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.
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Cancer letters
2022 Jun 01
Zhang, JY;Du, Y;Gong, LP;Shao, YT;Pan, LJ;Feng, ZY;Pan, YH;Huang, JT;Wen, JY;Sun, LP;Chen, GF;Chen, JN;Shao, CK;
PMID: 35304258 | DOI: 10.1016/j.canlet.2022.215646
Epstein-Barr virus (EBV) is a tumor virus that is associated with a variety of neoplasms, including EBV-associated gastric carcinoma (EBVaGC). Recently, EBV was reported to generate various circular RNAs (circRNAs). CircRNAs are important regulators of tumorigenesis by modulating the malignant behaviors of tumor cells. However, to date, the functions of ebv-circRNAs in EBVaGC remain poorly understood. In the present study, we observed high ebv-circRPMS1 expression in EBVaGC and showed that ebv-circRPMS1 promoted the proliferation, migration, and invasion and inhibited the apoptosis of EBVaGC cells. In addition, METTL3 was upregulated in GC cells overexpressing ebv-circRPMS1. Mechanistically, ebv-circRPMS1 bound to Sam68 to facilitate its physical interaction with the METTL3 promotor, resulting in the transactivation of METTL3 and cancer progression. In clinical EBVaGC samples, ebv-circRPMS1 was associated with distant metastasis and a poor prognosis. Based on these findings, ebv-circRPMS1 contributed to EBVaGC progression by recruiting Sam68 to the METTL3 promoter to induce METTL3 expression. ebv-circRPMS1, Sam68, and METTL3 might serve as therapeutic targets for EBVaGC.
Purinergic signalling
2022 Feb 15
Ye, M;Wang, M;Feng, Y;Shang, H;Yang, Y;Hu, L;Wang, M;Vakal, S;Lin, X;Chen, J;Zheng, W;
PMID: 35167016 | DOI: 10.1007/s11302-022-09847-5
The choroid plexus (CP) is one of the key gateways regulating the entry of peripheral immune cells into the CNS. However, the neuromodulatory mechanisms of maintaining its gateway activity are not fully understood. Here, we identified adenosine A2A receptor (A2AR) activity as a regulatory signal for the activity of CP gateway under physiological conditions. In association with a tightly closed CP gateway, we found that A2AR was present at low density in the CP. The RNA-seq analysis revealed that the A2AR antagonist KW6002 affected the expression of the cell adhesion molecules' (CAMs) pathway and cell response to IFN-γ in the CP. Furthermore, blocking or activating A2AR signaling in the CP resulted in a decreased and an increased, respectively, expression of lymphocyte trafficking determinants and disruption of the tight junctions (TJs). Furthermore, A2AR signaling regulates the CP permeability. Thus, A2AR activity in the CP may serve as a therapeutic target for remodeling the immune homeostasis in the CNS with implications for the treatment of neuroimmunological disorders.
SSRN Electronic Journal
2022 Jan 11
Webb, A;Schindell, B;Griffin, B;Soule, G;Siddik, A;Abrenica, B;Memon, H;Su, R;Kobasa, D;Safronetz, D;Kindrachuk, J;
| DOI: 10.2139/ssrn.4000892
Recent outbreaks of Ebola virus linked to chains of transmission from the 2014-2016 West African Ebola virus epidemic suggest a new paradigm for persistent Ebola virus infections as a lasting concern to public health. Cases of Ebola virus disease linked to sexual transmission and detection of Ebola virus in the male reproductive tract long after patients have recovered suggests that Ebola virus persistence occurs in this immune privileged area. However, little is known about Ebola virus cell tropism, viral kinetics, and host response to infection in the testis. In this study, we challenged immunocompromised mice and testicular tissue cultures with wild type Ebola virus. We utilized RT-qPCR and ISH to detect and quantify Ebola virus in the testis. We also employed RNAseq analysis to measure the transcriptomic response of specific testicular cell types to Ebola virus infection. Our results indicate that Ebola virus productively infects the cells at the blood-testis barrier, and that the interstitial space is more susceptible to infection compared to blood-testis barrier itself. In addition, the Sertoli cells that make up the physical structure of the blood-testis barrier maintain greater viability during Ebola virus infection, and this results from nonstandard immune response that prioritizes inhibited viral entry/replication and increased cell homeostatic activity. Our findings reinforce the need to further investigate viral persistence in the male reproductive tract as a reservoir for ongoing and future outbreaks of Ebola virus disease.
Immunological reviews
2021 Dec 02
Tan, Y;Tey, HL;Chong, SZ;Ng, LG;
PMID: 34859448 | DOI: 10.1111/imr.13049
As the largest organ of the body, the skin is a key barrier tissue with specialized structures where ongoing immune surveillance is critical for protecting the body from external insults. The innate immune system acts as first-responders in a coordinated manner to react to injury or infections, and recent developments in intravital imaging techniques have made it possible to delineate dynamic immune cell responses in a spatiotemporal manner. We review here key studies involved in understanding neutrophil, dendritic cell and macrophage behavior in skin and further discuss how this knowledge collectively highlights the importance of interactions and cellular functions in a systems biology manner. Furthermore, we will review emerging imaging technologies such as high-content proteomic screening, spatial transcriptomics and three-dimensional volumetric imaging and how these techniques can be integrated to provide a systems overview of the immune system that will further our current knowledge and lead to potential exciting discoveries in the upcoming decades.
Microorganisms
2021 Dec 08
Borrajo, A;Svicher, V;Salpini, R;Pellegrino, M;Aquaro, S;
PMID: 34946138 | DOI: 10.3390/microorganisms9122537
The chronic infection established by the human immunodeficiency virus 1 (HIV-1) produces serious CD4+ T cell immunodeficiency despite the decrease in HIV-1 ribonucleic acid (RNA) levels and the raised life expectancy of people living with HIV-1 (PLWH) through treatment with combined antiretroviral therapies (cART). HIV-1 enters the central nervous system (CNS), where perivascular macrophages and microglia are infected. Serious neurodegenerative symptoms related to HIV-associated neurocognitive disorders (HAND) are produced by infection of the CNS. Despite advances in the treatment of this infection, HAND significantly contribute to morbidity and mortality globally. The pathogenesis and the role of inflammation in HAND are still incompletely understood. Principally, growing evidence shows that the CNS is an anatomical reservoir for viral infection and replication, and that its compartmentalization can trigger the evolution of neurological damage and thus make virus eradication more difficult. In this review, important concepts for understanding HAND and neuropathogenesis as well as the viral proteins involved in the CNS as an anatomical reservoir for HIV infection are discussed. In addition, an overview of the recent advancements towards therapeutic strategies for the treatment of HAND is presented. Further neurological research is needed to address neurodegenerative difficulties in people living with HIV, specifically regarding CNS viral reservoirs and their effects on eradication.
Oncogene
2021 Oct 05
Hu, L;Chen, X;Narwade, N;Lim, MGL;Chen, Z;Tennakoon, C;Guan, P;Chan, UI;Zhao, Z;Deng, M;Xu, X;Sung, WK;Cheung, E;
PMID: 34611310 | DOI: 10.1038/s41388-021-02026-7
Androgen receptor (AR) plays a central role in driving prostate cancer (PCa) progression. How AR promotes this process is still not completely clear. Herein, we used single-cell transcriptome analysis to reconstruct the transcriptional network of AR in PCa. Our work shows AR directly regulates a set of signature genes in the ER-to-Golgi protein vesicle-mediated transport pathway. The expression of these genes is required for maximum androgen-dependent ER-to-Golgi trafficking, cell growth, and survival. Our analyses also reveal the signature genes are associated with PCa progression and prognosis. Moreover, we find inhibition of the ER-to-Golgi transport process with a small molecule enhanced antiandrogen-mediated tumor suppression of hormone-sensitive and insensitive PCa. Finally, we demonstrate AR collaborates with CREB3L2 in mediating ER-to-Golgi trafficking in PCa. In summary, our findings uncover a critical role for dysregulation of ER-to-Golgi trafficking expression and function in PCa progression, provide detailed mechanistic insights for how AR tightly controls this process, and highlight the prospect of targeting the ER-to-Golgi pathway as a therapeutic strategy for advanced PCa.
Subcellular localization of biomolecules and drug distribution by high-definition ion beam imaging
Nature communications
2021 Jul 30
Rovira-Clavé, X;Jiang, S;Bai, Y;Zhu, B;Barlow, G;Bhate, S;Coskun, AF;Han, G;Ho, CK;Hitzman, C;Chen, SY;Bava, FA;Nolan, GP;
PMID: 34330905 | DOI: 10.1038/s41467-021-24822-1
Simultaneous visualization of the relationship between multiple biomolecules and their ligands or small molecules at the nanometer scale in cells will enable greater understanding of how biological processes operate. We present here high-definition multiplex ion beam imaging (HD-MIBI), a secondary ion mass spectrometry approach capable of high-parameter imaging in 3D of targeted biological entities and exogenously added structurally-unmodified small molecules. With this technology, the atomic constituents of the biomolecules themselves can be used in our system as the "tag" and we demonstrate measurements down to ~30 nm lateral resolution. We correlated the subcellular localization of the chemotherapy drug cisplatin simultaneously with five subnuclear structures. Cisplatin was preferentially enriched in nuclear speckles and excluded from closed-chromatin regions, indicative of a role for cisplatin in active regions of chromatin. Unexpectedly, cells surviving multi-drug treatment with cisplatin and the BET inhibitor JQ1 demonstrated near total cisplatin exclusion from the nucleus, suggesting that selective subcellular drug relocalization may modulate resistance to this important chemotherapeutic treatment. Multiplexed high-resolution imaging techniques, such as HD-MIBI, will enable studies of biomolecules and drug distributions in biologically relevant subcellular microenvironments by visualizing the processes themselves in concert, rather than inferring mechanism through surrogate analyses.
Signaling through retinoic acid receptors is essential for mammalian uterine receptivity and decidualization
JCI insight
2021 Jul 22
Yin, Y;Haller, ME;Chadchan, SB;Kommagani, R;Ma, L;
PMID: 34292881 | DOI: 10.1172/jci.insight.150254
Retinoic Acid (RA) signaling has long been speculated to regulate embryo implantation, because many enzymes and proteins responsible for maintaining RA homeostasis and transducing RA signals are tightly regulated in the endometrium during this critical period. However, due to lack of genetic data, it was unclear whether RA signaling is truly required for implantation, and which specific RA signaling cascades are at play. Herein we utilize a genetic murine model that expresses a dominant negative form of RA receptor specifically in female reproductive organs to show that functional RA signaling is fundamental to female fertility, particularly implantation and decidualization. Reduction in RA signaling activity severely affects the ability of the uterus to achieve receptive status and decidualize, partially through dampening follistatin expression and downstream activin B/BMP2 signaling. To confirm translational relevance of these findings to humans, human endometrial stromal cells (hESCs) were treated with pan-RAR antagonist to show that in vitro decidualization is impaired. RNAi perturbation of individual RAR transcripts in hESCs revealed that RARα in particular is essential for proper decidualization. These data provide direct functional evidence that uterine RAR-mediated RA signaling is crucial for mammalian embryo implantation, and its disruption leads to failure of uterine receptivity and decidualization resulting in severely compromised fertility.
Astrocyte-derived CCL7 promotes microglia-mediated inflammation following traumatic brain injury
International immunopharmacology
2021 Jul 19
Xue, J;Zhang, Y;Zhang, J;Zhu, Z;Lv, Q;Su, J;
PMID: 34293712 | DOI: 10.1016/j.intimp.2021.107975
Microglia are immune cells of the central nervous system that mediate neuroinflammation. It is widely known that microglia-mediated inflammation in the brain contribute to the widespread tissue damage and neurological deficits in traumatic brain injury (TBI). However, the mechanisms responsible for this inflammatory response remain elusive. Here, we investigated the role of astrocyte-derived chemokine (C-C motif) ligand 7 (CCL7) in microglial-controlled inflammation following TBI. Our results demonstrated that astrocyte-derived CCL7 induced microglial activation and the release of proinflammatory mediators in the cortex and serum of rats that underwent experimental TBI. Furthermore, CCL7 knockout improved microglia-controlled inflammation, brain morphology and neurological dysfunction following TBI. In vitro, CCL7-siRNA attenuated the LPS-induced expression of pro-inflammatory markers in the co-culture of microglia and astrocytes. Collectively, our findings uncover an important role for astrocyte-derived CCL7 in promoting microglia-mediated inflammation after TBI and suggests CCL7 could serve as a potential therapeutic strategy for attenuating TBI by inhibiting microglial activation.
OMICs, Epigenetics, and Genome Editing Techniques for Food and Nutritional Security
Plants
2021 Jul 12
Gogolev, Y;Ahmar, S;Akpinar, B;Budak, H;Kiryushkin, A;Gorshkov, V;Hensel, G;Demchenko, K;Kovalchuk, I;Mora-Poblete, F;Muslu, T;Tsers, I;Yadav, N;Korzun, V;
| DOI: 10.3390/plants10071423
The incredible success of crop breeding and agricultural innovation in the last century greatly contributed to the Green Revolution, which significantly increased yields and ensures food security, despite the population explosion. However, new challenges such as rapid climate change, deteriorating soil, and the accumulation of pollutants require much faster responses and more effective solutions that cannot be achieved through traditional breeding. Further prospects for increasing the efficiency of agriculture are undoubtedly associated with the inclusion in the breeding strategy of new knowledge obtained using high-throughput technologies and new tools in the future to ensure the design of new plant genomes and predict the desired phenotype. This article provides an overview of the current state of research in these areas, as well as the study of soil and plant microbiomes, and the prospective use of their potential in a new field of microbiome engineering. In terms of genomic and phenomic predictions, we also propose an integrated approach that combines high-density genotyping and high-throughput phenotyping techniques, which can improve the prediction accuracy of quantitative traits in crop species.
Loss of Selenov predisposes mice to extra fat accumulation and attenuated energy expenditure
Redox biology
2021 Jun 17
Chen, LL;Huang, JQ;Wu, YY;Chen, LB;Li, SP;Zhang, X;Wu, S;Ren, FZ;Lei, XG;
PMID: 34167027 | DOI: 10.1016/j.redox.2021.102048
Selenoprotein V (SELENOV) is a new and the least conserved member of the selenoprotein family. Herein we generated Selenov knockout (KO) mice to determine its in vivo function. The KO led to 16-19% increases (P < 0.05) in body weight that were largely due to 54% higher (P < 0.05) fat mass accumulation, compared with the wild-type (WT) controls. The extra fat accumulation in the KO mice was mediated by up-regulations of genes and proteins involved in lipogenesis (Acc, Fas, Dgat, and Lpl; up by 40%-1.1-fold) and down-regulations of lipolysis (Atgl, Hsl, Ces1d, and Cpt1a; down by 36-89%) in the adipose tissues. The KO also decreased (P < 0.05) VO2 consumption (14-21%), VCO2 production (14-16%), and energy expenditure (14-23%), compared with the WT controls. SELENOV and O-GlcNAc transferase (OGT) exhibited a novel protein-protein interaction that explained the KO-induced decreases (P < 0.05) of OGT protein (15-29%), activity (33%), and function (O-GlcNAcylation, 10-21%) in the adipose tissues. A potential cascade of SELENOV-OGT-AMP-activated protein kinase might serve as a central mechanism to link the biochemical and molecular responses to the KO. Overall, our data revealed a novel in vivo function and mechanism of SELENOV as a new inhibitor of body fat accumulation, activator of energy expenditure, regulator of O-GlcNAcylation, and therapeutic target of such related disorders.
LncRNA H19 aggravates intervertebral disc degeneration by promoting the autophagy and apoptosis of nucleus pulposus cells via the miR-139/CXCR4/NF-κB axis
Stem cells and development
2021 May 20
Sun, Z;Tang, X;Wang, H;Sun, H;Chu, P;Sun, L;Tian, J;
PMID: 34015968 | DOI: 10.1089/scd.2021.0009
The etiology of lumbocrural pain is closely related to intervertebral disc degeneration (IDD). Long noncoding RNAs (LncRNAs) serve crucial roles in IDD progression. This study investigated the effect of lncRNA H19 on autophagy and apoptosis of nucleus pulposus cells (NPCs) in IDD. The rat model of IDD was established. Normal NPCs and degenerative NPCs (DNPCs) were cultured in vitro. H19 expression in IDD rat was detected. DNPCs were treated with si-H19 to evaluate autophagy and apoptosis of DNPCs. The binding relationships between H19 and miR-139-3p, and miR-139-3p and CXCR4 were verified. DNPCs were co-transfected si-H19 and miR-139-3p inhibitor. The phosphorylation of NF-κB pathway related p65 in DNPCs was detected. LncRNA H19 was upregulated in IDD rats. Downregulation of H19 inhibited autophagy and apoptosis of DNPCs. LncRNA H19 sponged miR-139-3p to inhibit CXCR4 expression. si-H19 and miR-139-3p inhibitor co-treatment induced autophagy and apoptosis, and enhanced CXCR4 expression. si-H19 decreased p-p65 phosphorylation, while si-H19 and miR-139-3p inhibitor co-treatment partially elevated p-p65 phosphorylation. In conclusion, lncRNA H19 facilitated the autophagy and apoptosis of DNPCs via the miR-139-3p/CXCR4/NF-κB axis, thereby aggravating IDD. This study may offer new insights for the management of IDD.
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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 | |
| EnEm | Probe targets exons n and m | |
| En-Em | Probe 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 | |
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