (pH 8.0), 0.15M NaCl, 10% glycerol and 1mM DTT. Greater than 85% as determined by SDS-PAGE. Application Solubility Biological Activity Shipping Format and Condition Lyophilized powder at room temperature. Optimal dilutions should be determined by each laboratory for each application.
[Show full text]
The Orphan Disease Networks
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector ARTICLE The Orphan Disease Networks Minlu Zhang,1,3,5 Cheng Zhu,1,5 Alexis Jacomy,4 Long J. Lu,1,2,3 and Anil G. Jegga1,2,3,* The low prevalence rate of orphan diseases (OD) requires special combined efforts to improve diagnosis, prevention, and discovery of novel therapeutic strategies. To identify and investigate relationships based on shared genes or shared functional features, we have con- ducted a bioinformatic-based global analysis of all orphan diseases with known disease-causing mutant genes. Starting with a bipartite network of known OD and OD-causing mutant genes and using the human protein interactome, we first construct and topologically analyze three networks: the orphan disease network, the orphan disease-causing mutant gene network, and the orphan disease-causing mutant gene interactome. Our results demonstrate that in contrast to the common disease-causing mutant genes that are predomi- nantly nonessential, a majority of orphan disease-causing mutant genes are essential. In confirmation of this finding, we found that OD-causing mutant genes are topologically important in the protein interactome and are ubiquitously expressed. Additionally, func- tional enrichment analysis of those genes in which mutations cause ODs shows that a majority result in premature death or are lethal in the orthologous mouse gene knockout models. To address the limitations of traditional gene-based disease networks, we also construct and analyze OD networks on the basis of shared enriched features (biological processes, cellular components, pathways, phenotypes, and literature citations).
[Show full text]
Bioinformatics Analysis Based on Gene Expression Omnibus
ANTICANCER RESEARCH 39 : 1689-1698 (2019) doi:10.21873/anticanres.13274 Chemo-resistant Gastric Cancer Associated Gene Expression Signature: Bioinformatics Analysis Based on Gene Expression Omnibus JUN-BAO LIU 1* , TUNYU JIAN 2* , CHAO YUE 3, DAN CHEN 4, WEI CHEN 5, TING-TING BAO 6, HAI-XIA LIU 7, YUN CAO 8, WEI-BING LI 6, ZHIJIAN YANG 9, ROBERT M. HOFFMAN 9 and CHEN YU 6 1Traditional Chinese Medicine Department, People's Hospital of Henan Province, People's Hospital of Zhengzhou University, Zhengzhou, P.R. China; 2Institute of Botany, Jiangsu Province and Chinese Academy of Sciences, Nanjing, P.R. China; 3Department of general surgery, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, P.R. China; 4Research Center of Clinical Oncology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, P.R. China; 5Department of Head and Neck Surgery, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, P.R. China; 6Department of Integrated TCM & Western Medicine, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, P.R. China; 7Emergency Department, The Second Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, P.R. China; 8Master candidate of Oncology, Nanjing University of Chinese Medicine, Nanjing, P.R. China; 9AntiCancer, Inc., San Diego, CA, U.S.A. Abstract. Background/Aim: This study aimed to identify identified, including 13 up-regulated and 1,473 down-regulated biomarkers for predicting the prognosis of advanced gastric genes.
[Show full text]
Recombinant Human ASPSCR1 Protein Catalog Number: ATGP2165
Recombinant human ASPSCR1 protein Catalog Number: ATGP2165 PRODUCT INPORMATION Expression system E.coli Domain 1-553aa UniProt No. Q9BZE9 NCBI Accession No. NP_076988 Alternative Names Tether containing uBX domain for GLuT4 isoform 1, ASPCR1, ASPL, ASPS, RCC17, TuG, uBXD9, uBXN9 PRODUCT SPECIFICATION Molecular Weight 62.6 kDa (576aa) Concentration 0.25mg/ml (determined by Bradford assay) Formulation Liquid in. 20mM Tris-HCl buffer (pH 8.0) containing 0.15M NaCl, 10% glycerol, 1mM DTT Purity > 85% by SDS-PAGE Tag His-Tag Application SDS-PAGE Storage Condition Can be stored at +2C to +8C for 1 week. For long term storage, aliquot and store at -20C to -80C. Avoid repeated freezing and thawing cycles. BACKGROUND Description ASPSCR1 contains a uBX domain and interacts with glucose transporter type 4 (GLuT4). This protein is a tether, which sequesters the GLuT4 in intracellular vesicles in muscle and fat cells in the absence of insulin, and redistributes the GLuT4 to the plasma membrane within minutes of insulin stimulation. Translocation t (X;17) (p11;q25) of this gene with transcription factor TFE3 gene results in a ASPSCR1-TFE3 fusion protein in alveolar soft part sarcoma and in renal cell carcinomas. Recombinant human ASPSCR1 protein, fused to His-tag at N- terminus, was expressed in E. coli and purified by using conventional chromatography techniques. 1 Recombinant human ASPSCR1 protein Catalog Number: ATGP2165 Amino acid Sequence MGSSHHHHHH SSGLVPRGSH MGSMAAPAGG GGSAVSVLAP NGRRHTVKVT PSTVLLQVLE DTCRRQDFNP CEYDLKFQRS VLDLSLQWRF ANLPNNAKLE
[Show full text]
TUG/ASPSCR1 Rabbit Pab
Leader in Biomolecular Solutions for Life Science TUG/ASPSCR1 Rabbit pAb Catalog No.: A7481 Basic Information Background Catalog No. The protein encoded by this gene contains a UBX domain and interacts with glucose A7481 transporter type 4 (GLUT4). This protein is a tether, which sequesters the GLUT4 in intracellular vesicles in muscle and fat cells in the absence of insulin, and redistributes Observed MW the GLUT4 to the plasma membrane within minutes of insulin stimulation. Translocation 80kDa t(X;17)(p11;q25) of this gene with transcription factor TFE3 gene results in a ASPSCR1- TFE3 fusion protein in alveolar soft part sarcoma and in renal cell carcinomas. Multiple Calculated MW alternatively spliced transcript variants have been found. 37kDa/54kDa/60kDa/69kDa Category Primary antibody Applications WB, IHC, IF, IP Cross-Reactivity Human, Mouse, Rat Recommended Dilutions Immunogen Information WB 1:500 - 1:2000 Gene ID Swiss Prot 79058 Q9BZE9 IHC 1:50 - 1:200 Immunogen 1:50 - 1:200 IF Recombinant fusion protein containing a sequence corresponding to amino acids 284-553 of human TUG/ASPSCR1 (NP_076988.1). IP 1:50 - 1:100 Synonyms ASPSCR1;ASPCR1;ASPL;ASPS;RCC17;TUG;UBXD9;UBXN9 Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using TUG/ASPSCR1 antibody (A7481) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution. Lysates/proteins: 25ug per lane.
[Show full text]
Download Special Issue
BioMed Research International Novel Bioinformatics Approaches for Analysis of High-Throughput Biological Data Guest Editors: Julia Tzu-Ya Weng, Li-Ching Wu, Wen-Chi Chang, Tzu-Hao Chang, Tatsuya Akutsu, and Tzong-Yi Lee Novel Bioinformatics Approaches for Analysis of High-Throughput Biological Data BioMed Research International Novel Bioinformatics Approaches for Analysis of High-Throughput Biological Data Guest Editors: Julia Tzu-Ya Weng, Li-Ching Wu, Wen-Chi Chang, Tzu-Hao Chang, Tatsuya Akutsu, and Tzong-Yi Lee Copyright © 2014 Hindawi Publishing Corporation. All rights reserved. This is a special issue published in “BioMed Research International.” All articles are open access articles distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Contents Novel Bioinformatics Approaches for Analysis of High-Throughput Biological Data,JuliaTzu-YaWeng, Li-Ching Wu, Wen-Chi Chang, Tzu-Hao Chang, Tatsuya Akutsu, and Tzong-Yi Lee Volume2014,ArticleID814092,3pages Evolution of Network Biomarkers from Early to Late Stage Bladder Cancer Samples,Yung-HaoWong, Cheng-Wei Li, and Bor-Sen Chen Volume 2014, Article ID 159078, 23 pages MicroRNA Expression Profiling Altered by Variant Dosage of Radiation Exposure,Kuei-FangLee, Yi-Cheng Chen, Paul Wei-Che Hsu, Ingrid Y. Liu, and Lawrence Shih-Hsin Wu Volume2014,ArticleID456323,10pages EXIA2: Web Server of Accurate and Rapid Protein Catalytic Residue Prediction, Chih-Hao Lu, Chin-Sheng
[Show full text]
Inferring Synthetic Lethal Interactions from Mutual Exclusivity of Genetic Events in Cancer
Inferring synthetic lethal interactions from mutual exclusivity of genetic events in cancer Sriganesh Srihari 1, Jitin Singla 2, Limsoon Wong 3* and Mark A. Ragan 1* 1 Institute for Molecular Bioscience, The University of Queensland, St. Lucia, Queensland 4072, Australia 2 Department of Computer Science and Engineering, Indian Institute of Technology Roorkee, Uttarakhand 247667, India 3 Department of Computer Science, National University of Singapore, Singapore 117417, Singapore *Correspondence should be addressed to Mark A. Ragan: [email protected] | +61 07 3346 2616 or Limsoon Wong: [email protected] | +65 6516 2902. Abstract Background: Synthetic lethality (SL) refers to the genetic interaction between two or more genes where only their co-alteration ( e.g. by mutations, amplifications or deletions) results in cell death. In recent years, SL has emerged as an attractive therapeutic strategy against cancer: by targeting the SL partners of altered genes in cancer cells, these cells can be selectively killed while sparing the normal cells. Consequently, a number of studies have attempted prediction of SL interactions in human, a majority by extrapolating SL interactions inferred through large-scale screens in model organisms. However, these predicted SL interactions either do not hold in human cells or do not include genes that are (frequently) altered in human cancers, and are therefore not attractive in the context of cancer therapy. Results: Here, we develop a computational approach to infer SL interactions directly from frequently altered genes in human cancers. It is based on the observation that pairs of genes that are altered in a (significantly) mutually exclusive manner in cancers are likely to constitute lethal combinations.
[Show full text]
Dynamic Changes of Muscle Insulin Sensitivity After Metabolic Surgery
ARTICLE https://doi.org/10.1038/s41467-019-12081-0 OPEN Dynamic changes of muscle insulin sensitivity after metabolic surgery Soﬁya Gancheva1,2,3,11, Meriem Ouni 3,4,11, Tomas Jelenik2,3, Chrysi Koliaki1,2,3,5, Julia Szendroedi1,2,3, Frederico G.S. Toledo6, Daniel F. Markgraf 2,3, Dominik H. Pesta 2,3, Lucia Mastrototaro2,3, Elisabetta De Filippo2,3, Christian Herder 1,2,3, Markus Jähnert 3,4, Jürgen Weiss3,7, Klaus Strassburger 3,8, Matthias Schlensak9, Annette Schürmann 3,4,10,12 & Michael Roden 1,2,3,12 1234567890():,; The mechanisms underlying improved insulin sensitivity after surgically-induced weight loss are still unclear. We monitored skeletal muscle metabolism in obese individuals before and over 52 weeks after metabolic surgery. Initial weight loss occurs in parallel with a decrease in muscle oxidative capacity and respiratory control ratio. Persistent elevation of intramyocel- lular lipid intermediates, likely resulting from unrestrained adipose tissue lipolysis, accom- panies the lack of rapid changes in insulin sensitivity. Simultaneously, alterations in skeletal muscle expression of genes involved in calcium/lipid metabolism and mitochondrial function associate with subsequent distinct DNA methylation patterns at 52 weeks after surgery. Thus, initial unfavorable metabolic changes including insulin resistance of adipose tissue and skeletal muscle precede epigenetic modiﬁcations of genes involved in muscle energy metabolism and the long-term improvement of insulin sensitivity. 1 Division of Endocrinology and Diabetology, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany. 2 Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research, Heinrich Heine University, Düsseldorf, Germany. 3 German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany.
[Show full text]
1 Epidemiology and Genetics of Preserved Ratio Impaired Spirometry
medRxiv preprint doi: https://doi.org/10.1101/2020.10.14.20212613; this version posted October 20, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-ND 4.0 International license . Epidemiology and Genetics of Preserved Ratio Impaired SpiroMetry (PRISm): An Analysis of UK Biobank Daniel H Higbee MBBS1,2, Raquel Granell PhD1, George Davey Smith FRS1, James W Dodd MB ChB, PhD1,2 1 MRC Integrative Epidemiology Unit (IEU), University of Bristol, Oakfield Grove, Bristol, BS8 2BN, UK. 2 Academic Respiratory Unit, University of Bristol, Southmead Hospital, Bristol, BS10 5NB UK Corresponding Author: Dr James W. Dodd [email protected] Tel +44117 4142012 Fax +44117 4149496 ORCID 0000-00034805-5759 JD & DH conceived the study and initial draft, all authors made substantial contributions to the analysis, drafting and final approval of the paper. Funding: This work was supported by the Medical Research Council and the University of Bristol Integrative Epidemiology Unit (MC_UU_00011). MRC CARP Fellowship (Grant ref: MR/T005114/1) NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. 1 medRxiv preprint doi: https://doi.org/10.1101/2020.10.14.20212613; this version posted October 20, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
[Show full text]
TUG (ASPSCR1) (NM 024083) Human Recombinant Protein Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TP305817 TUG (ASPSCR1) (NM_024083) Human Recombinant Protein Product data: Product Type: Recombinant Proteins Description: Recombinant protein of human alveolar soft part sarcoma chromosome region, candidate 1 (ASPSCR1) Species: Human Expression Host: HEK293T Tag: C-Myc/DDK Predicted MW: 60 kDa Concentration: >50 ug/mL as determined by microplate BCA method Purity: > 80% as determined by SDS-PAGE and Coomassie blue staining Buffer: 25 mM Tris.HCl, pH 7.3, 100 mM glycine, 10% glycerol Preparation: Recombinant protein was captured through anti-DDK affinity column followed by conventional chromatography steps. Storage: Store at -80°C. Stability: Stable for 12 months from the date of receipt of the product under proper storage and handling conditions. Avoid repeated freeze-thaw cycles. RefSeq: NP_076988 Locus ID: 79058 UniProt ID: Q9BZE9 RefSeq Size: 1858 Cytogenetics: 17q25.3 RefSeq ORF: 1659 Synonyms: ASPCR1; ASPL; ASPS; RCC17; TUG; UBXD9; UBXN9 This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 2 TUG (ASPSCR1) (NM_024083) Human Recombinant Protein – TP305817 Summary: The protein encoded by this gene contains a UBX domain and interacts with glucose transporter type 4 (GLUT4). This protein is a tether, which sequesters the GLUT4 in intracellular vesicles in muscle and fat cells in the absence of insulin, and redistributes the GLUT4 to the plasma membrane within minutes of insulin stimulation.
[Show full text]
32-3257: ASPSCR1 Recombinant Protein Description Product Info
9853 Pacific Heights Blvd. Suite D. San Diego, CA 92121, USA Tel: 858-263-4982 Email: [email protected] 32-3257: ASPSCR1 Recombinant Protein ASPCR1,ASPL,ASPS,RCC17,TUG,UBXD9,UBXN9,Tether containing UBX domain for GLUT4,Alveolar soft Alternative part sarcoma chromosomal region candidate gene 1 protein,Alveolar soft part sarcoma locus,Renal papillary Name : cell carcinoma protein 17,UBX domain-cont Description Source : Escherichia Coli. ASPSCR1 Human Recombinant produced in E. coli is a single polypeptide chain containing 576 amino acids (1-553) and having a molecular mass of 62.6kDa. ASPSCR1 is fused to a 23 amino acid His-tag at N-terminus & purified by proprietary chromatographic techniques. Alveolar Soft Part Sarcoma Chromosome Region, Candidate 1 (ASPSCR1) contains a UBX domain and interacts with glucose transporter type 4 (GLUT4). ASPSCR1 is a tether, which sequesters the GLUT4 in intracellular vesicles in muscle and fat cells in the lack of insulin, and redistributes the GLUT4 to the plasma membrane right after insulin stimulation. Translocation t(X;17)(p11;q25) of this ASPSCR1 with transcription factor TFE3 gene ends with a ASPSCR1-TFE3 fusion protein in alveolar soft part sarcoma and in renal cell carcinomas. Product Info Amount : 10 µg Purification : Greater than 85% as determined by SDS-PAGE. The ASPSCR1 solution (0.25mg/ml) contains 20mM Tris-HCl buffer (pH 8.0), 0.15M NaCl, 10% Content : glycerol and 1mM DTT. Store at 4°C if entire vial will be used within 2-4 weeks. Store, frozen at -20°C for longer periods of Storage condition : time. For long term storage it is recommended to add a carrier protein (0.1% HSA or BSA).Avoid multiple freeze-thaw cycles.
[Show full text]