Contact Us / Request a Quote Download Manuals
Advanced Cell Diagnostics Advanced Cell Diagnostics

Search form

Please sign in
  • Log In
  • Register
  • How to Order
  • What to Buy
0 My Cart
X

You have no items in your shopping cart.

Menu
X
  • Products +
    RNAscope™/BaseScope™/ miRNAscope™
    +
    • Assay Selection Guide
    Target Probes
    +
    • All About Probes
    • Catalog Probes
    • Probe Sets
    • New Probe Request
    Manual Assays
    +
    RNAscope™ Chromogenic
    • Overview
    • RNAscope™ 2.5 HD Assay-Brown
    • RNAscope™ 2.5 HD Assay-Red
    • RNAscope™ 2.5 HD Duplex Assay
    RNAscope™ Multiplex Fluorescent
    • Overview
    • RNAscope™ HiPlex v2 Assay
    • RNAscope™ Multiplex Fluorescent V2
    BaseScope™
    • Overview
    • BaseScope™ Assay Red
    • BaseScope™ Duplex Assay
    miRNAscope™
    • Overview
    • miRNAscope™ Assay red
    • RNAscope™ Plus smRNA-RNA Assay
    DNAscope™
    • Overview
    • DNAscope™ Duplex Assay
    Automated Assays
    +
    For Lunaphore COMET™
    • RNAscope™ HiPlex Pro for COMET™
    For Leica systems
    • Overview
    • RNAscope™ 2.5 LS Assay-Brown
    • RNAscope™ 2.5 LS Assay-Red
    • RNAscope™ 2.5 LS Duplex Assay
    • RNAscope™ Multiomic LS Assay
    • RNAscope™ 2.5 LS Fluorescent Multiplex Assay
    • RNAscope™ 2.5 LSx Reagent Kit-BROWN
    • RNAscope™ 2.5 LSx Reagent Kit-RED
    • BaseScope™ LS Reagent Kit – RED
    • miRNAscope LS Reagent Kit Red
    • RNAscope™ Plus smRNA-RNA LS Assay
    Roche DISCOVERY ULTRA system
    • Overview
    • RNAscope™ VS Universal HRP
    • RNAscope™ VS Universal AP
    • RNAscope™ VS Duplex Assay
    • BaseScope™ VS Reagent Kit – RED
    RNA-Protein Co-Detection Assay
    +
    • RNAscope HiPlex-IMC™ Co-Detection
    • Integrated Codetection Assay
    • Sequential RNA Protein Detection
    Software
    +
    • Overview
    • Aperio RNA ISH Algorithm
    • HALO® image analysis platform
    Controls & Accessories
    +
    • RNAscope™
    • BaseScope™
    • miRNAscope™
    • Accessories
    How to Order
    +
    • Ordering Instructions
    • What to Buy
  • Services +
    Professional Assay Services
    +
    • Our Services
    • Multiomic Services
    • Biomarker Assay Development
    • Cell & Gene Therapy Services
    • Clinical Assay Development
    • Tissue Bank & Sample Procurement
    • Image Analysis
    Benefits
    +
    • Your Benefits
    • Certified Providers
    How to Order
    +
    • Ordering Process
    • Contact Services
  • Areas of Research +
    Most Popular
    +
    • COVID-19 Coronavirus
    • Single Cell Analysis
    • Whole-Mount
    • Anatomic Pathology Panels
    • Neuroscience
    • Inflammation
    • Gene Therapy/AAV
    • Stem Cell
    • Immuno-oncology
    • Liver Research
    • Cardiovascular & Skeletal Muscle Research
    Cell & Gene Therapy
    +
    • Gene Therapy
    • Gene Therapy/AAV
    • siRNA/ASO
    • Cell Therapy
    Cancer
    +
    • Breast Cancer
    • EGFRvIII Splice Variant
    • HPV Related Cancer
    • Immuno-oncology
    • Lung Cancer
    • PDx
    • Prostate Cancer
    • Point Mutation
    • CDR3 for TCR
    Viral
    +
    • COVID-19 Coronavirus
    • HIV & SIV
    • Infectious Disease
    • Zika Virus
    Pathways
    +
    • AKT
    • JAK STAT
    • WNT B-Catenin
    Neuroscience
    +
    Neuroscience
    • Neural Development
    • Neuronal Cell Types
    • Learning and Memory
    • G-protein-coupled Receptors & Ion Channels
    • Post-mortem Brain Tissue
    Other
    +
    • Circular RNA
    • Gene Fusions
    • HT Transcript Validation
    • Long Non-coding RNA
    • RNAseq Validation
    • Single Cell Analysis
    • Splice Variant
    • miRNA
    RNA & Protein
    +
    • Antibody Challenges
    • Dual ISH + IHC Methods
    • No Antibodies
    • RNA & Protein Analysis
    Customer Innovations
    +
    • Dual RNA+DNA ISH
    • Very old FFPE ISH
    • Wholemount ISH
    Animal Models
    +
    • Any Species
    • Mouse Model
    • Preclincal Safety
  • Technology +
    Overview
    +
    • How it Works
    • Data Image Gallery
    • Technology Video
    • Webinars
    RNA Detection
    +
    • Why RNA?
    • RNA ISH and IHC
    Pretreatment Options
    +
    • RNAscope™ Pretreatment
    • PretreatPro™
    Spotlights
    +
    • Researchers Spotlights
    • RNA & DNA
    • WISH
    • FFPE
    • Testimonials
    Publications, Guides & Posters
    +
    • Search publications
    • RNAscope™ Reference Guide
    • RNAscope™ Data Analysis Guide
    • Download RNAscope™ Posters
  • Support +
    Overview
    +
    • Get Started
    • How to Order
    • Distributors
    • Contact Support
    Troubleshooting
    +
    • Troubleshooting Guide
    • FAQs
    • User Manuals, SDS and Product Inserts
    • Documents and Downloads
    Imaging Resource
    +
    • Image Analysis
    • Image Registration Software
    • QuPath
    • HALO® image analysis platform
    Learn More
    +
    • Webinars
    • Training Videos
  • Partners +
    Partners
    +
    • Overview
    Partners Directory
    +
    Automation Partners
    • Leica Biosystem
    • Roche Diagnostics
    Workflow Partners
    • NanoString
    Software Partners
    • indica labs
    Become a Partner
    +
    • Learn How
  • Diagnostics +
    Diagnostics
    +
    • Diagnostics
    • Literature
    • Diagnostics ASR Probes
    • Diagnostics CE-IVD Probes
    • Diagnostics CE-IVD Detection
    • Companion Diagnostics
  • Image Calendar +
    Image Calendar
    +
    • Image Contest
    • Data Image Gallery
Search

Probes for INS

ACD can configure probes for the various manual and automated assays for INS for RNAscope Assay, or for Basescope Assay compatible for your species of interest.

  • Probes for INS (0)
  • Kits & Accessories (0)
  • Support & Documents (0)
  • Publications (1426)
  • Image gallery (0)
Refine Probe List

Content for comparison

Gene

  • (-) Remove TBD filter TBD (1413)
  • Lgr5 (151) Apply Lgr5 filter
  • SARS-CoV-2 (136) Apply SARS-CoV-2 filter
  • Gad1 (90) Apply Gad1 filter
  • vGlut2 (80) Apply vGlut2 filter
  • HPV E6/E7 (78) Apply HPV E6/E7 filter
  • Slc17a6 (77) Apply Slc17a6 filter
  • Axin2 (74) Apply Axin2 filter
  • SLC32A1 (74) Apply SLC32A1 filter
  • FOS (73) Apply FOS filter
  • Sst (65) Apply Sst filter
  • TH (63) Apply TH filter
  • VGAT (58) Apply VGAT filter
  • Gad2 (54) Apply Gad2 filter
  • tdTomato (54) Apply tdTomato filter
  • DRD2 (53) Apply DRD2 filter
  • Slc17a7 (52) Apply Slc17a7 filter
  • GLI1 (51) Apply GLI1 filter
  • PVALB (47) Apply PVALB filter
  • egfp (46) Apply egfp filter
  • ZIKV (46) Apply ZIKV filter
  • DRD1 (42) Apply DRD1 filter
  • GFAP (39) Apply GFAP filter
  • COL1A1 (38) Apply COL1A1 filter
  • Crh (37) Apply Crh filter
  • Chat (37) Apply Chat filter
  • V-nCoV2019-S (37) Apply V-nCoV2019-S filter
  • Pomc (34) Apply Pomc filter
  • PDGFRA (33) Apply PDGFRA filter
  • Il-6 (33) Apply Il-6 filter
  • Cre (33) Apply Cre filter
  • AGRP (32) Apply AGRP filter
  • PECAM1 (32) Apply PECAM1 filter
  • Npy (32) Apply Npy filter
  • Wnt5a (31) Apply Wnt5a filter
  • CXCL10 (31) Apply CXCL10 filter
  • GLP1R (31) Apply GLP1R filter
  • Sox9 (29) Apply Sox9 filter
  • CD68 (28) Apply CD68 filter
  • Penk (28) Apply Penk filter
  • PD-L1 (28) Apply PD-L1 filter
  • ACTA2 (27) Apply ACTA2 filter
  • SHH (27) Apply SHH filter
  • VGluT1 (27) Apply VGluT1 filter
  • OLFM4 (26) Apply OLFM4 filter
  • GFP (26) Apply GFP filter
  • Rbfox3 (25) Apply Rbfox3 filter
  • MALAT1 (24) Apply MALAT1 filter
  • SOX2 (24) Apply SOX2 filter
  • Ccl2 (24) Apply Ccl2 filter

Product

  • RNAscope (220) Apply RNAscope filter
  • TBD (148) Apply TBD filter
  • RNAscope Multiplex Fluorescent Assay (39) Apply RNAscope Multiplex Fluorescent Assay filter
  • RNAscope 2.5 HD Brown Assay (12) Apply RNAscope 2.5 HD Brown Assay filter
  • Basescope (10) Apply Basescope filter
  • RNAscope Fluorescent Multiplex Assay (10) Apply RNAscope Fluorescent Multiplex Assay filter
  • DNAscope HD Duplex Reagent Kit (8) Apply DNAscope HD Duplex Reagent Kit filter
  • RNAscope 2.5 HD Red assay (8) Apply RNAscope 2.5 HD Red assay filter
  • RNAscope 2.5 HD Reagent Kit - BROWN (7) Apply RNAscope 2.5 HD Reagent Kit - BROWN filter
  • RNAscope HiPlex v2 assay (7) Apply RNAscope HiPlex v2 assay filter
  • RNAscope 2.5 HD Duplex (6) Apply RNAscope 2.5 HD Duplex filter
  • RNAscope Multiplex Fluorescent v2 (5) Apply RNAscope Multiplex Fluorescent v2 filter
  • BASEscope Assay RED (2) Apply BASEscope Assay RED filter
  • DNAscope Duplex Assay (1) Apply DNAscope Duplex Assay filter
  • miRNAscope (1) Apply miRNAscope filter
  • RNAscope 2.0 Assay (1) Apply RNAscope 2.0 Assay filter
  • RNAscope 2.5 HD Assay (1) Apply RNAscope 2.5 HD Assay filter
  • RNAscope 2.5 LS Assay (1) Apply RNAscope 2.5 LS Assay filter
  • RNAScope HiPlex assay (1) Apply RNAScope HiPlex assay filter
  • RNAscope HiPlex Image Registration Software (1) Apply RNAscope HiPlex Image Registration Software filter

Research area

  • Neuroscience (138) Apply Neuroscience filter
  • Cancer (109) Apply Cancer filter
  • Development (55) Apply Development filter
  • Other: Methods (44) Apply Other: Methods filter
  • Inflammation (33) Apply Inflammation filter
  • Infectious (18) Apply Infectious filter
  • HIV (15) Apply HIV filter
  • Stem Cells (15) Apply Stem Cells filter
  • Pain (14) Apply Pain filter
  • HPV (12) Apply HPV filter
  • Other: Neuromuscular Disorders (10) Apply Other: Neuromuscular Disorders filter
  • Other: Heart (9) Apply Other: Heart filter
  • Other: Lung (9) Apply Other: Lung filter
  • CGT (8) Apply CGT filter
  • Covid (8) Apply Covid filter
  • Other: Metabolism (8) Apply Other: Metabolism filter
  • Stem cell (8) Apply Stem cell filter
  • Infectious Disease (7) Apply Infectious Disease filter
  • Immunotherapy (6) Apply Immunotherapy filter
  • Metabolism (6) Apply Metabolism filter
  • Other: Reproduction (6) Apply Other: Reproduction filter
  • Endocrinology (5) Apply Endocrinology filter
  • LncRNAs (5) Apply LncRNAs filter
  • Obesity (5) Apply Obesity filter
  • Reproduction (5) Apply Reproduction filter
  • Aging (4) Apply Aging filter
  • Cystic Fibrosis (4) Apply Cystic Fibrosis filter
  • Heart (4) Apply Heart filter
  • Itch (4) Apply Itch filter
  • lncRNA (4) Apply lncRNA filter
  • Other (4) Apply Other filter
  • Other: Kidney (4) Apply Other: Kidney filter
  • Other: Skin (4) Apply Other: Skin filter
  • Skin (4) Apply Skin filter
  • Transcriptomics (4) Apply Transcriptomics filter
  • Alzheimer's Disease (3) Apply Alzheimer's Disease filter
  • diabetes (3) Apply diabetes filter
  • Immunology (3) Apply Immunology filter
  • Kidney (3) Apply Kidney filter
  • Memory (3) Apply Memory filter
  • other: Aging (3) Apply other: Aging filter
  • Other: Eyes (3) Apply Other: Eyes filter
  • Other: Gut (3) Apply Other: Gut filter
  • Other: Reproductive Biology (3) Apply Other: Reproductive Biology filter
  • Other: Transcriptomics (3) Apply Other: Transcriptomics filter
  • Other: Zoological Disease (3) Apply Other: Zoological Disease filter
  • Regeneration (3) Apply Regeneration filter
  • Reproductive Biology (3) Apply Reproductive Biology filter
  • Stress (3) Apply Stress filter
  • Tumor microenvironment (3) Apply Tumor microenvironment filter

Category

  • Publications (1426) Apply Publications filter
A Cell Atlas of the Human Amygdala

Biological Psychiatry

2021 May 01

Krienen, F;Goldman, M;Mullally, C;Reed, N;McCarroll, S;Berretta, S;
| DOI: 10.1016/j.biopsych.2021.02.049

Background: The amygdala is responsible for encoding valence, the biological value of aversive and rewarding stimuli; it plays a critical role in the formation and storage of emotional memories, assessment of threat-related stimuli, and fear consolidation. As a step toward identifying how specific cell populations contribute to these functions, we sought to systematically identify the cell types of the human amygdala, the genes (mRNAs) expressed by each cell type, and their relationships to cell types in mouse and marmoset amygdala. Methods: We used single-cell RNA-seq (Drop-seq and the 10X Genomics platform) to profile mRNA expression in nuclei sampled from the amygdala of n¼4 postmortem healthy donors. We used computational methods we have described previously (Sanders et al., Cell 2018; Krienen et al., Nature 2020) to organize these profiles into clusters of transcriptionally similar cells corresponding to cell types and cell states. We also analyzed these data in relationship to similar data we generated from mouse and marmoset amygdala. Results: We profiled mRNA expression in more than 100,000 nuclei sampled from the 4-human amygdala. Computational analysis revealed at least 30 transcriptionally distinct types of neurons in the amygdala, including 17 GABAergic and 13 glutamatergic types. We found homologs for these principal cell types in the amygdala of marmoset and mouse. However, the expression patterns of many individual genes (across these neuronal types) diverged considerably among the three species. Conclusions: Availability of this data resource will help enable diverse scientific investigations of the amygdala and its relationship to post-traumatic stress disorder and other psychiatric disorders.
Genetic deletion of Nox4 enhances cancerogen-induced formation of solid tumors

Proceedings of the National Academy of Sciences

2021 Mar 16

Helfinger, V;Freiherr von Gall, F;Henke, N;Kunze, M;Schmid, T;Rezende, F;Heidler, J;Wittig, I;Radeke, H;Marschall, V;Anderson, K;Shah, A;Fulda, S;Brüne, B;Brandes, R;Schröder, K;
| DOI: 10.1073/pnas.2020152118

Reactive oxygen species (ROS) can cause cellular damage and promote cancer development. Besides such harmful consequences of overproduction of ROS, all cells utilize ROS for signaling purposes and stabilization of cell homeostasis. In particular, the latter is supported by the NADPH oxidase 4 (Nox4) that constitutively produces low amounts of H2O2. By that mechanism, Nox4 forces differentiation of cells and prevents inflammation. We hypothesize a constitutive low level of H2O2 maintains basal activity of cellular surveillance systems and is unlikely to be cancerogenic. Utilizing two different murine models of cancerogen-induced solid tumors, we found that deletion of Nox4 promotes tumor formation and lowers recognition of DNA damage. Nox4 supports phosphorylation of H2AX (γH2AX), a prerequisite of DNA damage recognition, by retaining a sufficiently low abundance of the phosphatase PP2A in the nucleus. The underlying mechanism is continuous oxidation of AKT by Nox4. Interaction of oxidized AKT and PP2A captures the phosphatase in the cytosol. Absence of Nox4 facilitates nuclear PP2A translocation and dephosphorylation of γH2AX. Simultaneously AKT is left phosphorylated. Thus, in the absence of Nox4, DNA damage is not recognized and the increased activity of AKT supports proliferation. The combination of both events results in genomic instability and promotes tumor formation. By identifying Nox4 as a protective source of ROS in cancerogen-induced cancer, we provide a piece of knowledge for understanding the role of moderate production of ROS in preventing the initiation of malignancies.
Copy Number Variant Analysis and Genome-wide Association Study Identify Loci with Large Effect for Vesicoureteral Reflux

Journal of the American Society of Nephrology : JASN

2021 Feb 17

Verbitsky, M;Krithivasan, P;Batourina, E;Khan, A;Graham, SE;Marasà, M;Kim, H;Lim, TY;Weng, PL;Sánchez-Rodríguez, E;Mitrotti, A;Ahram, DF;Zanoni, F;Fasel, DA;Westland, R;Sampson, MG;Zhang, JY;Bodria, M;Kil, BH;Shril, S;Gesualdo, L;Torri, F;Scolari, F;Izzi, C;van Wijk, JAE;Saraga, M;Santoro, D;Conti, G;Barton, DE;Dobson, MG;Puri, P;Furth, SL;Warady, BA;Pisani, I;Fiaccadori, E;Allegri, L;Degl'Innocenti, ML;Piaggio, G;Alam, S;Gigante, M;Zaza, G;Esposito, P;Lin, F;Simões-E-Silva, AC;Brodkiewicz, A;Drozdz, D;Zachwieja, K;Miklaszewska, M;Szczepanska, M;Adamczyk, P;Tkaczyk, M;Tomczyk, D;Sikora, P;Mizerska-Wasiak, M;Krzemien, G;Szmigielska, A;Zaniew, M;Lozanovski, VJ;Gucev, Z;Ionita-Laza, I;Stanaway, IB;Crosslin, DR;Wong, CS;Hildebrandt, F;Barasch, J;Kenny, EE;Loos, RJF;Levy, B;Ghiggeri, GM;Hakonarson, H;Latos-Bieleńska, A;Materna-Kiryluk, A;Darlow, JM;Tasic, V;Willer, C;Kiryluk, K;Sanna-Cherchi, S;Mendelsohn, CL;Gharavi, AG;
PMID: 33597122 | DOI: 10.1681/ASN.2020050681

Vesicoureteral reflux (VUR) is a common, familial genitourinary disorder, and a major cause of pediatric urinary tract infection (UTI) and kidney failure. The genetic basis of VUR is not well understood. A diagnostic analysis sought rare, pathogenic copy number variant (CNV) disorders among 1737 patients with VUR. A GWAS was performed in 1395 patients and 5366 controls, of European ancestry. Altogether, 3% of VUR patients harbored an undiagnosed rare CNV disorder, such as the 1q21.1, 16p11.2, 22q11.21, and triple X syndromes ((OR, 3.12; 95% CI, 2.10 to 4.54; P=6.35×10-8) The GWAS identified three study-wide significant and five suggestive loci with large effects (ORs, 1.41-6.9), containing canonical developmental genes expressed in the developing urinary tract (WDPCP, OTX1, BMP5, VANGL1, and WNT5A). In particular, 3.3% of VUR patients were homozygous for an intronic variant in WDPCP (rs13013890; OR, 3.65; 95% CI, 2.39 to 5.56; P=1.86×10-9). This locus was associated with multiple genitourinary phenotypes in the UK Biobank and eMERGE studies. Analysis of Wnt5a mutant mice confirmed the role of Wnt5a signaling in bladder and ureteric morphogenesis. These data demonstrate the genetic heterogeneity of VUR. Altogether, 6% of patients with VUR harbored a rare CNV or a common variant genotype conferring an OR >3. Identification of these genetic risk factors has multiple implications for clinical care and for analysis of outcomes in VUR.
216: Nutritional and metabolic effects of elexacaftor/tezacaftor/ivacaftor in adults and adolescents with cystic fibrosis

Journal of Cystic Fibrosis

2021 Nov 01

Bailey, J;Wade, J;Redden, D;Rowe, S;Solomon, G;
| DOI: 10.1016/S1569-1993(21)01641-6

Background: Malnutrition has historically been a main clinical consequence of CF. Consensus recommendations have encouraged a highcalorie, high-fat diet but with little guidance related to nutrient density or quality of foods consumed to meet elevated metabolic needs. Highly effective modulators are associated with improved growth and increases in weight and body mass index (BMI) in subsets of the CF population. Recently elexacaftor/tezacaftor/ivacaftor was approved for use in up to 90% of people with CF. PROMISE is an open-label observational cohort study designed to longitudinally assess the effectiveness of elexacaftor/tezacaftor/ivacaftor in the clinical setting. Our single-center sub-study aimed to explore the changes in BMI, dietary intake, muscle strength, pancreatic enzyme replacement therapy (PERT), and resting energy expenditure with use of elexacaftor/tezacaftor/ivacaftor. Methods: Participants were enrolled and had baseline (V1) measurements performed prior to taking their first dose of elexacaftor/tezacaftor/ ivacaftor. Follow-up measurements were obtained at 2 visits. Short-term follow occurred at 28 days (V2) on elexacaftor/tezacaftor/ivacaftor and long-term follow measurements were obtained at > 6 months on drug (V3). Measurements at each time point included: resting energy expenditure as percent of predicted (REE%) using indirect calorimetry, hand grip strength (HGS), dietary intake using 3-day diet records, and PERT dosage. Diet records were reviewed by the study dietitian and were analyzed using NDSR software. The Healthy Eating Index (HEI) is a validated measure of diet quality based on the Dietary Guidelines for Americans 2015-2020. HEI-2015 scores range from 0 to 100, with a score of 100 indicating the best diet quality. Lung function and QOL (CFQ-r) were assessed at each visit as part of the parent PROMISE protocol. Wilcoxon sign rank tests were used to compare changes in outcomes at each time point. Results: A total of 22 participants enrolled and completed baseline assessments. Patients were 16-54 years of age (mean age 26 years), 68% were female, and 50% were not previously on CFTR modulators. V2 was completed by 20 participants and 17 participants completed all assessments through V3. Mean (± SD) BMI improved by 0.46 ± 0.93 kg/m² (P < 0.05) at V2 and 0.92 ± 0.88 kg/m² at V3 compared to V1 (P < 0.0001). REE% decreased by 6.6 ± 15.3 from V1 to V3 (P < 0.05). Total caloric intake increased by 297 ± 766 kcal/day (P < 0.05) and total fat intake increased by 19 ± 37 grams/day between V1 and V3 (P < 0.05). The average HEI for the cohort at baseline was 52.1 ± 10.7 and did not significantly change over the course of the study. There were no significant changes in HGS, PERT dosage, and intake of other macro and micro-nutrients, including fat-soluble vitamins. Conclusion: Elexacaftor/tezacaftor/ivacaftor improved BMI status rapidly, and this improvement was sustained through 6 or more months. Decreased energy expenditure combined with increased caloric intake are mechanisms of weight gain on elexacaftor/tezacaftor/ivacaftor. HEI in this CF cohort was similar to what is observed in adults in the general U.S. population. Diet quality did not improve with use of elexacaftor/tezacaftor/ ivacaftor therapy, despite increases in total caloric and fat intake. These findings highlight the need for individualized nutritional counseling to improve diet quality and manage weight changes on elexacaftor/tezacaftor/ ivacaftor in the clinical setting. Ongoing analyses are examining correlations between nutrition QOL domains (body image and eating disturbances) and changes in dietary intake on elexacaftor/tezacaftor/ivacaftor, as well as correlations between decreased REE% and lung function improvements.
A KIDNEY-ON-THE-CHIP APPROACH USING PRIMARY HUMAN TUBULAR CELLS IN A 3D CO-CULTURE SYSTEM

Kidney International Reports

2021 Apr 01

Martin, L;Wilken, G;MARSCHNER, J;Sartor, F;Romagnani, P;Anders, H;
| DOI: 10.1016/j.ekir.2021.03.086

Introduction: Conventional 2D mono-culture in vitro models using immortalized cell lines are still widely used in experimental nephrology, albeit their limited translatability and predictivity for the in vivo situation. The feasibility of more sophisticated assays is often reduced by complex protocols and long lasting procedures. We aimed to establish and validate an easy-to-use but yet (patho-) physiologically relevant 3D cell culture assay that mimics key aspects of the in vivo situation of renal tubules, including a leak-thight epithelium with a luminal and baso-lateral side, interstitial matrix, a peri-tubular capillary and circulating blood cells inside its lumen. Methods: We utilized the 3-lane OrganoPlate system (Mimetas, Leiden, Netherlands) as a scaffold. After infusing a collagen I matrix in the middle channel (C2), primary human renal progenitor cells are seeded into the upper channel (C1), adhering to the C2-matrix. The plate is put on a perfusion rocker, that facilitates continuous gravity-triggered bidirectional perfusion in all channels. Thereafter the cells form a leaktight tubular structure with a continuous lumen. Next, human endothelial cells are seeded into the bottom channel (C3), which adhered to the opposite site of C2 and formed a vessel-like structure with a continuous lumen, as well. Finally, primary human white blood cells (WBCs) were isolated and seeded into C3 (figure A). Results: The leak-tightness of the 3D-tubule increased significantly over time, as measured by tracing the diffusion of a 150 kDa FITClabeled dextran from C1 to C2 (time-to-leakage day 1: 3.3 2.6 min; day 9: 36.2 10.7 min), indicating the stability of the co-culture system as well as a cellular maturation resulting in significant barrier functionality as seen in vivo (figure B). In accordance with this and other studies, the primary human tubular cells expressed higher levels of functionally relevant proteins in 3D than under 2D, no-flow conditions, as indicated by cell-number normalized mean fluorescence intensity measured by immunofluorescence, e..g ZO-1 (2.1 0.4 vs. 82.2 20.8) and Na-KATPase (2.3 0.3 vs. 52.8 5.4). Additionally, the growth conditions of the OrganoPlate rendered the cells more resilient to stimuli of acute tubular necrosis, e.g. extracellular histones, as compared to standard cell culture, indicated by cell number normalized lactate dehydrogenase release.The primary WBCs seeded inside the endothelial lumen (C3) did not leave the compartment under normal culture conditions, but displayed extravasation and directed migration from C3 through C2 towards C1 when attracted by chemokines released from tubular cells in C1. This effect was inhibitable by pre-emptive treatment of the endothelium with an selective monoclonal anti-P-selectin antibody (percent migrated cells, medium: 0 0, chemokines: 4.59 0.6, chemokines + Pselectin AB: 1.0 0.5, figure C). This serves as a proof of principle, that the system is applicable to study complex cell-cell and cell-substrate interactions, such as chemokine-mediate immune cell homing. Conclusions: The results of this study suggest, that sophisticated 3D co-culture models of a renal tubule including an interstitial compartment, a peri-tubluar capillary and circulating immune cells are feasible and potentially suited for in depth mechanistic studies in vitro.
Neuromedin B-expressing neurons in the retrotrapezoid nucleus regulate respiratory homeostasis and promote stable breathing in adult mice

The Journal of neuroscience : the official journal of the Society for Neuroscience

2023 Jun 08

Souza, GMPR;Stornetta, DS;Shi, Y;Lim, E;Berry, FE;Bayliss, DA;Abbott, SBG;
PMID: 37290937 | DOI: 10.1523/JNEUROSCI.0386-23.2023

Respiratory chemoreceptor activity encoding arterial PCO2 and PO2 is a critical determinant of ventilation. Currently, the relative importance of several putative chemoreceptor mechanisms for maintaining eupneic breathing and respiratory homeostasis is debated. Transcriptomic and anatomical evidence suggest that bombesin-related peptide Neuromedin-B (Nmb) expression identifies chemoreceptor neurons in the retrotrapezoid nucleus (RTN) that mediate the hypercapnic ventilatory response, but functional support is missing. In this study, we generated a transgenic Nmb-Cre mouse and used Cre-dependent cell ablation and optogenetics to test the hypothesis that RTN Nmb neurons are necessary for the CO2-depedent drive to breathe in adult male and female mice. Selective ablation of ∼95% of RTN Nmb neurons causes compensated respiratory acidosis due to alveolar hypoventilation, as well as profound breathing instability and respiratory-related sleep disruption. Following RTN Nmb lesion, mice were hypoxemic at rest and were prone to severe apneas during hyperoxia, suggesting that oxygen-sensitive mechanisms, presumably the peripheral chemoreceptors, compensate for the loss of RTN Nmb neurons. Interestingly, ventilation following RTN Nmb -lesion was unresponsive to hypercapnia, but behavioral responses to CO2 (freezing and avoidance) and the hypoxia ventilatory response were preserved. Neuroanatomical mapping shows that RTN Nmb neurons are highly collateralized and innervate the respiratory-related centers in the pons and medulla with a strong ipsilateral preference. Together, this evidence suggests RTN Nmb neurons are dedicated to the respiratory effects of arterial PCO2/pH and maintain respiratory homeostasis in intact conditions and suggest that malfunction of these neurons could underlie the etiology of certain forms of sleep-disordered breathing in humans.Significance Statement:Respiratory chemoreceptors stimulate neural respiratory motor output to regulate arterial PCO2 and PO2, thereby maintaining optimal gas exchange. Neurons in the retrotrapezoid nucleus (RTN) that express the bombesin-related peptide Neuromedin-B are proposed to be important in this process, but functional evidence has not been established. Here, we developed a transgenic mouse model and demonstrated that RTN neurons are fundamental for respiratory homeostasis and mediate the stimulatory effects of CO2 on breathing. Our functional and anatomical data indicate that Nmb-expressing RTN neurons are an integral component of the neural mechanisms that mediate CO2-dependent drive to breathe and maintain alveolar ventilation. This work highlights the importance of the interdependent and dynamic integration of CO2- and O2-sensing mechanisms in respiratory homeostasis of mammals.
Abstract CT524: A phase 1, first in human (FIH) study of autologous anti-HER2 chimeric antigen receptor macrophages (CAR-M) in HER2-overexpressing solid tumors (ST)

Cancer Research

2022 Jun 15

Reiss, K;Yuan, Y;Ueno, N;Abdou, Y;Barton, D;Swaby, R;Ronczka, A;Cushing, D;Abramson, S;Condamine, T;Klichinsky, M;Dees, E;
| DOI: 10.1158/1538-7445.am2022-ct524

Background: Adoptive T cell therapies have led to remarkable advances in hematologic cancers but with less effect in ST. Actively recruited tumor associated macrophages (TAM) are abundant in the ST microenvironment (TME) and typically display immunosuppressive behavior. Macrophages engineered to be proinflammatory may be an ideal vector for adoptive ST cellular therapy. Engineered CAR-M selectively recognize and phagocytose antigen overexpressing cancer cells, reprogram TME and present neoantigens to T cells, leading to epitope spreading and immune memory. Human Epidermal Growth Factor Receptor 2 (HER2) overexpression promotes tumorigenesis in many cancers (Table 1). CT-0508 is a cell product comprised of autologous monocyte-derived proinflammatory macrophages expressing an anti-HER2 CAR. Pre-clinical studies show that CT-0508 induces targeted cancer cell phagocytosis while sparing normal cells, decreases tumor burden and prolongs survival, and was safe and effective in a semi-immunocompetent mouse model of human HER2-overexpressing ovarian cancer. Methods: This FIH Phase 1 study is evaluating safety, tolerability, cell manufacturing feasibility, trafficking, and preliminary efficacy in 18 subjects with locally advanced/unresectable or metastatic ST overexpressing HER2, with progression on available therapies, including anti-HER2 therapies. Filgrastim is used to mobilize autologous hematopoietic progenitor cells for monocyte collection by apheresis prior to CT-0508 CAR macrophage infusion. Group 1 subjects receive CT-0508 on D1, 3, & 5. Group 2 subjects will receive full dose on D1. A Safety Review Committee will review dose limiting toxicities. Pre/post-treatment biopsies and blood samples will be collected for correlative analysis of immunogenicity, trafficking (PCR, RNA scope), CT-0508 persistence in blood and tumor, target antigen engagement, TME modulation (single cell RNA sequencing), immune response (TCR sequencing) and others. Table 1. Her2 Overexpression Across Tumor Types Tumor HER2 Overexpression (%) Bladder 8-70 Salivary duct 30-40 Gastric 7-34 Ovarian 26 Breast 11-25 Salivary mucoepidermoid 17.6 Esophageal 12-14 Gallbladder 9.8-12.8 Cholangiocarcinoma 6.3-9 Colorectal 1.6-5 Cervical 2.8-3.9 Uterine 3 Testicular 2.4 Citation Format: Kim A. Reiss, Yuan Yuan, Naoto T. Ueno, Yara Abdou, Debora Barton, Ramona F. Swaby, Amy Ronczka, Daniel J. Cushing, Sascha Abramson, Thomas Condamine, Michael Klichinsky, E. Claire Dees. A phase 1, first in human (FIH) study of autologous anti-HER2 chimeric antigen receptor macrophages (CAR-M) in HER2-overexpressing solid tumors (ST) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr CT524.
92 Single cell and spatial multiplex profiling of immune cell markers in FFPE tumor tissues using the novel RNAscope HiPlex v2 in situ hybridization assay

Journal for ImmunoTherapy of Cancer

2021 Nov 01

Basak, S;Dikshit, A;Yu, M;Ji, H;Chang, C;Zhang, B;
| DOI: 10.1136/jitc-2021-sitc2021.092

BackgroundThe tumor microenvironment (TME) is highly complex, comprised of tumor cells, immune cells, stromal cells, and extracellular matrix. Understanding spatial interactions between various cell types and their activation states in the TME is crucial for implementing successful immunotherapy strategies against various types of cancer. This study demonstrates a highly sensitive and specific multiplexed technique, the RNAscope HiPlex v2 in situ hybridization (ISH) assay for spatial and transcriptomic profiling of target genes to assess immune regulation in human lung, breast, cervical and ovarian FFPE tumor tissues.MethodsWe have expanded our current RNAscope HiPlex assay capability of iteratively multiplexing up to 12 targets in fixed and fresh frozen samples to include formalin fixed paraffin embedded (FFPE) tissues. The novel FFPE reagent effectively reduces background autofluorescence, improving the signal to noise ratio. We have leveraged this technology to investigate spatial expression of 12 oncology and immuno-oncology target genes, including tumor markers, immune checkpoint markers, immunosuppression markers, immune cell markers and secreted chemokine RNA expression profile within the TME. The targets were simultaneously registered using HiPlex image registration software v2 that enables background subtraction.ResultsWe visualized T cell infiltration and identified T cell subsets within tumors using CD3and CD8 expression and activated T cells by IFNG expression. We further identified subsets of pro- and anti-inflammatory macrophages by CD68 and CD163 expression as well effector cells which secrete chemokines and cytokine. We also detected the hypoxia markers HIF1A and VEGF to elucidate the immunosuppressive state of tumor cells. Preliminary analysis and quantification of the HIF1A expression using HALO image analysis software showed higher copy numbers in the lung tumor as compared to the other tumors, demonstrating the sensitivity of the assay through differential expression. We additionally showed the differential expression of immune checkpoint markers PDCD1, and CD274 within the TME.ConclusionsUsing a highly sensitive multiplexed RNAscope HiPlex v2 ISH assay, we have demonstrated the capability of this technique to spatially resolve 12 targets in four different tumor types. The FFPE reagent efficiently quenched background autofluorescence in the tissues and identified immune cell signatures within the TME. Quantification of immunosuppressive markers further depicted a differential expression among various tumors. This technology is highly beneficial for investigating complex and spatial tumor-stroma interactions in basic science and translational research. The assay can also provide valuable understanding of the biological crosstalk among various cell types in complex and heterogeneous tissues.
Outer hair cell glutamate signaling through type II spiral ganglion afferents activates neurons in the cochlear nucleus in response to non-damaging sounds

The Journal of neuroscience : the official journal of the Society for Neuroscience

2021 Feb 10

Weisz, CJC;Williams, SG;Eckard, CS;Divito, CB;Ferreira, DW;Fantetti, KN;Dettwyler, SA;Cai, HM;Rubio, ME;Kandler, K;Seal, RP;
PMID: 33574178 | DOI: 10.1523/JNEUROSCI.0619-20.2021

Cochlear outer hair cells (OHCs) are known to uniquely participate in auditory processing through their electromotility, and like inner hair cells (IHCs), are also capable of releasing vesicular glutamate onto spiral ganglion (SG) neurons; in this case onto the sparse type II SG neurons. However, unlike glutamate signaling at the inner hair cell (IHC) -type I SG synapse, which is robust across a wide spectrum of sound intensities, glutamate signaling at the OHC-type II SG synapse is weaker and has been hypothesized to occur only at intense, possibly damaging sound levels. Here, we tested the ability of the OHC-type II SG pathway to signal to the brain in response to moderate, non-damaging sound (80 dB SPL) as well as to intense sound (115 dB SPL). First, we determined the vesicular glutamate transporters (VGLUTs) associated with OHC signaling and then confirmed the loss of glutamatergic synaptic transmission from OHCs to type II SG neurons in knockout mice using dendritic patch-clamp recordings. Next, we generated genetic mouse lines in which vesicular glutamate release occurs selectively from OHCs, and then assessed c-Fos expression in the cochlear nucleus (CN) in response to sound. From these analyses, we show for the first time that glutamatergic signaling at the OHC-type II SG synapse is capable of activating CN neurons even at moderate sound levels.SIGNIFICANCE STATEMENTEvidence suggests that cochlear outer hair cells (OHC) release glutamate onto type II spiral ganglion neurons only when exposed to loud sound, and that type II neurons are activated by tissue damage. Knowing whether moderate level sound, without tissue damage, activates this pathway has functional implications for this fundamental auditory pathway. We first determined that OHCs rely largely on VGLUT3 for synaptic glutamate release. We then used a genetic mouse line in which OHCs, but not IHCs, release vesicular glutamate to demonstrate that moderate sound exposure activates cochlear nucleus neurons via the OHC - type II SG pathway. Together these data indicate that glutamate signaling at the OHC-type II afferent synapse participates in auditory function at moderate sound levels.
A phase 1, first-in-human (FIH) study of adenovirally transduced autologous macrophages engineered to contain an anti-HER2 chimeric antigen receptor (CAR) in subjects with HER2 overexpressing solid tumors.

Journal of Clinical Oncology

2022 Feb 01

Reiss, K;Yuan, Y;Barton, D;Cushing, D;Ronczka, A;Klichinsky, M;Dees, E;
| DOI: 10.1200/JCO.2022.40.4_suppl.TPS668

TPS668 Background: Adoptive T cell therapies have led to remarkable advances among patients with hematologic malignancies, but not in those with solid tumors. Macrophages are actively recruited into, and are abundantly present in the solid tumor microenvironment (sTME). Tumor- associated macrophages typically display immunosuppressive behavior, but when engineered to be proinflammatory, may be an ideal vector to administer adoptive cellular therapy in solid tumors. Furthermore, insertion of a CAR on the macrophages allow them to selectively recognize and phagocytose antigen overexpressing cancer cells. CAR macrophages reprogram the sTME and present neoantigens to T cells, leading to epitope spreading and immune memory. Human Epidermal Growth Factor Receptor 2 (HER2) overexpression promotes tumorigenesis in many cancers (Table). CT-0508 is a cell product comprised of autologous monocyte-derived pro-inflammatory macrophages expressing an anti-HER2 CAR. Pre-clinical studies have shown that CT-0508 induced targeted cancer cell phagocytosis while sparing normal cells, decreased tumor burden and prolonged survival in relevant models. CT-0508 cells were safe and effective in a semi-immunocompetent mouse model of human HER2 overexpressing ovarian cancer. Methods: This is a FIH Phase 1 study to evaluate safety, tolerability, cell manufacturing feasibility, trafficking and preliminary evidence of efficacy of investigational product CT-0508 in 18 subjects with locally advanced (unresectable) or metastatic solid tumors overexpressing HER2, who have failed available therapies, including anti-HER2 therapies when indicated. Filgrastim is being used to mobilize autologous hematopoietic progenitor cells for monocyte collection by apheresis. The CT-0508 CAR macrophage product is manufactured, prepared and cryopreserved from mobilized peripheral blood monocytes. Group 1 subjects receive CT-0508 infusion split over D1, 3 and 5. Dose limiting toxicities will be observed and addressed by a Safety Review Committee. Group 2 subjects will receive the full CT-0508 infusion on D1. Pre and post treatment biopsies and blood samples will be collected to investigate correlates of safety (immunogenicity), trafficking (PCR, RNA scope), CT-0508 persistence in blood and in the tumor, target antigen engagement, TME modulation (single cell RNA sequencing), immune response (TCR sequencing) and others. Clinical trial information: NCT04660929. [Table: see text]
Transarterial Embolization Modulates the Immune Response within Target and Nontarget Hepatocellular Carcinomas in a Rat Model

Radiology

2022 Jan 11

Tischfield, DJ;Gurevich, A;Johnson, O;Gatmaytan, I;Nadolski, GJ;Soulen, MC;Kaplan, DE;Furth, E;Hunt, SJ;Gade, TPF;
PMID: 35014906 | DOI: 10.1148/radiol.211028

Background Transarterial embolization (TAE) is the most common treatment for hepatocellular carcinoma (HCC); however, there remain limited data describing the influence of TAE on the tumor immune microenvironment. Purpose To characterize TAE-induced modulation of the tumor immune microenvironment in a rat model of HCC and identify factors that modulate this response. Materials and Methods TAE was performed on autochthonous HCCs induced in rats with use of diethylnitrosamine. CD3, CD4, CD8, and FOXP3 lymphocytes, as well as programmed cell death protein ligand-1 (PD-L1) expression, were examined in three cohorts: tumors from rats that did not undergo embolization (control), embolized tumors (target), and nonembolized tumors from rats that had a different target tumor embolized (nontarget). Differences in immune cell recruitment associated with embolic agent type (tris-acryl gelatin microspheres [TAGM] vs hydrogel embolics) and vascular location were examined in rat and human tissues. A generalized estimating equation model and t, Mann-Whitney U, and χ2 tests were used to compare groups. Results Cirrhosis-induced alterations in CD8, CD4, and CD25/CD4 lymphocytes were partially normalized following TAE (CD8: 38.4%, CD4: 57.6%, and CD25/CD4: 21.1% in embolized liver vs 47.7% [P = .02], 47.0% [P = .01], and 34.9% [P = .03], respectively, in cirrhotic liver [36.1%, 59.6%, and 4.6% in normal liver]). Embolized tumors had a greater number of CD3, CD4, and CD8 tumor-infiltrating lymphocytes relative to controls (191.4 cells/mm2 vs 106.7 cells/mm2 [P = .03]; 127.8 cells/mm2 vs 53.8 cells/mm2 [P < .001]; and 131.4 cells/mm2 vs 78.3 cells/mm2 [P = .01]) as well as a higher PD-L1 expression score (4.1 au vs 1.9 au [P < .001]). A greater number of CD3, CD4, and CD8 lymphocytes were found near TAGM versus hydrogel embolics (4.1 vs 2.0 [P = .003]; 3.7 vs 2.0 [P = .01]; and 2.2 vs 1.1 [P = .03], respectively). The number of lymphocytes adjacent to embolics differed based on vascular location (17.9 extravascular CD68+ peri-TAGM cells vs 7.0 intravascular [P < .001]; 6.4 extravascular CD68+ peri-hydrogel embolic cells vs 3.4 intravascular [P < .001]). Conclusion Transarterial embolization-induced dynamic alterations of the tumor immune microenvironment are influenced by underlying liver disease, embolic agent type, and vascular location.
The role of pro-opiomelanocortin in the ACTH-cortisol dissociation of sepsis

Critical care (London, England)

2021 Feb 16

Téblick, A;Vander Perre, S;Pauwels, L;Derde, S;Van Oudenhove, T;Langouche, L;Van den Berghe, G;
PMID: 33593393 | DOI: 10.1186/s13054-021-03475-y

Sepsis is typically hallmarked by high plasma (free) cortisol and suppressed cortisol breakdown, while plasma adrenocorticotropic hormone (ACTH) is not increased, referred to as 'ACTH-cortisol dissociation.' We hypothesized that sepsis acutely activates the hypothalamus to generate, via corticotropin-releasing hormone (CRH) and vasopressin (AVP), ACTH-induced hypercortisolemia. Thereafter, via increased availability of free cortisol, of which breakdown is reduced, feedback inhibition at the pituitary level interferes with normal processing of pro-opiomelanocortin (POMC) into ACTH, explaining the ACTH-cortisol dissociation. We further hypothesized that, in this constellation, POMC leaches into the circulation and can contribute to adrenocortical steroidogenesis. In two human studies of acute (ICU admission to day 7, N = 71) and prolonged (from ICU day 7 until recovery; N = 65) sepsis-induced critical illness, POMC plasma concentrations were quantified in relation to plasma ACTH and cortisol. In a mouse study of acute (1 day), subacute (3 and 5 days) and prolonged (7 days) fluid-resuscitated, antibiotic-treated sepsis (N = 123), we further documented alterations in hypothalamic CRH and AVP, plasma and pituitary POMC and its glucocorticoid-receptor-regulated processing into ACTH, as well as adrenal cortex integrity and steroidogenesis markers. The two human studies revealed several-fold elevated plasma concentrations of the ACTH precursor POMC from the acute to the prolonged phase of sepsis and upon recovery (all p < 0.0001), coinciding with the known ACTH-cortisol dissociation. Elevated plasma POMC and ACTH-corticosterone dissociation were confirmed in the mouse model. In mice, sepsis acutely increased hypothalamic mRNA of CRH (p = 0.04) and AVP (p = 0.03) which subsequently normalized. From 3 days onward, pituitary expression of CRH receptor and AVP receptor was increased. From acute throughout prolonged sepsis, pituitary POMC mRNA was always elevated (all p < 0.05). In contrast, markers of POMC processing into ACTH and of ACTH secretion, negatively regulated by glucocorticoid receptor ligand binding, were suppressed at all time points (all p ≤ 0.05). Distorted adrenocortical structure (p < 0.05) and lipid depletion (p < 0.05) were present, while most markers of adrenocortical steroidogenic activity were increased at all time points (all p < 0.05). Together, these findings suggest that increased circulating POMC, through CRH/AVP-driven POMC expression and impaired processing into ACTH, could represent a new piece in the puzzling ACTH-cortisol dissociation.

Pages

  • « first
  • ‹ previous
  • …
  • 65
  • 66
  • 67
  • 68
  • 69
  • 70
  • 71
  • 72
  • 73
  • …
  • next ›
  • last »
X
Description
sense
Example: Hs-LAG3-sense
Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe.
Intron#
Example: Mm-Htt-intron2
Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection
Pool/Pan
Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G)
A mixture of multiple probe sets targeting multiple genes or transcripts
No-XSp
Example: Hs-PDGFB-No-XMm
Does not cross detect with the species (Sp)
XSp
Example: Rn-Pde9a-XMm
designed to cross detect with the species (Sp)
O#
Example: Mm-Islr-O1
Alternative design targeting different regions of the same transcript or isoforms
CDS
Example: Hs-SLC31A-CDS
Probe targets the protein-coding sequence only
EnEmProbe targets exons n and m
En-EmProbe targets region from exon n to exon m
Retired Nomenclature
tvn
Example: Hs-LEPR-tv1
Designed to target transcript variant n
ORF
Example: Hs-ACVRL1-ORF
Probe targets open reading frame
UTR
Example: Hs-HTT-UTR-C3
Probe targets the untranslated region (non-protein-coding region) only
5UTR
Example: Hs-GNRHR-5UTR
Probe targets the 5' untranslated region only
3UTR
Example: Rn-Npy1r-3UTR
Probe targets the 3' untranslated region only
Pan
Example: Pool
A mixture of multiple probe sets targeting multiple genes or transcripts

Enabling research, drug development (CDx) and diagnostics

Contact Us
  • Toll-free in the US and Canada
  • +1877 576-3636
  • 
  • 
  • 
Company
  • Overview
  • Leadership
  • Careers
  • Distributors
  • Quality
  • News & Events
  • Webinars
  • Patents
Products
  • RNAscope or BaseScope
  • Target Probes
  • Controls
  • Manual assays
  • Automated Assays
  • Accessories
  • Software
  • How to Order
Research
  • Popular Applications
  • Cancer
  • Viral
  • Pathways
  • Neuroscience
  • Other Applications
  • RNA & Protein
  • Customer Innovations
  • Animal Models
Technology
  • Overview
  • RNA Detection
  • Spotlight Interviews
  • Publications & Guides
Assay Services
  • Our Services
  • Biomarker Assay Development
  • Cell & Gene Therapy Services
  • Clinical Assay Development
  • Tissue Bank & Sample Procurement
  • Image Analysis
  • Your Benefits
  • How to Order
Diagnostics
  • Diagnostics
  • Companion Diagnostics
Support
  • Getting started
  • Contact Support
  • Troubleshooting Guide
  • FAQs
  • Manuals, SDS & Inserts
  • Downloads
  • Webinars
  • Training Videos

Visit Bio-Techne and its other brands

  • bio-technie
  • protein
  • bio-spacific
  • rd
  • novus
  • tocris
© 2025 Advanced Cell Diagnostics, Inc.
  • Terms and Conditions of Sale
  • Privacy Policy
  • Security
  • Email Preferences
  • 
  • 
  • 

For Research Use Only. Not for diagnostic use. Refer to appropriate regulations. RNAscope is a registered trademark; and HybEZ, EZ-Batch and DNAscope are trademarks of Advanced Cell Diagnostics, Inc. in the United States and other countries. All rights reserved. ©2025 Advanced Cell Diagnostics, Inc.

 

Contact Us / Request a Quote
Download Manuals
Request a PAS Project Consultation
Order online at
bio-techne.com
OK
X
Contact Us

Complete one of the three forms below and we will get back to you.

For Quote Requests, please provide more details in the Contact Sales form below

  • Contact Sales
  • Contact Support
  • Contact Services
  • Offices

Advanced Cell Diagnostics

Our new headquarters office starting May 2016:

7707 Gateway Blvd.  
Newark, CA 94560
Toll Free: 1 (877) 576-3636
Phone: (510) 576-8800
Fax: (510) 576-8798

 

Bio-Techne

19 Barton Lane  
Abingdon Science Park
Abingdon
OX14 3NB
United Kingdom
Phone 2: +44 1235 529449
Fax: +44 1235 533420

 

Advanced Cell Diagnostics China

20F, Tower 3,
Raffles City Changning Office,
1193 Changning Road, Shanghai 200051

021-52293200
info.cn@bio-techne.com
Web: www.acdbio.com/cn

For general information: Info.ACD@bio-techne.com
For place an order: order.ACD@bio-techne.com
For product support: support.ACD@bio-techne.com
For career opportunities: hr.ACD@bio-techne.com

See Distributors
×

You have already Quick ordered an Item in your cart . If you want to add a new item , Quick ordered Item will be removed form your cart. Do You want to continue?

OK Cancel
Need help?

How can we help you?