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Species

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Gene

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Platform

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Channel

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HiPlex Channel

  • T1 (85058) Apply T1 filter
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  • T11 (85039) Apply T11 filter
  • T9 (82563) Apply T9 filter
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  • S1 (32) Apply S1 filter
  • 8 (17) Apply 8 filter
  • 1 (1) Apply 1 filter
  • 10 (1) Apply 10 filter
  • 6 (1) Apply 6 filter

Product

  • RNAscope Multiplex Fluorescent Assay (1035) Apply RNAscope Multiplex Fluorescent Assay filter
  • RNAscope (998) Apply RNAscope filter
  • RNAscope Fluorescent Multiplex Assay (732) Apply RNAscope Fluorescent Multiplex Assay filter
  • RNAscope 2.5 HD Red assay (704) Apply RNAscope 2.5 HD Red assay filter
  • RNAscope 2.0 Assay (497) Apply RNAscope 2.0 Assay filter
  • RNAscope 2.5 HD Brown Assay (293) Apply RNAscope 2.5 HD Brown Assay filter
  • TBD (193) Apply TBD filter
  • RNAscope 2.5 LS Assay (191) Apply RNAscope 2.5 LS Assay filter
  • RNAscope 2.5 HD Duplex (160) Apply RNAscope 2.5 HD Duplex filter
  • RNAscope 2.5 HD Reagent Kit - BROWN (108) Apply RNAscope 2.5 HD Reagent Kit - BROWN filter
  • RNAscope Multiplex Fluorescent v2 (97) Apply RNAscope Multiplex Fluorescent v2 filter
  • BASEscope Assay RED (91) Apply BASEscope Assay RED filter
  • RNAscope 2.5 VS Assay (85) Apply RNAscope 2.5 VS Assay filter
  • Basescope (53) Apply Basescope filter
  • RNAscope HiPlex v2 assay (30) Apply RNAscope HiPlex v2 assay filter
  • miRNAscope (26) Apply miRNAscope filter
  • DNAscope HD Duplex Reagent Kit (15) Apply DNAscope HD Duplex Reagent Kit filter
  • RNAscope 2.5 HD duplex reagent kit (13) Apply RNAscope 2.5 HD duplex reagent kit filter
  • BaseScope Duplex Assay (12) Apply BaseScope Duplex Assay filter
  • RNAscope Multiplex fluorescent reagent kit v2 (6) Apply RNAscope Multiplex fluorescent reagent kit v2 filter
  • RNAscope Fluorescent Multiplex Reagent kit (5) Apply RNAscope Fluorescent Multiplex Reagent kit filter
  • RNAscope ISH Probe High Risk HPV (5) Apply RNAscope ISH Probe High Risk HPV filter
  • CTCscope (4) Apply CTCscope filter
  • RNAscope 2.5 HD Reagent Kit (4) Apply RNAscope 2.5 HD Reagent Kit filter
  • RNAscope HiPlex12 Reagents Kit (3) Apply RNAscope HiPlex12 Reagents Kit filter
  • DNAscope Duplex Assay (2) Apply DNAscope Duplex Assay filter
  • RNAscope 2.5 HD Assay (2) Apply RNAscope 2.5 HD Assay filter
  • RNAscope 2.5 LS Assay - RED (2) Apply RNAscope 2.5 LS Assay - RED filter
  • RNAscope Multiplex Fluorescent Assay v2 (2) Apply RNAscope Multiplex Fluorescent Assay v2 filter
  • BOND RNAscope Brown Detection (1) Apply BOND RNAscope Brown Detection filter
  • HybEZ Hybridization System (1) Apply HybEZ Hybridization System filter
  • miRNAscope Assay Red (1) Apply miRNAscope Assay Red filter
  • RNA-Protein CO-Detection Ancillary Kit (1) Apply RNA-Protein CO-Detection Ancillary Kit filter
  • RNAscope 2.0 HD Assay - Chromogenic (1) Apply RNAscope 2.0 HD Assay - Chromogenic filter
  • RNAscope 2.5 HD- Red (1) Apply RNAscope 2.5 HD- Red filter
  • RNAscope 2.5 LS Reagent Kits (1) Apply RNAscope 2.5 LS Reagent Kits filter
  • RNAScope HiPlex assay (1) Apply RNAScope HiPlex assay filter
  • RNAscope HiPlex Image Registration Software (1) Apply RNAscope HiPlex Image Registration Software filter
  • RNAscope LS Multiplex Fluorescent Assay (1) Apply RNAscope LS Multiplex Fluorescent Assay filter
  • RNAscope Multiplex Fluorescent Reagent Kit V3 (1) Apply RNAscope Multiplex Fluorescent Reagent Kit V3 filter
  • RNAscope Multiplex Fluorescent Reagent Kit v4 (1) Apply RNAscope Multiplex Fluorescent Reagent Kit v4 filter
  • RNAscope Multiplex Fluorescent v1 (1) Apply RNAscope Multiplex Fluorescent v1 filter
  • RNAscope Target Retrieval Reagents (1) Apply RNAscope Target Retrieval Reagents filter

Research area

  • Neuroscience (1849) Apply Neuroscience filter
  • Cancer (1385) Apply Cancer filter
  • Development (509) Apply Development filter
  • Inflammation (472) Apply Inflammation filter
  • Infectious Disease (410) Apply Infectious Disease filter
  • Other (406) Apply Other filter
  • Stem Cells (258) Apply Stem Cells filter
  • Covid (237) Apply Covid filter
  • Infectious (220) Apply Infectious filter
  • HPV (187) Apply HPV filter
  • lncRNA (135) Apply lncRNA filter
  • Metabolism (91) Apply Metabolism filter
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  • Immunotherapy (72) Apply Immunotherapy filter
  • Other: Methods (67) Apply Other: Methods filter
  • HIV (64) Apply HIV filter
  • CGT (62) Apply CGT filter
  • Pain (62) Apply Pain filter
  • diabetes (57) Apply diabetes filter
  • LncRNAs (46) Apply LncRNAs filter
  • Aging (43) Apply Aging filter
  • Other: Heart (40) Apply Other: Heart filter
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  • Obesity (29) Apply Obesity filter
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  • Behavior (27) Apply Behavior filter
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  • Other: Kidney (27) Apply Other: Kidney filter
  • Alzheimer's Disease (26) Apply Alzheimer's Disease filter
  • Bone (24) Apply Bone filter
  • Stress (21) Apply Stress filter
  • Other: Zoological Disease (20) Apply Other: Zoological Disease filter
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  • Other: Endocrinology (16) Apply Other: Endocrinology filter
  • Other: Skin (16) Apply Other: Skin filter
  • Injury (15) Apply Injury filter
  • Anxiety (14) Apply Anxiety filter
  • Memory (14) Apply Memory filter
  • Reproductive Biology (14) Apply Reproductive Biology filter

Product sub type

  • Target Probes (256568) Apply Target Probes filter
  • Control Probe - Automated Leica (409) Apply Control Probe - Automated Leica filter
  • Control Probe - Automated Leica Multiplex (284) Apply Control Probe - Automated Leica Multiplex filter
  • Control Probe - Automated Leica Duplex (168) Apply Control Probe - Automated Leica Duplex filter
  • Control Probe- Manual RNAscope Multiplex (148) Apply Control Probe- Manual RNAscope Multiplex filter
  • Control Probe - Automated Ventana (143) Apply Control Probe - Automated Ventana filter
  • Control Probe - Manual RNAscope Singleplex (142) Apply Control Probe - Manual RNAscope Singleplex filter
  • Control Probe - Manual RNAscope Duplex (137) Apply Control Probe - Manual RNAscope Duplex filter
  • Control Probe (73) Apply Control Probe filter
  • Control Probe - Manual BaseScope Singleplex (51) Apply Control Probe - Manual BaseScope Singleplex filter
  • Control Probe - VS BaseScope Singleplex (41) Apply Control Probe - VS BaseScope Singleplex filter
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  • L-HBsAG (15) Apply L-HBsAG filter
  • Cancer (13) Apply Cancer filter
  • Automated Assay 2.5: Leica System (8) Apply Automated Assay 2.5: Leica System filter
  • Control Probe- Manual BaseScope Duplex (8) Apply Control Probe- Manual BaseScope Duplex filter
  • 1765 (8) Apply 1765 filter
  • 1379 (8) Apply 1379 filter
  • 2184 (8) Apply 2184 filter
  • 38322 (8) Apply 38322 filter
  • Manual Assay 2.5: Pretreatment Reagents (5) Apply Manual Assay 2.5: Pretreatment Reagents filter
  • Controls: Manual Probes (5) Apply Controls: Manual Probes filter
  • Control Probe- Manual RNAscope HiPlex (5) Apply Control Probe- Manual RNAscope HiPlex filter
  • Manual Assay RNAscope Brown (4) Apply Manual Assay RNAscope Brown filter
  • Manual Assay RNAscope Duplex (4) Apply Manual Assay RNAscope Duplex filter
  • Manual Assay RNAscope Multiplex (4) Apply Manual Assay RNAscope Multiplex filter
  • Manual Assay BaseScope Red (4) Apply Manual Assay BaseScope Red filter
  • IA: Other (4) Apply IA: Other filter
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  • Manual Assay miRNAscope Red (4) Apply Manual Assay miRNAscope Red filter
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  • Control Probe - Automated Ventana Duplex (3) Apply Control Probe - Automated Ventana Duplex filter
  • Manual Assay BaseScope Duplex (3) Apply Manual Assay BaseScope Duplex filter
  • Manual Assay RNAscope Red (2) Apply Manual Assay RNAscope Red filter
  • Controls: Control Slides (2) Apply Controls: Control Slides filter
  • Control Probe- Manual BaseScope Singleplex (2) Apply Control Probe- Manual BaseScope Singleplex filter
  • Control Probe - Manual BaseScope™Singleplex (2) Apply Control Probe - Manual BaseScope™Singleplex filter
  • Manual Assay: Accessory Reagent (1) Apply Manual Assay: Accessory Reagent filter
  • Accessory Reagent (1) Apply Accessory Reagent filter
  • Controls: Manual RNAscope Multiplex (1) Apply Controls: Manual RNAscope Multiplex filter
  • IA: HybEZ (1) Apply IA: HybEZ filter
  • Automated Assay BaseScope: LS (1) Apply Automated Assay BaseScope: LS filter
  • Automated Assay BaseScope: VS (1) Apply Automated Assay BaseScope: VS filter
  • Software: RNAscope HiPlex Image Registration (1) Apply Software: RNAscope HiPlex Image Registration filter
  • miRNAscope Automated Assay: Leica System (1) Apply miRNAscope Automated Assay: Leica System filter
  • Automated Assay: VS (1) Apply Automated Assay: VS filter
  • Control Probe - VS BaseScope™Singleplex (1) Apply Control Probe - VS BaseScope™Singleplex filter
  • Controls:2.5VS Probes (1) Apply Controls:2.5VS Probes filter
  • Control Probe - Manual RNAscope Multiplex (1) Apply Control Probe - Manual RNAscope Multiplex filter

Sample Compatibility

  • Cell pellets (49) Apply Cell pellets filter
  • FFPE (41) Apply FFPE filter
  • Fixed frozen tissue (31) Apply Fixed frozen tissue filter
  • TMA (31) Apply TMA filter
  • Adherent cells (26) Apply Adherent cells filter
  • Freshfrozen tissue (18) Apply Freshfrozen tissue filter
  • Fresh frozen tissue (13) Apply Fresh frozen tissue filter
  • Cell Cultures (12) Apply Cell Cultures filter
  • TMA(Tissue Microarray) (9) Apply TMA(Tissue Microarray) filter
  • FFPE,Freshfrozen tissue,Fixed frozen tissue,TMA,Cell pellets,Adherent cells (7) Apply FFPE,Freshfrozen tissue,Fixed frozen tissue,TMA,Cell pellets,Adherent cells filter
  • CTC (4) Apply CTC filter
  • PBMC's (4) Apply PBMC's filter
  • Adherent or Cultured Cells (1) Apply Adherent or Cultured Cells filter
  • Fixed frozen (1) Apply Fixed frozen filter
  • FFPE,TMA (1) Apply FFPE,TMA filter
  • Fixed frozen tissues (for chromogenic assays) (1) Apply Fixed frozen tissues (for chromogenic assays) filter

Category

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Application

  • Cancer (139875) Apply Cancer filter
  • Neuroscience (51010) Apply Neuroscience filter
  • Cancer, Neuroscience (32227) Apply Cancer, Neuroscience filter
  • Non-coding RNA (24365) Apply Non-coding RNA filter
  • Cancer, Inflammation (16436) Apply Cancer, Inflammation filter
  • Cancer, Inflammation, Neuroscience (12591) Apply Cancer, Inflammation, Neuroscience filter
  • Inflammation (9879) Apply Inflammation filter
  • Cancer, Stem Cell (7932) Apply Cancer, Stem Cell filter
  • Cancer, Neuroscience, Stem Cell (7028) Apply Cancer, Neuroscience, Stem Cell filter
  • Cancer, Immunotherapy, Inflammation, Neuroscience, Stem Cell (6854) Apply Cancer, Immunotherapy, Inflammation, Neuroscience, Stem Cell filter
  • Cancer, Inflammation, Neuroscience, Stem Cell (5424) Apply Cancer, Inflammation, Neuroscience, Stem Cell filter
  • Immunotherapy (5368) Apply Immunotherapy filter
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  • Cancer, Immunotherapy, Inflammation (2844) Apply Cancer, Immunotherapy, Inflammation filter
  • Cancer, Immunotherapy, Inflammation, Neuroscience (1878) Apply Cancer, Immunotherapy, Inflammation, Neuroscience filter
  • Cancer, Immunotherapy, Neuroscience (1786) Apply Cancer, Immunotherapy, Neuroscience filter
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GLP-1-, but not GDF-15-, receptor activation increases the number of IL-6-expressing cells in the external lateral parabrachial nucleus

Neuroendocrinology

2019 Mar 20

Anesten F, Mishra D, Dalmau Gasull A, Engstrom-Ruud L, Bellman J, Palsdottir V, Zhang FP, Trapp S, Skibicka KP, Poutanen M and Jansson JO
PMID: 30889580 | DOI: 10.1159/000499693

Background/Aims IL-6 in the hypothalamus and hindbrain is an important downstream mediator of suppression of body weight and food intake by glucagon-like peptide-1 (GLP-1) receptor stimulation. CNS GLP-1 is produced almost exclusively in prepro-glucagon neurons in the nucleus of the solitary tract. These neurons innervate energy balance-regulating areas, such as the external lateral parabrachial nucleus (PBNel); essential for induction of anorexia. Methods Using a validated novel IL-6-reporter mouse strain, we investigated the interactions in PBNel between GLP-1, IL-6 and calcitonin gene related peptide (CGRP, a well-known mediator of anorexia). We show that PBNel GLP-1R-containing cells highly (to about 80%) overlap with IL-6-containing cells on both protein and mRNA level. Results Intraperitoneal administration of a GLP-1 analogue exendin-4 to mice increased the proportion of IL-6 containing cells in PBNel 3-fold, while there was no effect in the rest of the lateral PBN. In contrast, injections of an anorexigenic peptide growth and differentiation factor 15 (GDF15) markedly increased the proportion of CGRP-containing cells, while IL-6-containing cells were not affected. Conclusion In summary, GLP-1R are found on IL-6 producing cells in PBNel, and GLP-1R stimulation leads to an increase in the proportion of cells with IL-6 reporter fluorescence, supporting IL-6 mediation of GLP-1 effects on energy balance.
A whole-brain atlas of monosynaptic input targeting four different cell types in the medial prefrontal cortex of the mouse

Nat Neurosci

2019 Mar 18

Ahrlund-Richter S, Xuan Y, van Lunteren JA, Kim H, Ortiz C, Pollak Dorocic I, Meletis K and Carlen M
PMID: 30886408 | DOI: 10.1038/s41593-019-0354-y

The local and long-range connectivity of cortical neurons are considered instrumental to the functional repertoire of the cortical region in which they reside. In cortical networks, distinct cell types build local circuit structures enabling computational operations. Computations in the medial prefrontal cortex (mPFC) are thought to be central to cognitive operation, including decision-making and memory. We used a retrograde trans-synaptic rabies virus system to generate brain-wide maps of the input to excitatory neurons as well as three inhibitory interneuron subtypes in the mPFC. On the global scale the input patterns were found to be mainly cell type independent, with quantitative differences in key brain regions, including the basal forebrain. Mapping of the local mPFC network revealed high connectivity between the different subtypes of interneurons. The connectivity mapping gives insight into the information that the mPFC processes and the structural architecture underlying the mPFC's unique functions.
Clinical significance of BRCA1 and BRCA2 mRNA and protein expression in patients with sporadic gastric cancer

Oncology Letters

2019 Mar 08

Kim H, Hwang I, Min H, Bang Y and Kim W
| DOI: 10.3892/ol.2019.10132

Differential regulation of thyrotropin-releasing hormone mRNA expression in the paraventricular nucleus and dorsomedial hypothalamus in OLETF rats

Neurosci Lett

2019 Mar 19

Zhang N, Zhang HY, Bi SA, Moran TH and Bi S
PMID: 30902570 | DOI: 10.1016/j.neulet.2019.03.030

Thyrotropin-releasing hormone (TRH) plays an important role in the regulation of energy balance. While the regulation of TRH in the paraventricular nucleus (PVN) in response to changes of energy balance has been well studied, how TRH is regulated in the dorsomedial hypothalamus (DMH) in maintaining energy homeostasis remains unclear. Here, we assessed the effects of food restriction and exercise on hypothalamic Trh expression using Otsuka Long-Evens Tokushima Fatty (OLETF) rats. Sedentary ad lib fed OLETF rats (OLETF-SED) became hyperphagic and obese. These alterations were prevented in OLETF rats with running wheel access (OLETF-RW) or food restriction in which their food was pair-fed (OLETF-PF) to the intake of lean control rats (LETO-SED). Evaluation of hypothalamic gene expression revealed that Trh mRNA expression was increased in the PVN of OLETF-SED rats and normalized in OLETF-RW and OLETF-PF rats compared to LETO-SED rats. In contrast, the expression of Trh in the DMH was decreased in OLETF-SED rats relative to LETO-SED rats. This alteration was reversed in OLETF-RW rats as seen in LETO-SED rats, but food restriction resulted in a significant increase in DMH Trh expression in OLETF-PF rats compared to LETO-SED rats. Strikingly, while Trh mRNA expression was decreased in the PVN of intact rats in response to acute food deprivation, food deprivation resulted in increased expression of Trh in the DMH. Together, these results demonstrate the differential regulation of Trh expression in the PVN and DMH in OLETF rats and suggest that DMH TRH also contributes to hypothalamic regulation of energy balance.
The Familial dementia gene ITM2b/BRI2 facilitates glutamate transmission via both presynaptic and postsynaptic mechanisms

Sci Rep

2019 Mar 19

Yao W, Yin T, Tambini MD and D'Adamio L
PMID: 30890756 | DOI: 10.1038/s41598-019-41340-9

Mutations in the Integral membrane protein 2B (ITM2b/BRI2) gene, which codes for a protein called BRI2, cause familial British and Danish dementia (FBD and FDD). Loss of BRI2 function and/or accumulation of amyloidogenic mutant BRI2-derived peptides have been proposed to mediate FDD and FBD pathogenesis by impairing synaptic Long-term potentiation (LTP). However, the precise site and nature of the synaptic dysfunction remain unknown. Here we use a genetic approach to inactivate Itm2b in either presynaptic (CA3), postsynaptic (CA1) or both (CA3 + CA1) neurons of the hippocampal Schaeffer-collateral pathway in both female and male mice. We show that after CA3 + CA1 Itm2b inactivation, spontaneous glutamate release and AMPAR-mediated responses are decreased, while short-term synaptic facilitation is increased. Moreover, AMPAR-mediated responses are decreased after postsynaptic but not presynaptic deletion of Itm2b. In contrast, the probability of spontaneous glutamate release is decreased, while short-term synaptic facilitation is increased, primarily after presynaptic deletion of Itm2b. Collectively, these results indicate a dual physiological role of Itm2b in the regulation of excitatory synaptic transmission at both presynaptic termini and postsynaptic termini and suggest that presynaptic and postsynaptic dysfunctions may be a pathogenic event leading to dementia and neurodegeneration in FDD and FBD.
Chimeric antigen receptor costimulation domains modulate human regulatory T cell function

JCI Insight

2019 Mar 14

Boroughs AC, Larson RC, Choi BD, Bouffard AA, Riley LS, Schiferle E, Kulkarni AS, Cetrulo CL, Ting D, Blazar BR, Demehri S and Maus MV
PMID: 30869654 | DOI: 10.1172/jci.insight.126194

Regulatory T cells (Tregs) are key modulators of inflammation and are important for the maintenance of peripheral tolerance. Adoptive immunotherapy with polyclonal Tregs holds promise in organ transplantation, graft-versus-host disease, and autoimmune diseases, but may be enhanced by antigen-specific, long-lived Treg cells. We modified primary human Tregs with chimeric antigen-receptors (CARs) bearing different costimulatory domains and performed in vitro analyses of their phenotype and function. While neither the presence of a CAR nor the type of costimulation domain influenced Foxp3 expression in Tregs, the costimulation domain of the CARs affected CAR Treg surface phenotype and functions such as cytokine production. Furthermore, signaling from the CD28 costimulation domain maintained CAR Treg suppressor function, whereas 4-1B costimulation did not. In vivo, CAR Tregs accumulated at sites expressing target antigen, and suppressed antigen specific effector T cell responses; however, only CAR Tregs with CD28 signaling domains were potent inhibitors of effector T cell mediated graft rejection in vivo. Our findings support the use of CD28 based CAR-Tregs for tissue specific immune suppression in the clinic.
Defining the role of NG2-expressing cells in experimental models of multiple sclerosis. A biofunctional analysis of the neurovascular unit in wild type and NG2 null mice

PLoS One

2019 Mar 14

Girolamo F, Errede M, Longo G, Annese T, Alias C, Ferrara G, Morando S, Trojano M, Kerlero de Rosbo N, Uccelli A and Virgintino D
PMID: 30870435 | DOI: 10.1371/journal.pone.0213508

During experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis associated with blood-brain barrier (BBB) disruption, oligodendrocyte precursor cells (OPCs) overexpress proteoglycan nerve/glial antigen 2 (NG2), proliferate, and make contacts with the microvessel wall. To explore whether OPCs may actually be recruited within the neurovascular unit (NVU), de facto intervening in its cellular and molecular composition, we quantified by immunoconfocal morphometry the presence of OPCs in contact with brain microvessels, during postnatal cerebral cortex vascularization at postnatal day 6, in wild-type (WT) and NG2 knock-out (NG2KO) mice, and in the cortex of adult naive and EAE-affected WT and NG2KO mice. As observed in WT mice during postnatal development, a higher number of juxtavascular and perivascular OPCs was revealed in adult WT mice during EAE compared to adult naive WT mice. In EAE-affected mice, OPCs were mostly associated with microvessels that showed altered claudin-5 and occludin tight junction (TJ) staining patterns and barrier leakage. In contrast, EAE-affected NG2KO mice, which did not show any significant increase in vessel-associated OPCs, seemed to retain better preserved TJs and BBB integrity. As expected, absence of NG2, in both OPCs and pericytes, led to a reduced content of vessel basal lamina molecules, laminin, collagen VI, and collagen IV. In addition, analysis of the major ligand/receptor systems known to promote OPC proliferation and migration indicated that vascular endothelial growth factor A (VEGF-A), platelet-derived growth factor-AA (PDGF-AA), and the transforming growth factor-beta (TGF-beta) were the molecules most likely involved in proliferation and recruitment of vascular OPCs during EAE. These results were confirmed by real time-PCR that showed Fgf2, Pdgfa and Tgfb expression on isolated cerebral cortex microvessels and by dual RNAscope-immunohistochemistry/in situ hybridization (IHC/ISH), which detected Vegfa and Vegfr2 transcripts on cerebral cortex sections. Overall, this study suggests that vascular OPCs, in virtue of their developmental arrangement and response to neuroinflammation and growth factors, could be integrated among the classical NVU cell components. Moreover, the synchronized activation of vascular OPCs and pericytes during both BBB development and dysfunction, points to NG2 as a key regulator of vascular interactions.
GPR139 and Dopamine D2 Receptor Co-express in the Same Cells of the Brain and May Functionally Interact

Frontiers in Neuroscience

2019 Mar 26

Wang L, Lee G, Kuei C, Yao X, Harrington A, Bonaventure P, Lovenberg TW and Liu C
| DOI: 10.3389/fnins.2019.00281

GPR139, a Gq-coupled receptor that is activated by the essential amino acids L-tryptophan and L-phenylalanine, is predominantly expressed in the brain and pituitary. The physiological function of GPR139 remains elusive despite the availability of pharmacological tool agonist compounds and knock-out mice. Whole tissue RNA sequencing data from human, mouse and rat tissues revealed that GPR139 and the dopamine D2 receptor (DRD2) exhibited some similarities in their distribution patterns in the brain and pituitary gland. To determine if there was true co-expression of these two receptors, we applied double in situ hybridization in mouse tissues using the RNAscope™ technique. GPR139 and DRD2 mRNA co-localized in a majority of cells within part of the dopaminergic mesolimbic pathways (ventral tegmental area and olfactory tubercle), the nigrostriatal pathway (compact part of substantia nigra and caudate putamen) and also the tuberoinfundibular pathway (arcuate hypothalamic nucleus and anterior lobe of pituitary). Both receptors mRNA also co-localized in brain regions involved in responses to negative stimulus and stress, such as lateral habenula, lateral septum, interpeduncular nucleus and medial raphe nuclei. GPR139 mRNA expression was detected in the dentate gyrus and the pyramidal cell layer of the hippocampus as well as the paraventricular hypothalamic nucleus. The functional interaction between GPR139 and DRD2 was studied in vitro using a calcium mobilization assay in cells co-transfected with both receptors from several species (human, rat and mouse). The dopamine DRD2 agonist did not stimulate calcium response in cells expressing DRD2 alone consistent with the Gi signaling transduction pathway of this receptor. In cells co-transfected with DRD2 and GPR139 the DRD2 agonist was able to stimulate calcium response and its effect was blocked by either a DRD2 or a GPR139 antagonist supporting an in vitro interaction between GPR139 and DRD2. Taken together, these data showed that GPR139 and DRD2 are in position to functionally interact in native tissue.
LRG1 Promotes Diabetic Kidney Disease Progression by Enhancing TGF-beta-Induced Angiogenesis

J Am Soc Nephrol

2019 Mar 11

Hong Q, Zhang L, Fu J, Verghese DA, Chauhan K, Nadkarni GN, Li Z, Ju W, Kretzler M, Cai GY, Chen XM, D'Agati VD, Coca SG, Schlondorff D, He JC and Lee K
PMID: 30858225 | DOI: 10.1681/asn.2018060599

BACKGROUND: Glomerular endothelial dysfunction and neoangiogenesis have long been implicated in the pathogenesis of diabetic kidney disease (DKD). However, the specific molecular pathways contributing to these processes in the early stages of DKD are not well understood. Our recent transcriptomic profiling of glomerular endothelial cells identified a number of proangiogenic genes that were upregulated in diabetic mice, including leucine-rich alpha-2-glycoprotein 1 (LRG1). LRG1 was previously shown to promote neovascularization in mouse models of ocular disease by potentiating endothelial TGF-beta/activin receptor-like kinase 1 (ALK1) signaling. However, LRG1's role in the kidney, particularly in the setting of DKD, has been unclear. METHODS: We analyzed expression of LRG1 mRNA in glomeruli of diabetic kidneys and assessed its localization by RNA in situ hybridization. We examined the effects of genetic ablation of Lrg1 on DKD progression in unilaterally nephrectomized, streptozotocin-induced diabetic mice at 12 and 20 weeks after diabetes induction. We also assessed whether plasma LRG1 was associated with renal outcome in patients with type 2 diabetes. RESULTS: LRG1 localized predominantly to glomerular endothelial cells, and its expression was elevated in the diabetic kidneys. LRG1 ablation markedly attenuated diabetes-induced glomerular angiogenesis, podocyte loss, and the development of diabetic glomerulopathy. These improvements were associated with reduced ALK1-Smad1/5/8 activation in glomeruli of diabetic mice. Moreover, increased plasma LRG1 was associated with worse renal outcome in patients with type 2 diabetes. CONCLUSIONS: These findings identify LRG1 as a potential novel pathogenic mediator of diabetic glomerular neoangiogenesis and a risk factor in DKD progression.
Increased SLC38A4 Amino Acid Transporter Expression in Human Pancreatic α-Cells Following Glucagon Receptor Inhibition

Endocrinology

2019 Mar 11

Kim J, Dominguez Gutierrez G, Xin Y, Cavino K, Sung B, Sipos B, Kloeppel G, Gromada J and Okamoto H
| DOI: 10.1210/en.2019-00022

p53-targeted lincRNA-p21 acts as a tumor suppressor by inhibiting JAK2/STAT3 signaling pathways in head and neck squamous cell carcinoma

Mol Cancer

2019 Mar 11

Jin S, Yang X, Li J, Yang W, Ma H and Zhang Z
PMID: 30857539 | DOI: 10.1186/s12943-019-0993-3

BACKGROUND: Long intergenic noncoding RNA p21 (lincRNA-p21) is considered a target of wild-type p53, but little is known about its regulation by mutant p53 and its functions during the progression of head and neck squamous cell carcinoma (HNSCC). METHODS: RNAscope was used to detect the expression and distribution of lincRNA-p21. Chromatin immunoprecipitation and electrophoretic mobility shift assays were performed to analyze the transcriptional regulation of lincRNA-p21 in HNSCC cells. The biological functions of lincRNA-p21 were investigated in vitro and in vivo. RNA immunoprecipitation and pull-down assays were used to detect the direct binding of lincRNA-p21. RESULTS: Lower lincRNA-p21 expression was observed in HNSCC tissues and indicated worse prognosis. Both wild and mutant type p53 transcriptionally regulated lincRNA-p21, but nuclear transcription factor Y subunit alpha (NF-YA) was essential for mutant p53 in the regulation of lincRNA-p21. Ectopic expression of lincRNA-p21 significantly inhibited cell proliferation capacity in vitro and in vivo and vice versa. Moreover, the overexpression of lincRNA-p21 induced G1 arrest and apoptosis. Knockdown NF-YA expression reversed tumor suppressor activation of lincRNA-p21 in mutant p53 cells, not wild-type p53 cells. A negative correlation was observed between lincRNA-p21 and the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) in HNSCC tissues. High lincRNA-p21 expression inhibited Janus kinase 2 (JAK2)/STAT3 signal activation and vice versa. Further, we observed direct binding to STAT3 by lincRNA-p21 in HNSCC cells, which suppressed STAT3-induced oncogenic potential. CONCLUSIONS: Our results revealed the transcriptional regulation of lincRNA-p21 by the mutant p53/NF-YA complex in HNSCC. LincRNA-p21 acted as a tumor suppressor in HNSCC progression, which was attributed to direct binding to STAT3 and blocking of JAK2/STAT3 signaling.
Brf1 loss and not overexpression disrupts tissues homeostasis in the intestine, liver and pancreas

Cell Death Differ

2019 Mar 11

Liko D, Mitchell L, Campbell KJ, Ridgway RA, Jones C, Dudek K, King A, Bryson S, Stevenson D, Blyth K, Strathdee D, Morton JP, Bird TG, Knight JRP, Willis AE and Sansom OJ
PMID: 30858608 | DOI: 10.1038/s41418-019-0316-7

RNA polymerase III (Pol-III) transcribes tRNAs and other small RNAs essential for protein synthesis and cell growth. Pol-III is deregulated during carcinogenesis; however, its role in vivo has not been studied. To address this issue, we manipulated levels of Brf1, a Pol-III transcription factor that is essential for recruitment of Pol-III holoenzyme at tRNA genes in vivo. Knockout of Brf1 led to embryonic lethality at blastocyst stage. In contrast, heterozygous Brf1 mice were viable, fertile and of a normal size. Conditional deletion of Brf1 in gastrointestinal epithelial tissues, intestine, liver and pancreas, was incompatible with organ homeostasis. Deletion of Brf1 in adult intestine and liver induced apoptosis. However, Brf1 heterozygosity neither had gross effects in these epithelia nor did it modify tumorigenesis in the intestine or pancreas. Overexpression of BRF1 rescued the phenotypes of Brf1 deletion in intestine and liver but was unable to initiate tumorigenesis. Thus, Brf1 and Pol-III activity are absolutely essential for normal homeostasis during development and in adult epithelia. However, Brf1 overexpression or heterozygosity are unable to modify tumorigenesis, suggesting a permissive, but not driving role for Brf1 in the development of epithelial cancers of the pancreas and gut.

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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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