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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.

Your search for "INS" returned results. Search for our Top genes LGR5, vglut2, gad67, brca1

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    Gene

    • HPV E6/E7 (30) Apply HPV E6/E7 filter
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    Category

    • Publications (4) Apply Publications filter
    Long non-coding RNA chromogenic in situ hybridisation signal pattern correlation with breast tumour pathology.

    J Clin Pathol.

    2015 Aug 31

    Zhang Z, Weaver DL, Olsen D, deKay J, Peng Z, Ashikaga T, Evans MF.
    PMID: 26323944 | DOI: 10.1136/jclinpath-2015-203275

    Abstract

    AIM:
    Long non-coding RNAs (lncRNAs) are potential biomarkers for breast cancer risk stratification. LncRNA expression has been investigated primarily by RNA sequencing, quantitative reverse transcription PCR or microarray techniques. In this study, six breast cancer-implicated lncRNAs were investigated by chromogenic in situ hybridisation (CISH).

    METHODS:
    Invasive breast carcinoma (IBC), ductal carcinoma in situ (DCIS) and normal adjacent (NA) breast tissues from 52 patients were screened by CISH. Staining was graded by modified Allred scoring.

    RESULTS:
    HOTAIR, H19 and KCNQ1OT1 had significantly higher expression levels in IBC and DCIS than NA (p<0.05), and HOTAIR and H19 were expressed more strongly in IBC than in DCIS tissues (p<0.05). HOTAIR and KCNQ101T were expressed in tumour cells; H19 and MEG3 were expressed in stromal microenvironment cells; MALAT1 was expressed in all cells strongly and ZFAS1 was negative or weakly expressed in all specimens.

    CONCLUSION:
    These data corroborate the involvement of three lncRNAs (HOTAIR, H19 and KCNQ1OT1) in breast tumourigenesis and support lncRNA CISH as a potential clinical assay. Importantly, CISH allows identification of the tissue compartment expressing lncRNA.

    Intestinal Stem Cell Markers in the Intestinal Metaplasia of Stomach and Barrett's Esophagus.

    PLoS One. 2015 May 21;10(5):e0127300.

    Jang BG, Lee BL, Kim WH.
    PMID: 26015511 | DOI: clincanres.3357.2014.

    Gastric intestinal metaplasia (IM) is a highly prevalent preneoplastic lesion; however, the molecular mechanisms regulating its development remain unclear. We have previously shown that a population of cells expressing the intestinal stem cell (ISC) marker LGR5 increases remarkably in IM. In this study, we further investigated the molecular characteristics of these LGR5+ cells in IM by examining the expression profile of several ISC markers. Notably, we found that ISC markers-including OLFM4 and EPHB2-are positively associated with the CDX2 expression in non-tumorous gastric tissues. This finding was confirmed in stomach lesions with or without metaplasia, which demonstrated that OLFM4 and EPHB2 expression gradually increased with metaplastic progression. Moreover, RNA in situ hybridization revealed that LGR5+ cells coexpress several ISC markers and remained confined to the base of metaplastic glands, reminiscent to that of normal intestinal crypts, whereas those in normal antral glands expressed none of these markers. Furthermore, a large number of ISC marker-expressing cells were diffusely distributed in gastric adenomas, suggesting that these markers may facilitate gastric tumorigenesis. In addition, Barrett's esophagus (BE)-which is histologically similar to intestinal metaplasia-exhibited a similar distribution of ISC markers, indicating the presence of a stem cell population with intestinal differentiation potential. In conclusion, we identified that LGR5+ cells in gastric IM and BE coexpress ISC markers, and exhibit the same expression profile as those found in normal intestinal crypts. Taken together, these results implicate an intestinal-like stem cell population in the pathogenesis of IM, and provide an important basis for understanding the development and maintenance of this disease.
    Long Non-Coding RNA H19 Prevents Lens Fibrosis through Maintaining Lens Epithelial Cell Phenotypes

    Cells

    2022 Aug 17

    Xiong, L;Sun, Y;Huang, J;Ma, P;Wang, X;Wang, J;Chen, B;Chen, J;Huang, M;Huang, S;Liu, Y;
    PMID: 36010635 | DOI: 10.3390/cells11162559

    The integrity of lens epithelial cells (LECs) lays the foundation for lens function and transparency. By contrast, epithelial-mesenchymal transition (EMT) of LECs leads to lens fibrosis, such as anterior subcapsular cataracts (ASC) and fibrotic forms of posterior capsule opacification (PCO). However, the underlying mechanisms remain unclear. Here, we aimed to explore the role of long non-coding RNA (lncRNA) H19 in regulating TGF-β2-induced EMT during lens fibrosis, revealing a novel lncRNA-based regulatory mechanism. In this work, we identified that lncRNA H19 was highly expressed in LECs, but downregulated by exposure to TGF-β2. In both human lens epithelial explants and SRA01/04 cells, knockdown of H19 aggravated TGF-β2-induced EMT, while overexpressing H19 partially reversed EMT and restored lens epithelial phenotypes. Semi-in vivo whole lens culture and H19 knockout mice demonstrated the indispensable role of H19 in sustaining lens clarity through maintaining LEC features. Bioinformatic analyses further implied a potential H19-centered regulatory mechanism via Smad-dependent pathways, confirmed by in vitro experiments. In conclusion, we uncovered a novel role of H19 in inhibiting TGF-β2-induced EMT of the lens by suppressing Smad-dependent signaling, providing potential therapeutic targets for treating lens fibrosis.
    Functional significance of gain-of-function H19 lncRNA in skeletal muscle differentiation and anti-obesity effects

    Genome medicine

    2021 Aug 28

    Li, Y;Zhang, Y;Hu, Q;Egranov, SD;Xing, Z;Zhang, Z;Liang, K;Ye, Y;Pan, Y;Chatterjee, SS;Mistretta, B;Nguyen, TK;Hawke, DH;Gunaratne, PH;Hung, MC;Han, L;Yang, L;Lin, C;
    PMID: 34454586 | DOI: 10.1186/s13073-021-00937-4

    Exercise training is well established as the most effective way to enhance muscle performance and muscle building. The composition of skeletal muscle fiber type affects systemic energy expenditures, and perturbations in metabolic homeostasis contribute to the onset of obesity and other metabolic dysfunctions. Long noncoding RNAs (lncRNAs) have been demonstrated to play critical roles in diverse cellular processes and diseases, including human cancers; however, the functional importance of lncRNAs in muscle performance, energy balance, and obesity remains elusive. We previously reported that the lncRNA H19 regulates the poly-ubiquitination and protein stability of dystrophin (DMD) in muscular dystrophy.Here, we identified mouse/human H19-interacting proteins using mouse/human skeletal muscle tissues and liquid chromatography-mass spectrometry (LC-MS). Human induced pluripotent stem-derived skeletal muscle cells (iPSC-SkMC) from a healthy donor and Becker Muscular Dystrophy (BMD) patients were utilized to study DMD post-translational modifications and associated proteins. We identified a gain-of-function (GOF) mutant of H19 and characterized the effects on myoblast differentiation and fusion to myotubes using iPSCs. We then conjugated H19 RNA gain-of-function oligonucleotides (Rgof) with the skeletal muscle enrichment peptide agrin (referred to as AGR-H19-Rgof) and evaluated AGR-H19-Rgof's effects on skeletal muscle performance using wild-type (WT) C57BL/6 J mice and its anti-obesity effects using high-fat diet (HFD)- and leptin deficiency-induced obese mouse models.We demonstrated that both human and mouse H19 associated with DMD and that the H19 GOF exhibited enhanced interaction with DMD compared to WT H19. DMD was found to associate with serine/threonine-protein kinase MRCK alpha (MRCKα) and α-synuclein (SNCA) in iPSC-SkMC derived from BMD patients. Inhibition of MRCKα and SNCA-mediated phosphorylation of DMD antagonized the interaction between H19 and DMD. These signaling events led to improved skeletal muscle cell differentiation and myotube fusion. The administration of AGR-H19-Rgof improved the muscle mass, muscle performance, and base metabolic rate of WT mice. Furthermore, mice treated with AGR-H19-Rgof exhibited resistance to HFD- or leptin deficiency-induced obesity.Our study suggested the functional importance of the H19 GOF mutant in enhancing muscle performance and anti-obesity effects.
    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

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