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 (497)
  • Image gallery (0)
Refine Probe List

Content for comparison

Gene

  • HPV E6/E7 (30) Apply HPV E6/E7 filter
  • Lgr5 (20) Apply Lgr5 filter
  • PD-L1 (9) Apply PD-L1 filter
  • Axin2 (6) Apply Axin2 filter
  • FGFR1 (6) Apply FGFR1 filter
  • IFN-γ (5) Apply IFN-γ filter
  • HER2 (5) Apply HER2 filter
  • OLFM4 (5) Apply OLFM4 filter
  • MALAT1 (4) Apply MALAT1 filter
  • Wnt4 (4) Apply Wnt4 filter
  • Wnt5a (4) Apply Wnt5a filter
  • MYC (4) Apply MYC filter
  • OLFM4 (4) Apply OLFM4 filter
  • PTEN (4) Apply PTEN filter
  • TERT (4) Apply TERT filter
  • TNF-α (4) Apply TNF-α filter
  • TGF-β (4) Apply TGF-β filter
  • IL-17A (4) Apply IL-17A filter
  • HPV (4) Apply HPV filter
  • AR-V7 (4) Apply AR-V7 filter
  • Wnt7a (3) Apply Wnt7a filter
  • AR (3) Apply AR filter
  • BRCA1 (3) Apply BRCA1 filter
  • MET (3) Apply MET filter
  • CXCL10 (3) Apply CXCL10 filter
  • HEY2 (3) Apply HEY2 filter
  • HOTAIR (3) Apply HOTAIR filter
  • IL-10 (3) Apply IL-10 filter
  • H19 (3) Apply H19 filter
  • HIV (3) Apply HIV filter
  • Lgr4 (3) Apply Lgr4 filter
  • COL11A1 (3) Apply COL11A1 filter
  • ASPM (3) Apply ASPM filter
  • IL-8 (3) Apply IL-8 filter
  • VEGF (3) Apply VEGF filter
  • Il-6 (3) Apply Il-6 filter
  • MERS-CoV (3) Apply MERS-CoV filter
  • HPV HR7 (3) Apply HPV HR7 filter
  • LINC00473 (3) Apply LINC00473 filter
  • PD-l2 (3) Apply PD-l2 filter
  • HIV-1 (3) Apply HIV-1 filter
  • TNFA (3) Apply TNFA filter
  • CD274 (2) Apply CD274 filter
  • TGFB1 (2) Apply TGFB1 filter
  • Wnt10a (2) Apply Wnt10a filter
  • Wnt10b (2) Apply Wnt10b filter
  • Wnt16 (2) Apply Wnt16 filter
  • Wnt1 (2) Apply Wnt1 filter
  • Wnt6 (2) Apply Wnt6 filter
  • Wnt7b (2) Apply Wnt7b filter

Product

  • (-) Remove RNAscope 2.0 Assay filter RNAscope 2.0 Assay (497)

Research area

  • Cancer (244) Apply Cancer filter
  • Infectious Disease (87) Apply Infectious Disease filter
  • Other (72) Apply Other filter
  • Neuroscience (50) Apply Neuroscience filter
  • Inflammation (38) Apply Inflammation filter
  • lncRNA (36) Apply lncRNA filter
  • HPV (34) Apply HPV filter
  • Stem Cells (28) Apply Stem Cells filter
  • Developmental (14) Apply Developmental filter
  • diabetes (14) Apply diabetes filter
  • Immunotherapy (11) Apply Immunotherapy filter
  • Development (9) Apply Development filter
  • Stem cell (5) Apply Stem cell filter
  • Infectious (3) Apply Infectious filter
  • LncRNAs (3) Apply LncRNAs filter
  • Metabolism (3) Apply Metabolism filter
  • Diet (2) Apply Diet filter
  • Infammation (2) Apply Infammation filter
  • Reproduction (2) Apply Reproduction filter
  • Alzheimer's Disease (1) Apply Alzheimer's Disease filter
  • Colon (1) Apply Colon filter
  • Endocrinology-Development (1) Apply Endocrinology-Development filter
  • Excretory (1) Apply Excretory filter
  • Eyes (1) Apply Eyes filter
  • Gut (1) Apply Gut filter
  • Gut microbiome (1) Apply Gut microbiome filter
  • Heart (1) Apply Heart filter
  • HIV (1) Apply HIV filter
  • Hypertension (1) Apply Hypertension filter
  • Hypoglycemia (1) Apply Hypoglycemia filter
  • Infectious Disease: Epstein-Barr virus (1) Apply Infectious Disease: Epstein-Barr virus filter
  • Infectiouse Disease: Yellow Fever (1) Apply Infectiouse Disease: Yellow Fever filter
  • Inflammatory Bowel Disease (1) Apply Inflammatory Bowel Disease filter
  • Intestinal Stem Cells (1) Apply Intestinal Stem Cells filter
  • IO (1) Apply IO filter
  • Kidney (1) Apply Kidney filter
  • Lnc (1) Apply Lnc filter
  • Locomotion (1) Apply Locomotion filter
  • Lung (1) Apply Lung filter
  • Metabolic (1) Apply Metabolic filter
  • Nonalcoholic Fatty Liver Disease (1) Apply Nonalcoholic Fatty Liver Disease filter
  • Other: Liver (1) Apply Other: Liver filter
  • Other: Metabolism (1) Apply Other: Metabolism filter
  • Parasite (1) Apply Parasite filter
  • Sex Differences (1) Apply Sex Differences filter
  • Signalling (1) Apply Signalling filter
  • Skin (1) Apply Skin filter
  • Tumourigenesis (1) Apply Tumourigenesis filter
  • Wound healing (1) Apply Wound healing filter

Category

  • Publications (497) Apply Publications filter
Lgr5+ cells regenerate hair cells via proliferation and direct transdifferentiation in damaged neonatal mouse utricle

Nat Commun. 2015 Apr 7;6:6613.

Wang T, Chai R, Kim GS, Pham N, Jansson L, Nguyen DH, Kuo B, May LA, Zuo J, Cunningham LL, Cheng AG.
PMID: 25849379 | DOI: 10.1038/ncomms7613.

Recruitment of endogenous progenitors is critical during tissue repair. The inner ear utricle requires mechanosensory hair cells (HCs) to detect linear acceleration. After damage, non-mammalian utricles regenerate HCs via both proliferation and direct transdifferentiation. In adult mammals, limited transdifferentiation from unidentified progenitors occurs to regenerate extrastriolar Type II HCs. Here we show that HC damage in neonatal mouse utricle activates the Wnt target gene Lgr5 in striolar supporting cells. Lineage tracing and time-lapse microscopy reveal that Lgr5+ cells transdifferentiate into HC-like cells in vitro. In contrast to adults, HC ablation in neonatal utricles in vivo recruits Lgr5+ cells to regenerate striolar HCs through mitotic and transdifferentiation pathways. Both Type I and II HCs are regenerated, and regenerated HCs display stereocilia and synapses. Lastly, stabilized ß-catenin in Lgr5+ cells enhances mitotic activity and HC regeneration. Thus Lgr5 marks Wnt-regulated, damage-activated HC progenitors and may help uncover factors driving mammalian HC regeneration.
Pharmacological stimulation of Edar signaling in the adult enhances sebaceous gland size and function.

J Invest Dermatol. 2015 Feb;135(2):359-68.

Kowalczyk-Quintas C, Schuepbach-Mallepell S, Willen L, Smith TK, Huttner K, Kirby N, Headon DJ, Schneider P.

Impaired ectodysplasin A (EDA) receptor (EDAR) signaling affects ectodermally derived structures including teeth, hair follicles, and cutaneous glands. The X-linked hypohidrotic ectodermal dysplasia (XLHED), resulting from EDA deficiency, can be rescued with lifelong benefits in animal models by stimulation of ectodermal appendage development with EDAR agonists. Treatments initiated later in the developmental period restore progressively fewer of the affected structures. It is unknown whether EDAR stimulation in adults with XLHED might have beneficial effects. In adult Eda mutant mice treated for several weeks with agonist anti-EDAR antibodies, we find that sebaceous gland size and function can be restored to wild-type levels. This effect is maintained upon chronic treatment but reverses slowly upon cessation of treatment. Sebaceous glands in all skin regions respond to treatment, although to varying degrees, and this is accompanied in both Eda mutant and wild-type mice by sebum secretion to levels higher than those observed in untreated controls. Edar is expressed at the periphery of the glands, suggesting a direct homeostatic effect of Edar stimulation on the sebaceous gland. Sebaceous gland size and sebum production may serve as biomarkers for EDAR stimulation, and EDAR agonists may improve skin dryness and eczema frequently observed in XLHED.
Local expression of complement factor I in breast cancer cells correlates with poor survival and recurrence

Cancer Immunol Immunother. 2015 Jan 25.

Okroj M, Holmquist E, Nilsson E, Anagnostaki L, Jirström K, Blom AM.
PMID: 25618258

Tumor cells often evade killing by the complement system by overexpressing membrane-bound complement inhibitors. However, production of soluble complement inhibitors in cells other than hepatocytes was rarely reported. We screened several breast cancer cell lines for expression of soluble complement inhibitor, complement factor I (FI). We also analyzed local production of FI in tissue microarrays with tumors from 130 breast cancer patients by in situ hybridization and immunohistochemistry. We found expression of FI in breast adenocarcinoma cell line MDA-MB-468 and confirmed its functional activity. Expression of FI at mRNA and protein levels was also confirmed in tumor cells and tumor stroma, both in fibroblasts and infiltrating immune cells. Multivariate Cox regression analyses revealed that high expression of FI protein in tumor cells was correlated with significantly shorter cancer-specific survival (HR 2.8; 95 % CI 1.0–7.5; p = 0.048) and recurrence-free survival (HR 3.4; 95 % CI 1.5–7.4; p = 0.002). High FI expression was positively correlated with tumor size (p < 0.001), and Nottingham histological grade (p = 0.015) and associated with estrogen and progesterone receptor status (p = 0.03 and p = 0.009, respectively). Our data show that FI is expressed in breast cancer and is associated with unfavorable clinical outcome.
Mucoepidermoid Carcinoma Does Not Harbor Transcriptionally Active High Risk Human Papillomavirus Even in the Absence of the MAML2 Translocation

Head Neck Pathol. 2014 Apr 5

Bishop JA, Yonescu R, Batista D, Yemelyanova A, Ha PK, Westra WH
PMID: 24706055 | DOI: 10.1007/s12105-014-0541-9

High risk human papillomavirus (HPV) is firmly established as an important cause of oropharyngeal carcinoma. Recent studies have also implicated HPV as a cause of mucoepidermoid carcinoma (MEC)—a tumor of salivary gland origin that frequently harbors MAML2 translocations. The purpose of this study was to determine the prevalence of transcriptionally active HPV in a large group of MECs and to determine whether HPV infection and the MAML2 translocation are mutually exclusive events. Break-apart fluorescence in situ hybridization for MAML2 was performed on a tissue microarray containing 92 MECs. HPV testing was performed using RNA in situ hybridization targeting high risk HPV mRNA E6/E7 transcripts. Of the 71 MECs that could be evaluated by FISH, 57 (80 %) harbored the MAML2 rearrangement. HPV was not detected in any of the 57 MECs that contained a MAML2 rearrangement, in any of the 14 MECs that did not contain the rearrangement, or in any of the 21 MECs where MAML2 status was unknown. High risk HPV does not appear to play any significant role in the development of MEC. It neither complements nor replaces MAML2 translocation in the tumorigenesis of MEC
Disruption of murine Adamtsl4 results in zonular fiber detachment from the lens and retinal pigment epithelium dedifferentiation.

Hum Mol Genet.

2015 Sep 24

Collin GB, Hubmacher D, Charette JR, Hicks WL, Stone L, Yu M, Naggert JK, Krebs MP, Peachey NS, Apte SS, Nishina PM.
PMID: 26405179 | DOI: -

Human gene mutations have revealed that a significant number of ADAMTS (a disintegrin-like and metalloproteinase (reprolysin type) with thrombospondin-type 1 motifs) proteins are necessary for normal ocular development and eye function. Mutations in human ADAMTSL4, encoding an ADAMTS-like protein which has been implicated in fibrillin microfibril biogenesis, cause ectopia lentis (EL) and EL et pupillae. Here, we report the first ADAMTSL4 mouse model, tvrm267, bearing a nonsense mutation in Adamtsl4. Homozygous Adamtsl4tvrm267 mice recapitulate the EL phenotype observed in humans, and our analysis strongly suggests that ADAMTSL4 is required for stable anchorage of zonule fibers to the lens capsule. Unexpectedly, homozygous Adamtsl4tvrm267 mice exhibit focal retinal pigment epithelium (RPE) defects primarily in the inferior eye. RPE dedifferentiation was indicated by reduced pigmentation, altered cellular morphology, and a reduction in RPE-specific transcripts. Finally, as with a subset of patients with ADAMTSL4 mutations, increased axial length, relative to age-matched controls, was observed and was associated with the severity of the RPE phenotype. In summary, the Adamtsl4tvrm267 model provides a valuable tool to further elucidate the molecular basis of zonule formation, the pathophysiology of ectopia lentis and ADAMTSL4 function in the maintenance of the RPE.

Aspm sustains postnatal cerebellar neurogenesis and medulloblastoma growth in mice.

Development.

2015 Nov 15

Williams SE, Garcia I, Crowther AJ, Li S, Stewart A, Liu H, Lough KJ, O'Neill S, Veleta K, Oyarzabal EA, Merrill JR, Shih YY, Gershon TR.
PMID: 26450969 | DOI: 10.1242/dev.124271

Alterations in genes that regulate brain size may contribute to both microcephaly and brain tumor formation. Here, we report that Aspm, a gene that is mutated in familial microcephaly, regulates postnatal neurogenesis in the cerebellum and supports the growth of medulloblastoma, the most common malignant pediatric brain tumor. Cerebellar granule neuron progenitors (CGNPs) express Aspm when maintained in a proliferative state by sonic hedgehog (Shh) signaling, and Aspm is expressed in Shh-driven medulloblastoma in mice. Genetic deletion of Aspm reduces cerebellar growth, while paradoxically increasing the mitotic rate of CGNPs. Aspm-deficient CGNPs show impaired mitotic progression, altered patterns of division orientation and differentiation, and increased DNA damage, which causes progenitor attrition through apoptosis. Deletion of Aspm in mice with Smo-induced medulloblastoma reduces tumor growth and increases DNA damage. Co-deletion of Aspm and either of the apoptosis regulators Bax or Trp53 (also known as p53) rescues the survival of neural progenitors and reduces the growth restriction imposed by Aspm deletion. Our data show that Aspm functions to regulate mitosis and to mitigate DNA damage during CGNP cell division, causes microcephaly through progenitor apoptosis when mutated, and sustains tumor growth in medulloblastoma.

Decreased FOXJ1 expression and its ciliogenesis program in aggressive ependymoma and choroid plexus tumours.

J Pathol.

2015 Dec 22

Abedalthagafi MS, Wu MP, Merrill PH, Du Z, Woo T, Sheu SH, Hurwitz S, Ligon KL, Santagata S.
PMID: 26690880 | DOI: 10.1002/path.4682.

Well-differentiated human cancers share transcriptional programs with the normal tissue counterparts from which they arise. These programs broadly influence cell behaviour and function and are integral modulators of malignancy. Here, we show that the master regulator of motile ciliogenesis, FOXJ1, is highly expressed in cells along the ventricular surface of the human brain. Strong expression is present in cells of the ependyma and the choroid plexus as well as in a subset of cells residing in the subventricular zone. Expression of FOXJ1 and its transcriptional program is maintained in many well-differentiated human tumours that arise along the ventricle, including low-grade ependymal tumours and choroid plexus papilloma. Anaplastic ependymoma as well as choroid plexus carcinoma show decreased FOXJ1 expression and its associated ciliogenesis program genes. In ependymoma and choroid plexus tumours, reduced expression of FOXJ1 and its ciliogenesis program are markers of poor outcome and are therefore useful biomarkers for assessing these tumours. Transitions in ciliogenesis define distinct differentiation states in ependymal and choroid plexus tumours with important implications for patient care.

APOBEC3B expression in drug resistant MCF-7 breast cancer cell lines

Biomedicine & Pharmacotherapy

2016 Feb 16

Ongurua O, Yalcinc S, Rosemblitd C, Zhangb PJ, Kilice S, Gunduzf U.
PMID: - | DOI: 10.1016/j.biopha.2016.02.004

APOBEC3B belongs to a protein family of cytidine deaminases that can insert mutations in DNA and RNA as a result of their ability to deaminate cytidine to uridine. It has been shown that APOBEC3B-catalysed deamination provides a chronic source of DNA damage in breast cancers. We investigated APOBEC3B expression in four drug resistant breast cancer cell lines (Doxorubicin, Etoposide, Paclitaxel and Docetaxel resistant MCF-7 cell lines) using a novel RNA in situ hybridization technology (RNAscope) and compared expression levels with drug sensitive MCF-7 cell line. After RNAscope staining, slides were scanned and saved as digital images using Aperio scanner and software. Quantitative scoring utilizing the number of punctate dots present within each cell boundary was performed for the parameters including positive cell percentage and signal intensity per positive cell. In Doxorubicin and Etoposide resistant MCF-7 cell lines, APOBEC3B expression was approximately five-fold increased (23% and 24% respectively) with higher signal intensity (1.92 and 1.44 signal/cell, respectively) compared to drug sensitive MCF-7 cell line (5%, 1.00 signal/cell) with statistical significance. The increase of APOBEC3B expression in Docataxel resitant and Paclitaxel resistant MCF-7 cell lines was not very high. In conclusion, APOBEC3B expression was increased in some population of tumor cells of drug resistant cell lines. At least for some drugs, APOBEC3B expression may be related to drug resistance, subjecting to some tumor cells to frequent mutation.

A new protoparvovirus in human fecal samples and cutaneous T cell lymphomas (mycosis fungoides).

Virology

2016 Jul 06

Phan TG, Dreno B, da Costa AC, Li L, Orlandi P, Deng X, Kapusinszky B, Siqueira J, Knol AC, Halary F, Dantal J, Alexander KA, Pesavento PA, Delwart E.
PMID: 27393975 | DOI: 10.1016/j.virol.2016.06.013

We genetically characterized seven nearly complete genomes in the protoparvovirus genus from the feces of children with diarrhea. The viruses, provisionally named cutaviruses (CutaV), varied by 1-6% nucleotides and shared ~76% and ~82% amino acid identity with the NS1 and VP1 of human bufaviruses, their closest relatives. Using PCR, cutavirus DNA was found in 1.6% (4/245) and 1% (1/100) of diarrhea samples from Brazil and Botswana respectively. In silico analysis of pre-existing metagenomics datasets then revealed closely related parvovirus genomes in skin biopsies from patients with epidermotropic cutaneous T-cell lymphoma (CTCL or mycosis fungoides). PCR of skin biopsies yielded cutavirus DNA in 4/17 CTCL, 0/10 skin carcinoma, and 0/21 normal or noncancerous skin biopsies. In situ hybridization of CTCL skin biopsies detected viral genome within rare individual cells in regions of neoplastic infiltrations. The influence of cutavirus infection on human enteric functions and possible oncolytic role in CTCL progression remain to be determined.

Favorable prognosis in colorectal cancer patients with co-expression of c-MYC and ß-catenin.

BMC Cancer.

2016 Sep 13

Lee KS, Kwak Y, Nam KH, Kim DW, Kang SB, Choe G, Kim WH, Lee HS.
PMID: 27619912 | DOI: 10.1186/s12885-016-2770-7

BACKGROUND:

The purpose of our research was to determine the prognostic impact and clinicopathological feature of c-MYC and β-catenin overexpression in colorectal cancer (CRC) patients.

METHODS:

Using immunohistochemistry (IHC), we measured the c-MYC and β-catenin expression in 367 consecutive CRC patientsretrospectively (cohort 1). Also, c-MYC expression was measured by mRNA in situ hybridization. Moreover, to analyze regional heterogeneity, three sites of CRC including the primary, distant and lymph node metastasis were evaluated in 176 advanced CRC patients (cohort 2).

RESULTS:

In cohort 1, c-MYC protein and mRNA overexpression and ß-catenin nuclear expression were found in 201 (54.8 %), 241 (65.7 %) and 221 (60.2 %) of 367 patients, respectively, each of which was associated with improved prognosis (P = 0.011, P = 0.012 and P = 0.033, respectively). Moreover, co-expression of c-MYC and ß-catenin was significantly correlated with longer survival by univariate (P = 0.012) and multivariate (P = 0.048) studies. Overexpression of c-MYC protein was associated with mRNA overexpression (ρ, 0.479; P < 0.001) and nuclear ß-catenin expression (ρ, 0.282; P < 0.001). Expression of c-MYC and ß-catenin was heterogeneous depending on location in advanced CRCpatients (cohort 2). Nevertheless, both c-MYC and ß-catenin expression in primary cancer were significantly correlated with improved survival in univariate (P = 0.001) and multivariate (P = 0.002) analyses. c-MYC and ß-catenin expression of lymph node or distant metastatic tumor was not significantly correlated with patients' prognosis (P > 0.05).

CONCLUSIONS:

Co-expression of c-MYC and ß-catenin was independently correlated with favorable prognosis in CRC patient. We concluded that the expression of c-MYC and ß-catenin might be useful predicting indicator of CRC patient's prognosis.

Gremlin1 plays a key role in kidney development and renal fibrosis

Am J Physiol Renal Physiol.

2017 Jan 18

Church RH, Ali I, Tate M, Lavin D, Krishnakumar A, Kok HM, Goldschmeding R, Martin F, Brazil D.
PMID: 28100499 | DOI: 10.1152/ajprenal.00344.2016

Grem1, an antagonist of bone morphogenetic proteins, plays a key role in embryogenesis. A highly specific temporospatial gradient of Grem1 and BMP signalling is critical to normal lung, kidney and limb development. Grem1 levels are increased in renal fibrotic conditions including acute kidney injury, diabetic nephropathy, chronic allograft nephropathy and immune glomerulonephritis. A small number of grem1-/- whole body knockout mice on a mixed genetic background (8 %) are viable, with a single, enlarged left kidney and grossly normal histology. Grem1-/- mice displayed mild renal dysfunction at 4 wk, which recovered by 16 wk. Tubular epithelial specific targeted deletion of Grem1 (Grem1-TEC-/-) mice displayed a milder response in both the acute injury and recovery phase of the folic acid model. Grem1-TEC-/- mice had smaller increases in indices of kidney damage compared to wild-type. In the recovery phase of the folic acid model, associated with renal fibrosis, Grem1-TEC-/- mice displayed reduced histological damage and an attenuated fibrotic gene response compared to wild-type controls. Together, these data demonstrated that Grem1 expression in the tubular epithelial compartment plays a significant role in the fibrotic response to renal injury in vivo.

Oncogenic S1P signalling in EBV-associated nasopharyngeal carcinoma activates AKT and promotes cell migration through S1P receptor 3

J Pathol.

2017 Feb 27

Lee HM, Lo KW, Wei W, Tsao SW, Chung GT, Ibrahim MH, Dawson CW, Murray PG, Paterson IC, Yap LF.
PMID: 28240350 | DOI: 10.1002/path.4879

Undifferentiated nasopharyngeal carcinoma (NPC) is a cancer with high metastatic potential that is consistently associated with Epstein-Barr virus (EBV) infection. In this study, we have investigated the functional contribution of sphingosine-1-phosphate (S1P) signalling to the pathogenesis of NPC. We show that EBV infection or ectopic expression of the EBV-encoded latent genes (EBNA1, LMP1 and LMP2A) can up-regulate sphingosine kinase 1 (SPHK1), the key enzyme that produces S1P, in NPC cell lines. Exogenous addition of S1P promotes the migration of NPC cells through the activation of AKT; shRNA knockdown of SPHK1 resulted in a reduction in the levels of activated AKT and inhibition of cell migration. We also show that S1P receptor 3 (S1PR3) mRNA is over-expressed in EBV-positive NPC patient-derived xenografts and a subset of primary NPC tissues, and that knockdown of S1PR3 suppressed the activation of AKT and the S1P-induced migration of NPC cells. Taken together, our data point to a central role for EBV in mediating the oncogenic effects of S1P in NPC and identify S1P signalling as a potential therapeutic target in this disease.

Pages

  • « first
  • ‹ previous
  • …
  • 9
  • 10
  • 11
  • 12
  • 13
  • 14
  • 15
  • 16
  • 17
  • …
  • 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?