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 discovery
2023 Apr 26
Wan, L;Lin, KT;Rahman, MA;Ishigami, Y;Wang, Z;Jensen, MA;Wilkinson, JE;Park, Y;Tuveson, DA;Krainer, AR;
PMID: 37098965 | DOI: 10.1158/2159-8290.CD-22-1013
Inflammation is strongly associated with pancreatic ductal adenocarcinoma (PDAC), a highly lethal malignancy. Dysregulated RNA splicing factors have been widely reported in tumorigenesis, but their involvement in pancreatitis and PDAC is not well understood. Here, we report that the splicing factor SRSF1 is highly expressed in pancreatitis, PDAC precursor lesions, and tumors. Increased SRSF1 is sufficient to induce pancreatitis and accelerate KRASG12D-mediated PDAC. Mechanistically, SRSF1 activates MAPK signaling-partly by upregulating interleukin 1 receptor type 1 (IL1R1) through alternative-splicing-regulated mRNA stability. Additionally, SRSF1 protein is destabilized through a negative feedback mechanism in phenotypically normal epithelial cells expressing KRASG12D in mouse pancreas, and in pancreas organoids acutely expressing KRASG12D, buffering MAPK signaling and maintaining pancreas-cell homeostasis. This negative-feedback regulation of SRSF1 is overcome by hyperactive MYC, facilitating PDAC tumorigenesis. Our findings implicate SRSF1 in the etiology of pancreatitis and PDAC, and point to SRSF1-misregulated alternative splicing as a potential therapeutic target.
Science immunology
2023 Feb 03
Sahu, SK;Ozantürk, AN;Kulkarni, DH;Ma, L;Barve, RA;Dannull, L;Lu, A;Starick, M;McPhatter, J;Garnica, L;Sanfillipo-Burchman, M;Kunen, J;Wu, X;Gelman, AE;Brody, SL;Atkinson, JP;Kulkarni, HS;
PMID: 36735773 | DOI: 10.1126/sciimmunol.abp9547
The complement component C3 is a fundamental plasma protein for host defense, produced largely by the liver. However, recent work has demonstrated the critical importance of tissue-specific C3 expression in cell survival. Here, we analyzed the effects of local versus peripheral sources of C3 expression in a model of acute bacterial pneumonia induced by Pseudomonas aeruginosa. Whereas mice with global C3 deficiency had severe pneumonia-induced lung injury, those deficient only in liver-derived C3 remained protected, comparable to wild-type mice. Human lung transcriptome analysis showed that secretory epithelial cells, such as club cells, express high levels of C3 mRNA. Mice with tamoxifen-induced C3 gene ablation from club cells in the lung had worse pulmonary injury compared with similarly treated controls, despite maintaining normal circulating C3 levels. Last, in both the mouse pneumonia model and cultured primary human airway epithelial cells, we showed that stress-induced death associated with C3 deficiency parallels that seen in Factor B deficiency rather than C3a receptor deficiency. Moreover, C3-mediated reduction in epithelial cell death requires alternative pathway component Factor B. Thus, our findings suggest that a pathway reliant on locally derived C3 and Factor B protects the lung mucosal barrier.
Experimental eye research
2023 Mar 01
Peperstraete, K;Baes, M;Swinkels, D;
PMID: 36740160 | DOI: 10.1016/j.exer.2023.109406
Utilizing cell type-specific knockout mice has been an excellent tool for decades not only to explore the role of a gene in a specific cell, but also to unravel the underlying mechanism in diseases. To investigate the mechanistic association between dysfunction of the peroxisomal protein multifunctional protein 2 (MFP2) and retinopathy, we generated and phenotyped multiple transgenic mouse models with global or cell type-specific MFP2 deletion. These studies pointed to a potential role of MFP2 specifically in rod bipolar cells. To explore this, we aimed to create rod bipolar cell specific knockout mice of Mfp2 by crossing Mfp2L/L mice with L7Cre-2 mice (also known as PCP2Cre), generating L7-Mfp2-/- mice. L7Cre-2 mice express Cre recombinase under the control of the L7 promoter, which is believed to be exclusively expressed in rod bipolar cells and cerebellar Purkinje cells. Unexpectedly, only sporadic Cre activity was observed in the rod bipolar cells of L7-Mfp2-/- mice, despite efficient Cre recombination in cerebellar Purkinje cells. Moreover, a variable fraction of photoreceptors was targeted, which does not correspond with the supposed specificity of L7Cre-2 mice. These observations indicate that L7Cre-2 mice can be exploited to manipulate Purkinje cells in the cerebellum, whereas they cannot be used to generate rod bipolar cell specific knockout mice. For this aim, we suggest utilizing an independently generated mouse line named BAC-L7-IRES-Cre.
Life (Basel, Switzerland)
2023 Feb 14
Ross, AM;Leahy, CI;Neylon, F;Steigerova, J;Flodr, P;Navratilova, M;Urbankova, H;Vrzalikova, K;Mundo, L;Lazzi, S;Leoncini, L;Pugh, M;Murray, PG;
PMID: 36836878 | DOI: 10.3390/life13020521
Epstein-Barr virus (EBV), defined as a group I carcinogen by the World Health Organization (WHO), is present in the tumour cells of patients with different forms of B-cell lymphoma, including Burkitt lymphoma, Hodgkin lymphoma, post-transplant lymphoproliferative disorders, and, most recently, diffuse large B-cell lymphoma (DLBCL). Understanding how EBV contributes to the development of these different types of B-cell lymphoma has not only provided fundamental insights into the underlying mechanisms of viral oncogenesis, but has also highlighted potential new therapeutic opportunities. In this review, we describe the effects of EBV infection in normal B-cells and we address the germinal centre model of infection and how this can lead to lymphoma in some instances. We then explore the recent reclassification of EBV+ DLBCL as an established entity in the WHO fifth edition and ICC 2022 classifications, emphasising the unique nature of this entity. To that end, we also explore the unique genetic background of this entity and briefly discuss the potential role of the tumour microenvironment in lymphomagenesis and disease progression. Despite the recent progress in elucidating the mechanisms of this malignancy, much work remains to be done to improve patient stratification, treatment strategies, and outcomes.
American journal of physiology. Renal physiology
2022 Dec 22
Dickinson, K;Hammond, L;Akpa, M;Chu, LL;Lalonde, CT;Goumba, A;Goodyer, P;
PMID: 36546838 | DOI: 10.1152/ajprenal.00207.2022
Mammalian nephrons arise from a population of nephron progenitor cells (NPCs) expressing the master transcription factor, WT1, which is crucial for NPC proliferation, migration, and differentiation. In humans, biallelic loss of WT1 precludes nephrogenesis and leads to formation of Wilms tumor precursor lesions. We hypothesize that WT1 normally primes the NPC for nephrogenesis by inducing expression of NPC-specific DNA-repair genes that protect the genome. We analyzed transcript levels for a panel of DNA-repair genes in E17.5 vs adult mouse kidneys and noted seven that were increased >20-fold. We then isolated d1(+) NPCs from E17.5 kidneys and found that only one, Neil3, was enriched. RNAscope ISH of E17.5 mouse kidneys showed increased Neil3 expression in the nephrogenic zone vs mature nephron structures. To determine whether Neil3-expression is WT1-dependent, we knocked down Wt1 in d1(+) NPCs (60% knockdown efficiency) and noted a 58% reduction in Neil3 transcript levels. We showed that WT1 directly binds to the Neil3 promoter and that activity of a Neil3 promoter-reporter vector was increased two-fold in WT1(+) vs WT1(-) cells. We propose that Neil3 is a WT1-dependent DNA-repair gene, expressed at high levels in d1(+) NPCs where it repairs mutational injury to the genome during nephrogenesis. NEIL3 is likely just one of many such lineage-specific repair mechanisms that respond to genomic injury during kidney development.
Brain, behavior, and immunity
2022 Aug 29
Reinl, EL;Blanchard, AC;Graham, EL;Edwards, S;Dionisos, C;McCarthy, MM;
PMID: 36049705 | DOI: 10.1016/j.bbi.2022.08.012
Little is known about the peripheral immune cell (PIC) profile of the developing brain despite growing appreciation for these cells in the mature nervous system. To address this gap, the PIC profile, defined as which cells are present, where they are located, and for how long, was examined in the developing rat using spectral flow cytometry. Select regions of the rat brain (cerebellum, hippocampus, and hypothalamus) were examined at embryonic day 20, and postnatal days 0, 7 and 16. At their peak (E20), PICs were most abundant in the cerebellum, then the hippocampus and hypothalamus. Within the PIC pool, monocytes were most prevalent in all regions and time points, and shifted from being majority classical at E20 to non-classical by PN7. T cells increased over time, and shifted from majority cytotoxic to T-helper cells by PN7. This suggests the PIC profile transitions from reactive to adaptive and surveilling in the second postnatal week. NK cells and mast cells increased temporarily, and mast cells were restricted to the hippocampus and hypothalamus, suggesting they may play a specific role in the development of those regions. Mimicking a viral infection by administration of Poly I:C increased the influx of PICs into the neonatal brain, particularly of NK cells and in the case of males only, non-classical monocytes. This work provides a map for researchers as they study immune cell contributions to healthy and pathological brain development.
Cancer research
2022 Aug 11
Pitter, KL;Grbovic-Huezo, O;Joost, S;Singhal, A;Blum, M;Wu, K;Holm, M;Ferrena, A;Bhutkar, A;Hudson, A;Lecomte, N;de Stanchina, E;Chaligne, R;Iacobuzio-Donahue, CA;Pe'er, D;Tammela, T;
PMID: 35952360 | DOI: 10.1158/0008-5472.CAN-22-1742
Intra-tumoral heterogeneity and cellular plasticity have emerged as hallmarks of cancer, including pancreatic ductal adenocarcinoma (PDAC). As PDAC portends a dire prognosis, a better understanding of the mechanisms underpinning cellular diversity in PDAC is crucial. Here, we investigated the cellular heterogeneity of PDAC cancer cells across a range of in vitro and in vivo growth conditions using single-cell genomics. Heterogeneity contracted significantly in 2D and 3D cell culture models but was restored upon orthotopic transplantation. Orthotopic transplants reproducibly acquired cell states identified in autochthonous PDAC tumors, including a basal state exhibiting co-expression and co-accessibility of epithelial and mesenchymal genes. Lineage-tracing combined with single-cell transcriptomics revealed that basal cells display high plasticity in situ. This work defines the impact of cellular growth conditions on phenotypic diversity and uncovers a highly plastic cell state with the capacity to facilitate state transitions and promote intra-tumoral heterogeneity in PDAC.
Journal of Swine Health and Production
2022 May 02
Buckley, A;Lager, K;
| DOI: 10.54846/jshap/1270
Senecavirus A (SVA) has been demonstrated to be a causative agent for vesicular disease in swine. It is clinically indistinguishable from other agents that cause vesicular disease such as foot-and-mouth disease virus (FMDV), which is a reportable foreign animal disease (FAD). Thus, an investigation is initiated to rule out FMDV every time a vesicle is observed. Senecavirus A has now been reported across the Americas and Asia, and it appears the ecology of this virus has changed from sporadic infections to an endemic disease in some areas. In addition to vesicular disease, there have also been reports of increased neonatal mortality on affected sow farms. Knowledge about the pathogenesis of SVA in swine can provide many benefits to the swine industry. Understanding how long the virus can be detected in various sample types after infection can aide in choosing the correct samples to collect for diagnosis. In addition, the duration of virus shedding can help determine measures to control virus spread between animals. Prevention of SVA infection and disease with an efficacious vaccine could improve swine welfare, minimize SVA transmission, and reduce the burden of FAD investigations.
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.
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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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