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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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    Intraamniotic Zika virus inoculation of pregnant rhesus macaques produces fetal neurologic disease

    Nat. Commun.

    2018 Jun 20

    Coffey LL, Keesler RI, Pesavento PA, Woolard K, Singapuri A, Watanabe J, Cruzen C, Christe KL, Usachenko J, Yee JA, Heng VA, Bliss-Moreau E, Reader JR, von Morgenland W, Gibbons AM, Jackson K, Ardeshir A, Heimsath H, Permar S, Senthamaraikannan P, Presicc
    PMID: - | DOI: 10.1038/s41467-018-04777-6

    Zika virus (ZIKV) infection of pregnant women can cause fetal microcephaly and other neurologic defects. We describe the development of a non-human primate model to better understand fetal pathogenesis. To reliably induce fetal infection at defined times, four pregnant rhesus macaques are inoculated intravenously and intraamniotically with ZIKV at gestational day (GD) 41, 50, 64, or 90, corresponding to first and second trimester of gestation. The GD41-inoculated animal, experiencing fetal death 7 days later, has high virus levels in fetal and placental tissues, implicating ZIKV as cause of death. The other three fetuses are carried to near term and euthanized; while none display gross microcephaly, all show ZIKV RNA in many tissues, especially in the brain, which exhibits calcifications and reduced neural precursor cells. Given that this model consistently recapitulates neurologic defects of human congenital Zika syndrome, it is highly relevant to unravel determinants of fetal neuropathogenesis and to explore interventions.

    A ZNRF3-dependent Wnt/β-catenin signaling gradient is required for adrenal homeostasis.

    Genes Dev.

    2019 Jan 28

    Basham KJ, Rodriguez S, Turcu AF, Lerario AM, Logan CY, Rysztak MR, Gomez-Sanchez CE, Breault DT, Koo BK, Clevers H, Nusse R, Val P, Hammer GD.
    PMID: 30692207 | DOI: 10.1101/gad.317412.118

    Spatiotemporal control of Wnt signaling is essential for the development and homeostasis of many tissues. The transmembrane E3 ubiquitin ligases ZNRF3 (zinc and ring finger 3) and RNF43 (ring finger protein 43) antagonize Wnt signaling by promoting degradation of frizzled receptors. ZNRF3 and RNF43 are frequently inactivated in human cancer, but the molecular and therapeutic implications remain unclear. Here, we demonstrate that adrenocortical-specific loss of ZNRF3, but not RNF43, results in adrenal hyperplasia that depends on Porcupine-mediated Wnt ligand secretion. Furthermore, we discovered a Wnt/β-catenin signaling gradient in the adrenal cortex that is disrupted upon loss of ZNRF3. Unlike β-catenin gain-of-function models, which induce high Wnt/β-catenin activation and expansion of the peripheral cortex, ZNRF3 loss triggers activation of moderate-level Wnt/β-catenin signaling that drives proliferative expansion of only the histologically and functionally distinct inner cortex. Genetically reducing β-catenin dosage significantly reverses the ZNRF3-deficient phenotype. Thus, homeostatic maintenance of the adrenal cortex is dependent on varying levels of Wnt/β-catenin activation, which is regulated by ZNRF3.

    CARMIL2 Deficiency Presenting as Very Early Onset Inflammatory Bowel Disease.

    Inflamm Bowel Dis

    2019 May 22

    Magg T, Shcherbina A, Arslan D, Desai MM, Wall S, Mitsialis V, Conca R, Unal E, Karacabey N, Mukhina A, Rodina Y, Taur PD, Illig D, Marquardt B, Hollizeck S, Jeske T, Gothe F, Schober T, Rohlfs M, Koletzko S, Lurz E, Muise AM, Snapper SB, Hauck F, Klein C, Kotlarz D.
    PMID: 31115454 | DOI: 10.1093/ibd/izz103

    BACKGROUND:

    Children with very early onset inflammatory bowel diseases (VEO-IBD) often have a refractory and severe disease course. A significant number of described VEO-IBD-causing monogenic disorders can be attributed to defects in immune-related genes. The diagnosis of the underlying primary immunodeficiency (PID) often has critical implications for the treatment of patients with IBD-like phenotypes.

    METHODS:

    To identify the molecular etiology in 5 patients from 3 unrelated kindred with IBD-like symptoms, we conducted whole exome sequencing. Immune workup confirmed an underlying PID.

    RESULTS:

    Whole exome sequencing revealed 3 novel CARMIL2 loss-of-function mutations in our patients. Immunophenotyping of peripheral blood mononuclear cells showed reduction of regulatory and effector memory T cells and impaired B cell class switching. The T cell proliferation and activation assays confirmed defective responses to CD28 costimulation, consistent with CARMIL2 deficiency.

    CONCLUSION:

    Our study highlights that human CARMIL2 deficiency can manifest with IBD-like symptoms. This example illustrates that early diagnosis of underlying PID is crucial for the treatment and prognosis of children with VEO-IBD.

    Robust Colonic Epithelial Regeneration and Amelioration of Colitis via FZD-Specific Activation of Wnt Signaling

    Cellular and molecular gastroenterology and hepatology

    2022 May 13

    Xie, L;Fletcher, RB;Bhatia, D;Shah, D;Phipps, J;Deshmukh, S;Zhang, H;Ye, J;Lee, S;Le, L;Newman, M;Chen, H;Sura, A;Gupta, S;Sanman, LE;Yang, F;Meng, W;Baribault, H;Vanhove, GF;Yeh, WC;Li, Y;Lu, C;
    PMID: 35569814 | DOI: 10.1016/j.jcmgh.2022.05.003

    Current management of inflammatory bowel disease leaves a clear unmet need to treat the severe epithelial damage. Modulation of Wnt signaling might present an opportunity to achieve histological remission and mucosal healing when treating IBD. Exogenous R-spondin, which amplifies Wnt signals by maintaining cell surface expression of Frizzled (Fzd) and low-density lipoprotein receptor-related protein receptors, not only helps repair intestine epithelial damage, but also induces hyperplasia of normal epithelium. Wnt signaling may also be modulated with the recently developed Wnt mimetics, recombinant antibody-based molecules mimicking endogenous Wnts.We first compared the epithelial healing effects of RSPO2 and a Wnt mimetic with broad Fzd specificity in an acute dextran sulfate sodium mouse colitis model. Guided by Fzd expression patterns in the colon epithelium, we also examined the effects of Wnt mimetics with subfamily Fzd specificities.In the DSS model, Wnt mimetics repaired damaged colon epithelium and reduced disease activity and inflammation and had no apparent effect on uninjured tissue. We further identified that the FZD5/8 and LRP6 receptor-specific Wnt mimetic, SZN-1326-p, was associated with the robust repair effect. Through a range of approaches including single-cell transcriptome analyses, we demonstrated that SZN-1326-p directly impacted epithelial cells, driving transient expansion of stem and progenitor cells, promoting differentiation of epithelial cells, histologically restoring the damaged epithelium, and secondarily to epithelial repair, reducing inflammation.It is feasible to design Wnt mimetics such as SZN-1326-p that impact damaged intestine epithelium specifically and restore its physiological functions, an approach that holds promise for treating epithelial damage in inflammatory bowel disease.
    Neutralizing human antibodies prevent Zika virus replication and fetal disease in mice.

    Nature.

    2016 Nov 07

    Sapparapu G, Fernandez E, Kose N, Cao B, Fox JM, Bombardi RG, Zhao H, Nelson CA, Bryan AL, Barnes T, Davidson E, Mysorekar IU, Fremont DH, Doranz BJ, Diamond MS, Crowe JE.
    PMID: 27819683 | DOI: 10.1038/nature20564

    Zika virus (ZIKV) is an emerging mosquito-transmitted flavivirus that can cause severe disease, including congenital birth defects during pregnancy1. To develop candidate therapeutic agents against ZIKV, we isolated a panel of human monoclonal antibodies (mAbs) from subjects with prior ZIKV infection. A subset of mAbs recognized diverse epitopes on the envelope (E) protein and exhibited potently neutralizing activity. One of the most inhibitory mAbs, ZIKV-117, broadly neutralized infection of ZIKV strains corresponding to African, Asian, and American lineages. Epitope mapping studies revealed that ZIKV-117 recognized a unique quaternary epitope on the E protein dimer-dimer interface. We evaluated the therapeutic efficacy of ZIKV-117 in pregnant and non-pregnant mice. mAb treatment markedly reduced tissue pathology, placental and fetal infection, and mortality in mice. Thus, neutralizing human mAbs can protect against maternal-fetal transmission, infection and disease, and reveal important determinants for structure-based rational vaccine design efforts.

    Differential Wnt signaling activity limits epithelial gland development to the anti-mesometrial side of the mouse uterus.

    Dev Biol.

    2017 Jan 30

    Goad J, Ko YA, Kumar M, Syed SM, Tanwar PS.
    PMID: 28153546 | DOI: 10.1016/j.ydbio.2017.01.015

    In mice, implantation always occurs towards the antimesometrial side of the uterus, while the placenta develops at the mesometrial side. What determines this particular orientation of the implanting blastocyst remains unclear. Uterine glands are critical for implantation and pregnancy. In this study, we showed that uterine gland development and active Wnt signalling activity is limited to the antimesometrial side of the uterus. Dkk2, a known antagonist of Wnt signalling, is only present at the mesometrial side of the uterus. Imaging of whole uterus, thick uterine sections (100-1000μm), and individual glands revealed that uterine glands are simple tubes with branches that are directly connected to the luminal epithelium and are only present towards the antimesometrial side of the uterus. By developing a unique mouse model targeting the uterine epithelium, we demonstrated that Wnt/β-catenin signaling is essential for prepubertal gland formation and normal implantation, but dispensable for postpartum gland development and regeneration. Our results for the first time have provided a probable explanation for the antimesometrial bias for implantation.

    Stem cell plasticity enables hair regeneration following Lgr5+ cell loss.

    Nat Cell Biol.

    2017 May 29

    Hoeck JD, Biehs B, Kurtova AV, Kljavin NM, de Sousa E Melo F, Alicke B, Koeppen H, Modrusan Z, Piskol R, de Sauvage FJ.
    PMID: 28553937 | DOI: 10.1038/ncb3535

    Under injury conditions, dedicated stem cell populations govern tissue regeneration. However, the molecular mechanisms that induce stem cell regeneration and enable plasticity are poorly understood. Here, we investigate stem cell recovery in the context of the hair follicle to understand how two molecularly distinct stem cell populations are integrated. Utilizing diphtheria-toxin-mediated cell ablation of Lgr5+(leucine-rich repeat-containing G-protein-coupled receptor 5) stem cells, we show that killing of Lgr5+ cells in mice abrogates hair regeneration but this is reversible. During recovery, CD34+ (CD34 antigen) stem cells activate inflammatory response programs and start dividing. Pharmacological attenuation of inflammation inhibits CD34+ cell proliferation. Subsequently, the Wnt pathway controls the recovery of Lgr5+ cells and inhibition of Wnt signalling prevents Lgr5+ cell and hair germ recovery. Thus, our study uncovers a compensatory relationship between two stem cell populations and the underlying molecular mechanisms that enable hair follicle regeneration.

    Neuropathogenesis of Zika Virus in a Highly Susceptible Immunocompetent Mouse Model after Antibody Blockade of Type I Interferon

    PLoS Negl Trop Dis.

    2017 Jan 09

    Smith DR, Hollidge B, Daye S, Zeng X, Blancett C, Kuszpit K, Bocan T, Koehler JW, Coyne S, Minogue T, Kenny T, Chi X, Yim S, Miller L, Schmaljohn C, Bavari S, Golden JW.
    PMID: 28068342 | DOI: 10.1371/journal.pntd.0005296

    Animal models are needed to better understand the pathogenic mechanisms of Zika virus (ZIKV) and to evaluate candidate medical countermeasures. Adult mice infected with ZIKV develop a transient viremia, but do not demonstrate signs of morbidity or mortality. Mice deficient in type I or a combination of type I and type II interferon (IFN) responses are highly susceptible to ZIKV infection; however, the absence of a competent immune system limits their usefulness for studying medical countermeasures. Here we employ a murine model for ZIKV using wild-type C57BL/6 mice treated with an antibody to disrupt type I IFN signaling to study ZIKV pathogenesis. We observed 40% mortality in antibody treated mice exposed to ZIKV subcutaneously whereas mice exposed by intraperitoneal inoculation were highlysusceptible incurring 100% mortality. Mice infected by both exposure routes experienced weight loss, high viremia, and severe neuropathologic changes. The most significant histopathological findings occurred in the central nervous system where lesions represent an acute to subacute encephalitis/encephalomyelitis that is characterized by neuronal death, astrogliosis, microgliosis, scattered necrotic cellular debris, and inflammatory cell infiltrates. This model of ZIKV pathogenesis will be valuable for evaluating medical countermeasures and the pathogenic mechanisms of ZIKV because it allows immune responses to be elicited in immunologically competent mice with IFN I blockade only induced at the time of infection.

    Pluripotent stem cell-derived endometrial stromal fibroblasts in a cyclic, hormone-responsive, coculture model of human decidua

    Cell reports

    2021 May 18

    Cheung, VC;Peng, CY;Marinić, M;Sakabe, NJ;Aneas, I;Lynch, VJ;Ober, C;Nobrega, MA;Kessler, JA;
    PMID: 34010658 | DOI: 10.1016/j.celrep.2021.109138

    Various human diseases and pregnancy-related disorders reflect endometrial dysfunction. However, rodent models do not share fundamental biological processes with the human endometrium, such as spontaneous decidualization, and no existing human cell cultures recapitulate the cyclic interactions between endometrial stromal and epithelial compartments necessary for decidualization and implantation. Here we report a protocol differentiating human pluripotent stem cells into endometrial stromal fibroblasts (PSC-ESFs) that are highly pure and able to decidualize. Coculture of PSC-ESFs with placenta-derived endometrial epithelial cells generated organoids used to examine stromal-epithelial interactions. Cocultures exhibited specific endometrial markers in the appropriate compartments, organization with cell polarity, and hormone responsiveness of both cell types. Furthermore, cocultures recapitulate a central feature of the human decidua by cyclically responding to hormone withdrawal followed by hormone retreatment. This advance enables mechanistic studies of the cyclic responses that characterize the human endometrium.
    LAG3+ Regulatory T Cells Restrain Interleukin-23-Producing CX3CR1+ Gut-Resident Macrophages during Group 3 Innate Lymphoid Cell-Driven Colitis

    Immunity

    2018 Aug 07

    Bauché D, Joyce-Shaikh B, Jain R, Grein J, Ku KS, Blumenschein WM, Ganal-Vonarburg SC, Wilson DC, McClanahan TK, Malefyt RdW, Macpherson AJ, Annamalai L, Yearley JH, Cua, Daniel J.
    PMID: - | DOI: 10.1016/j.immuni.2018.07.007

    Interleukin-22 (IL-22)-producing group 3 innate lymphoid cells (ILC3) maintains gut homeostasis but can also promote inflammatory bowel disease (IBD). The regulation of ILC3-dependent colitis remains to be elucidated. Here we show that Foxp3 + regulatory T cells (Treg cells) prevented ILC3-mediated colitis in an IL-10-independent manner. Treg cells inhibited IL-23 and IL-1β production from intestinal-resident CX3CR1 + macrophages but not CD103 + dendritic cells. Moreover, Treg cells restrained ILC3 production of IL-22 through suppression of CX3CR1 + macrophage production of IL-23 and IL-1β. This suppression was contact dependent and was mediated by latent activation gene-3 (LAG-3)—an immune checkpoint receptor—expressed on Treg cells. Engagement of LAG-3 on MHC class II drove profound immunosuppression of CX3CR1+ tissue-resident macrophages. Our study reveals that the health of the intestinal mucosa is maintained by an axis driven by Treg cells communication with resident macrophages that withhold inflammatory stimuli required for ILC3 function.

    Stromal R-spondin orchestrates gastric epithelial stem cells and gland homeostasis.

    Nature

    2017 Aug 16

    Sigal M, Logan CY, Kapalczynska M, Mollenkopf HJ, Berger H, Wiedenmann B, Nusse R, Amieva MR, Meyer TF.
    PMID: 28813421 | DOI: 10.1038/nature23642

    The constant regeneration of stomach epithelium is driven by long-lived stem cells, but the mechanism that regulates their turnover is not well understood. We have recently found that the gastric pathogen Helicobacter pylori can activate gastric stem cells and increase epithelial turnover, while Wnt signalling is known to be important for stem cell identity and epithelial regeneration in several tissues. Here we find that antral Wnt signalling, marked by the classic Wnt target gene Axin2, is limited to the base and lower isthmus of gastric glands, where the stem cells reside. Axin2 is expressed by Lgr5+ cells, as well as adjacent, highly proliferative Lgr5- cells that are able to repopulate entire glands, including the base, upon depletion of the Lgr5+ population. Expression of both Axin2 and Lgr5 requires stroma-derived R-spondin 3 produced by gastric myofibroblasts proximal to the stem cell compartment. Exogenous R-spondin administration expands and accelerates proliferation of Axin2+/Lgr5- but not Lgr5+ cells. Consistent with these observations, H. pylori infection increases stromal R-spondin 3 expression and expands the Axin2+ cell pool to cause hyperproliferation and gland hyperplasia. The ability of stromal niche cells to control and adapt epithelial stem cell dynamics constitutes a sophisticated mechanism that orchestrates epithelial regeneration and maintenance of tissue integrity.

    Low-Dose Interleukin-2 Ameliorates Colitis in a Preclinical Humanized Mouse Model.

    Cell Mol Gastroenterol Hepatol.

    2019 May 09

    Goettel JA, Kotlarz D, Emani R, Canavan JB, Konnikova L, Illig D, Frei SM, Field M, Kowalik M, Peng K, Gringauz J, Mitsalis V, Wall SM, Tsou A, Griffith AE, Friedman JR, Towne JE, Plevy SE, O'Hara Hall A, Snapper SB.
    PMID: 31078723 | DOI: 10.1016/j.jcmgh.2019.05.001

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    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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