APOL3 Goat Polyclonal Antibody – TA305719 | Origene

Total Page：16

File Type：pdf, Size：1020Kb

APOL3 Goat Polyclonal Antibody – TA305719 | Origene

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 TA305719 APOL3 Goat Polyclonal Antibody Product data: Product Type: Primary Antibodies Applications: WB Recommended Dilution: WB: 1-3ug/ml. Reactivity: Human Host: Goat Isotype: IgG Clonality: Polyclonal Immunogen: Peptide with sequence ELTQIYQRLNPCHTH, from the C Terminus of the protein sequence according to NP_663615.1, NP_055164.1, NP_663616.1. Formulation: 0.5 mg/ml in Tris saline, 0.02% sodium azide, pH7.3 with 0.5% bovine serum albumin Concentration: lot specific Purification: Purified from goat serum by ammonium sulphate precipitation followed by antigen affinity chromatography using the immunizing peptide. Supplied at 0.5 mg/ml in Tris saline, 0.02% sodium azide, pH7.3 with 0.5% bovine serum albumin. Aliquot and store at -20C. Minimize freezing and thawing. Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Gene Name: apolipoprotein L3 Database Link: NP_055164 Entrez Gene 80833 Human O95236 Background: This gene is a member of the apolipoprotein L gene family. The encoded protein is found in the cytoplasm, where it may affect the movement of lipids or allow the binding of lipids to organelles. In addition, expression of this gene is upregulated by tumor necrosis factor-alpha in endothelial cells lining the normal and atherosclerotic iliac artery and aorta. Six transcript variants encoding three different isoforms have been found for this gene. 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 APOL3 Goat Polyclonal Antibody – TA305719 Synonyms: 3; APOLIII; apolipoprotein L; apolipoprotein L-III; apolipoprotein L3; CG12-1; OTTHUMP00000028913; TNF-inducible protein CG12-1 Product images: TA305719 (1ug/ml) staining of DAUDI lysate (35ug protein in RIPA buffer). Primary incubation was 1 hour. Detected by chemiluminescence. This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 2 / 2.

Copy Link

Recommended publications

The Expression of the Human Apolipoprotein Genes and Their Regulation by Ppars
CORE Metadata, citation and similar papers at core.ac.uk Provided by UEF Electronic Publications The expression of the human apolipoprotein genes and their regulation by PPARs Juuso Uski M.Sc. Thesis Biochemistry Department of Biosciences University of Kuopio June 2008 Abstract The expression of the human apolipoprotein genes and their regulation by PPARs. UNIVERSITY OF KUOPIO, the Faculty of Natural and Environmental Sciences, Curriculum of Biochemistry USKI Juuso Oskari Thesis for Master of Science degree Supervisors Prof. Carsten Carlberg, Ph.D. Merja Heinäniemi, Ph.D. June 2008 Keywords: nuclear receptors; peroxisome proliferator-activated receptor; PPAR response element; apolipoprotein; lipid metabolism; high density lipoprotein; low density lipoprotein. Lipids are any fat-soluble, naturally-occurring molecules and one of their main biological functions is energy storage. Lipoproteins carry hydrophobic lipids in the water and salt-based blood environment for processing and energy supply in liver and other organs. In this study, the genomic area around the apolipoprotein genes was scanned in silico for PPAR response elements (PPREs) using the in vitro data-based computer program. Several new putative REs were found in surroundings of multiple lipoprotein genes. The responsiveness of those apolipoprotein genes to the PPAR ligands GW501516, rosiglitazone and GW7647 in the HepG2, HEK293 and THP-1 cell lines were tested with real-time PCR. The APOA1, APOA2, APOB, APOD, APOE, APOF, APOL1, APOL3, APOL5 and APOL6 genes were found to be regulated by PPARs in direct or secondary manners. Those results provide new insights in the understanding of lipid metabolism and so many lifestyle diseases like atherosclerosis, type 2 diabetes, heart disease and stroke.
[Show full text]
JUN-Mediated Downregulation of EGFR Signaling Is Associated With
Published OnlineFirst May 31, 2017; DOI: 10.1158/1535-7163.MCT-16-0564 Cancer Biology and Signal Transduction Molecular Cancer Therapeutics JUN-Mediated Downregulation of EGFR Signaling Is Associated with Resistance to Gefitinib in EGFR- mutant NSCLC Cell Lines Kian Kani1,2, Carolina Garri1, Katrin Tiemann1, Paymaneh D. Malihi1, Vasu Punj3, Anthony L. Nguyen1, Janet Lee1, Lindsey D. Hughes1, Ruth M. Alvarez1, Damien M. Wood1, Ah Young Joo1, Jonathan E. Katz1, David B. Agus1,2, and Parag Mallick1,4 Abstract Mutations or deletions in exons 18–21 in the EGFR)are HCC827 cells increased gefitinib IC50 from 49 nmol/L to 8 present in approximately 15% of tumors in patients with non– mmol/L (P < 0.001). Downregulation of JUN expression small cell lung cancer (NSCLC). They lead to activation of the through shRNA resensitized HCC827 cells to gefitinib (IC50 EGFR kinase domain and sensitivity to molecularly targeted from 49 nmol/L to 2 nmol/L; P < 0.01). Inhibitors targeting therapeutics aimed at this domain (gefitinib or erlotinib). JUNwere3-foldmoreeffectiveinthegefitinib-resistant cells These drugs have demonstrated objective clinical response in than in the parental cell line (P < 0.01). Analysis of gene many of these patients; however, invariably, all patients acquire expression in patient tumors with EGFR-activating mutations resistance. To examine the molecular origins of resistance, we and poor response to erlotinib revealed a similar pattern as the derivedasetofgefitinib-resistant cells by exposing lung ade- top 260 differentially expressed genes in the gefitinib-resistant nocarcinoma cell line, HCC827, with an activating mutation in cells (Spearman correlation coefficient of 0.78, P < 0.01).
[Show full text]
APOL3 (NM 030644) Human Tagged ORF Clone – RC218012L4 | Origene
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 RC218012L4 APOL3 (NM_030644) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: APOL3 (NM_030644) Human Tagged ORF Clone Tag: mGFP Symbol: APOL3 Synonyms: apoL-III; APOLIII; CG12_1; CG121 Vector: pLenti-C-mGFP-P2A-Puro (PS100093) E. coli Selection: Chloramphenicol (34 ug/mL) Cell Selection: Puromycin ORF Nucleotide The ORF insert of this clone is exactly the same as(RC218012). Sequence: Restriction Sites: SgfI-MluI Cloning Scheme: ACCN: NM_030644 ORF Size: 993 bp 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 APOL3 (NM_030644) Human Tagged ORF Clone – RC218012L4 OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. RefSeq: NM_030644.1 RefSeq Size: 2328 bp RefSeq ORF: 996 bp Locus ID: 80833 UniProt ID: O95236, A0A024R1G6 MW: 36.4 kDa Gene Summary: This gene is a member of the apolipoprotein L gene family, and it is present in a cluster with other family members on chromosome 22.
[Show full text]
The Apolipoprotein L Gene Cluster Has Emerged Recently in Evolution and Is Expressed in Human Vascular Tissue
doi:10.1006/geno.2002.6729, available online at http://www.idealibrary.com on IDEAL Article The Apolipoprotein L Gene Cluster Has Emerged Recently in Evolution and Is Expressed in Human Vascular Tissue Houshang Monajemi, Ruud D. Fontijn, Hans Pannekoek, and Anton J. G. Horrevoets* Department of Biochemistry of the Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands 1105 AZ *To whom correspondence and reprint requests should be addressed. Fax: (31) 20-6915519. E-mail: [email protected]. We previously isolated APOL3 (CG12-1) cDNA and now describe the isolation of APOL1 and APOL2 cDNA from an activated endothelial cell cDNA library and show their endothelial- specific expression in human vascular tissue. APOL1–APOL4 are clustered on human chro- mosome 22q13.1, as a result of tandem gene duplication, and were detected only in primates (humans and African green monkeys) and not in dogs, pigs, or rodents, showing that this gene cluster has arisen recently in evolution. The specific tissue distribution and gene organiza- tion suggest that these genes have diverged rapidly after duplication. This has resulted in the emergence of an additional signal peptide encoding exon that ensures secretion of the plasma high-density lipoprotein-associated APOL1. Our results show that the APOL1–APOL4 clus- ter might contribute to the substantial differences in the lipid metabolism of humans and mice, as dictated by the variable expression of genes involved in this process. Key Words: apolipoprotein L, gene cluster, duplication, evolution, endothelial cells, atherosclerosis, vascular wall, mouse lipid metabolism INTRODUCTION on chromosome 22, consisting of APOL1–APOL6 [6,7].
[Show full text]
Common Homozygosity for Predicted Loss-Of-Function Variants Reveals Both Redundant and Advantageous Effects of Dispensable Human Genes
Common homozygosity for predicted loss-of-function variants reveals both redundant and advantageous effects of dispensable human genes Antonio Rausella,b,1,2, Yufei Luoa,b,1, Marie Lopezc, Yoann Seeleuthnerb,d, Franck Rapaporte, Antoine Faviera,b, Peter D. Stensonf, David N. Cooperf, Etienne Patinc, Jean-Laurent Casanovab,d,e,g,h,2, Lluis Quintana-Murcic,i, and Laurent Abelb,d,e,2 aClinical Bioinformatics Laboratory, INSERM UMR1163, Necker Hospital for Sick Children, 75015 Paris, France; bUniversity of Paris, Imagine Institute, 75015 Paris, France; cHuman Evolutionary Genetics Unit, Institut Pasteur, UMR2000, CNRS, Paris 75015, France; dLaboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR1163, Necker Hospital for Sick Children, 75015 Paris, France; eSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065; fInstitute of Medical Genetics, School of Medicine, Cardiff University, CF14 4XN Cardiff, United Kingdom; gHoward Hughes Medical Institute, New York, NY 10065; hPediatric Hematology and Immunology Unit, Necker Hospital for Sick Children, 75015 Paris, France; and iHuman Genomics and Evolution, Collège de France, Paris 75005, France Contributed by Jean-Laurent Casanova, January 10, 2020 (sent for review October 24, 2019; reviewed by Philippe Froguel, John M. Greally, and Lennart Hammarström). Humans homozygous or hemizygous for variants predicted to in-frame insertions−deletions (indels), missense variants, splice cause a loss of function (LoF) of the corresponding protein do not region variants not affecting the essential splice regions, and even necessarily present with overt clinical phenotypes. We report here synonymous or deep intronic mutations, that may actually be LoF 190 autosomal genes with 207 predicted LoF variants, for which but cannot be systematically identified as such in silico.
[Show full text]
The Mechanism of Kidney Disease Due to APOL1 Risk Variants
PERSPECTIVE www.jasn.org The Mechanism of Kidney Disease Due to APOL1 Risk Variants Etienne Pays Laboratory of Molecular Parasitology, IBMM, Université Libre de Bruxelles, Gosselies, Belgium JASN 31: 2502–2505, 2020. doi: https://doi.org/10.1681/ASN.2020070954 The apoL1 C-terminal variants G1 and PI4KB, because autophagy and mito- induced by the viral mimetic poly(I:C) G2 are linked to CKD.1 Expression of chondrial fission are dependent on the is linked to apoL1 involvement in these variants induces effacement of po- transfer of PI4KB-containing vesicles apoptosis.2,5 It is tempting to propose docyte foot processes, leading to the loss carrying the autophagy marker ATG9A that, as occurs for apoptotic Bcl2 of these cells from glomeruli and impair- from the Golgi to the endoplasmic retic- proteins,9 apoL oligomerization re- ment of the blood filtration activity of ulum (ER).4,6,7 sulting from high protein expression the kidney. A characteristic of G1/G2- Thus, podocyte dysfunctions could triggers the formation of mitochon- linked disease is the strong association result from interference of apoL1 G1/ drial megapores.10 As occurs for Bcl2 of glomerular pathology with the type I G2 variants with PI4KB activity. This homologous antagonist killer (Bak) IFN inflammatory response, such as oc- conclusion differs from that of many or Bcl2–associated X (Bax), hydro- curs with viral infection.1 studies, which have concluded that G1 phobic residues exposed on apoL1 he- In podocytes, either truncation of the and G2 induce nonspecificcytotoxicity.1 lices
[Show full text]
Downloadable Synaptic Protein Database
bioRxiv preprint doi: https://doi.org/10.1101/643783; this version posted May 25, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Title Page Title Dynamics of murine brain protein synthesis in vivo identify the hippocampus, cortex and cerebellum as highly active metabolic sites Authors Names and Affiliations: Ser Sue Ng1, Jung Eun Park1, Wei Meng1, Christopher Li-Hsian Chen2,3, Raj N. Kalaria4, Neil E. McCarthy5, Siu Kwan Sze1,* 1School of Biological Science, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore. 2Memory, Aging and Cognition Centre, National University Health System, Singapore. 3Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. 4Institute of Neuroscience, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, United Kingdom, NE4 5PL. 5Centre for Immunobiology, The Blizard Institute, Bart's and The London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom. *Corresponding author Corresponding author email address: [email protected] Special note: Due to the large file size and excel file format is not accepted by Biorxiv submission system, all the Tables (except Table1) in this manuscript have submitted as supplementary. bioRxiv preprint doi: https://doi.org/10.1101/643783; this version posted May 25, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Abstract Identification of proteins that are synthesized de novo in response to specific microenvironmental cues is critical to understanding the molecular mechanisms that underpin key physiological processes and pathologies.
[Show full text]
Transcriptional Profile of Human Anti-Inflamatory Macrophages Under Homeostatic, Activating and Pathological Conditions
UNIVERSIDAD COMPLUTENSE DE MADRID FACULTAD DE CIENCIAS QUÍMICAS Departamento de Bioquímica y Biología Molecular I TESIS DOCTORAL Transcriptional profile of human anti-inflamatory macrophages under homeostatic, activating and pathological conditions Perfil transcripcional de macrófagos antiinflamatorios humanos en condiciones de homeostasis, activación y patológicas MEMORIA PARA OPTAR AL GRADO DE DOCTOR PRESENTADA POR Víctor Delgado Cuevas Directores María Marta Escribese Alonso Ángel Luís Corbí López Madrid, 2017 © Víctor Delgado Cuevas, 2016 Universidad Complutense de Madrid Facultad de Ciencias Químicas Dpto. de Bioquímica y Biología Molecular I TRANSCRIPTIONAL PROFILE OF HUMAN ANTI-INFLAMMATORY MACROPHAGES UNDER HOMEOSTATIC, ACTIVATING AND PATHOLOGICAL CONDITIONS Perfil transcripcional de macrófagos antiinflamatorios humanos en condiciones de homeostasis, activación y patológicas. Víctor Delgado Cuevas Tesis Doctoral Madrid 2016 Universidad Complutense de Madrid Facultad de Ciencias Químicas Dpto. de Bioquímica y Biología Molecular I TRANSCRIPTIONAL PROFILE OF HUMAN ANTI-INFLAMMATORY MACROPHAGES UNDER HOMEOSTATIC, ACTIVATING AND PATHOLOGICAL CONDITIONS Perfil transcripcional de macrófagos antiinflamatorios humanos en condiciones de homeostasis, activación y patológicas. Este trabajo ha sido realizado por Víctor Delgado Cuevas para optar al grado de Doctor en el Centro de Investigaciones Biológicas de Madrid (CSIC), bajo la dirección de la Dra. María Marta Escribese Alonso y el Dr. Ángel Luís Corbí López Fdo. Dra. María Marta Escribese
[Show full text]
Table S1. 103 Ferroptosis-Related Genes Retrieved from the Genecards
Table S1. 103 ferroptosis-related genes retrieved from the GeneCards. Gene Symbol Description Category GPX4 Glutathione Peroxidase 4 Protein Coding AIFM2 Apoptosis Inducing Factor Mitochondria Associated 2 Protein Coding TP53 Tumor Protein P53 Protein Coding ACSL4 Acyl-CoA Synthetase Long Chain Family Member 4 Protein Coding SLC7A11 Solute Carrier Family 7 Member 11 Protein Coding VDAC2 Voltage Dependent Anion Channel 2 Protein Coding VDAC3 Voltage Dependent Anion Channel 3 Protein Coding ATG5 Autophagy Related 5 Protein Coding ATG7 Autophagy Related 7 Protein Coding NCOA4 Nuclear Receptor Coactivator 4 Protein Coding HMOX1 Heme Oxygenase 1 Protein Coding SLC3A2 Solute Carrier Family 3 Member 2 Protein Coding ALOX15 Arachidonate 15-Lipoxygenase Protein Coding BECN1 Beclin 1 Protein Coding PRKAA1 Protein Kinase AMP-Activated Catalytic Subunit Alpha 1 Protein Coding SAT1 Spermidine/Spermine N1-Acetyltransferase 1 Protein Coding NF2 Neurofibromin 2 Protein Coding YAP1 Yes1 Associated Transcriptional Regulator Protein Coding FTH1 Ferritin Heavy Chain 1 Protein Coding TF Transferrin Protein Coding TFRC Transferrin Receptor Protein Coding FTL Ferritin Light Chain Protein Coding CYBB Cytochrome B-245 Beta Chain Protein Coding GSS Glutathione Synthetase Protein Coding CP Ceruloplasmin Protein Coding PRNP Prion Protein Protein Coding SLC11A2 Solute Carrier Family 11 Member 2 Protein Coding SLC40A1 Solute Carrier Family 40 Member 1 Protein Coding STEAP3 STEAP3 Metalloreductase Protein Coding ACSL1 Acyl-CoA Synthetase Long Chain Family Member 1 Protein
[Show full text]
Impact of AHR Ligand TCDD on Human Embryonic Stem Cells and Early Differentiation
International Journal of Molecular Sciences Article Impact of AHR Ligand TCDD on Human Embryonic Stem Cells and Early Differentiation Indrek Teino 1,* , Antti Matvere 1 , Martin Pook 1, Inge Varik 1, Laura Pajusaar 1, 1 1 1 1 2,3, Keyt Uudeküll , Helen Vaher , Annika Trei , Arnold Kristjuhan ,Tõnis Org y 1, and Toivo Maimets y 1 Chair of Cell Biology, Institute of Molecular and Cell Biology, University of Tartu, Riia 23, 51010 Tartu, Estonia; [email protected] (A.M.); [email protected] (M.P.); [email protected] (I.V.); [email protected] (L.P.); [email protected] (K.U.); [email protected] (H.V.); [email protected] (A.T.); [email protected] (A.K.); [email protected] (T.M.) 2 Chair of Biotechnology, Institute of Molecular and Cell Biology, University of Tartu, Riia 23, 51010 Tartu, Estonia; [email protected] 3 Institute of Genomics, University of Tartu, Riia 23b, 51010 Tartu, Estonia * Correspondence: [email protected]; Tel.: +372-737-5023 These authors contributed equally. y Received: 6 November 2020; Accepted: 26 November 2020; Published: 28 November 2020 Abstract: Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor, which mediates the effects of a variety of environmental stimuli in multiple tissues. Recent advances in AHR biology have underlined its importance in cells with high developmental potency, including pluripotent stem cells. Nonetheless, there is little data on AHR expression and its role during the initial stages of stem cell differentiation. The purpose of this study was to investigate the temporal pattern of AHR expression during directed differentiation of human embryonic stem cells (hESC) into neural progenitor, early mesoderm and definitive endoderm cells.
[Show full text]
Supplementary Table I
Supplementary Table I TNF-inducible genes (360) identified by the microarrays are listed. These genes were identified by the formula M+T/M+M ≥2, and shown is the log2 induction (mean±SD). The Table contains the gene (alphabetical order), the systematic name, and the probe name. Gene Systematic Name Probe Name log2 induction (mean±SD) 7A5 NM_182762 A_32_P131031 3,06 ± 0,68 ABTB2 NM_145804 A_23_P356616 2,65 ± 0,53 ACSL1 NM_001995 A_23_P110212 2,95 ± 0,36 ACSL5 NM_203380 A_24_P201360 1,97 ± 0,61 ACVR2A NM_001616 A_23_P153930 2,80 ± 0,20 ADA NM_000022 A_23_P210482 1,63 ± 0,30 ADM NM_001124 A_23_P127948 3,15 ± 0,31 ADORA2A NM_000675 A_23_P109436 3,89 ± 0,22 AK3L1 NM_001005353 A_32_P108655 3,81 ± 1,22 AK3L2 NM_001002921 A_23_P200524 3,27 ± 1,40 ALS2CR4 NM_152388 A_23_P370097 1,69 ± 0,40 AMPD3 NM_000480 A_23_P116286 1,77 ± 0,32 AMZ1 NM_133463 A_24_P383649 3,08 ± 0,64 ANKRD15 NM_153186 A_32_P64570 4,34 ± 0,48 ANKRD22 NM_144590 A_23_P161428 1,56 ± 0,65 APOL3 NM_145641 A_24_P416997 2,36 ± 0,69 AQP9 NM_020980 A_23_P106362 2,84 ± 0,94 AREG NM_001657 A_23_P259071 2,62 ± 0,63 ARHGAP20 NM_020809 A_23_P422933 1,69 ± 0,44 ARHGEF7 NM_145735 A_23_P417891 2,01 ± 0,41 ARL5B NM_178815 A_23_P378588 3,64 ± 0,73 ARNTL2 NM_020183 A_23_P53345 2,07 ± 0,40 ARRDC3 NM_020801 A_24_P274615 1,84 ± 0,38 ARRDC4 NM_183376 A_23_P339818 1,89 ± 0,25 ATF5 NM_012068 A_23_P119337 1,66 ± 0,28 ATP2B1 NM_001682 A_23_P128319 2,36 ± 0,20 AXUD1 NM_033027 A_23_P121011 2,03 ± 0,46 B4GALT1 NM_001497 A_24_P103803 2,04 ± 0,20 B4GALT5 NM_004776 A_24_P239731 2,10 ± 0,60 BAZ1A NM_013448 A_23_P76799
[Show full text]
APOL3 (NM 145641) 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 TP761559 APOL3 (NM_145641) Human Recombinant Protein Product data: Product Type: Recombinant Proteins Description: Purified recombinant protein of Human apolipoprotein L, 3 (APOL3), transcript variant beta/a, full length, with N-terminal GST and C-terminal HIS tag, expressed in E. coli, 50ug Species: Human Expression Host: E. coli Tag: N-GST and C-His Predicted MW: 49.4 kDa Concentration: >50 ug/mL as determined by microplate BCA method Purity: > 80% as determined by SDS-PAGE and Coomassie blue staining Buffer: 25mM Tris, pH8.0,150mM NaCl,10% glycerol,1%Sarkosyl. 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_663616 Locus ID: 80833 UniProt ID: O95236 RefSeq Size: 3627 Cytogenetics: 22q12.3 RefSeq ORF: 606 Synonyms: apoL-III; APOLIII; CG12_1; CG121 Summary: This gene is a member of the apolipoprotein L gene family, and it is present in a cluster with other family members on chromosome 22. The encoded protein is found in the cytoplasm, where it may affect the movement of lipids, including cholesterol, and/or allow the binding of lipids to organelles. In addition, expression of this gene is up-regulated by tumor necrosis factor-alpha in endothelial cells lining the normal and atherosclerotic iliac artery and aorta. Alternative splicing results in multiple transcript variants.
[Show full text]