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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Evaluation of Human Kidney Injury Molecule 1 (hKIM-1) Expression in Tumors From Various Organs by Messenger RNA In Situ Hybridization
American journal of clinical pathology
2021 Feb 20
Sarami, I;Shi, J;Lin, B;Liu, H;Monroe, R;Lin, F;
PMID: 33608720 | DOI: 10.1093/ajcp/aqaa236
Human kidney injury molecule 1 (hKIM-1) is a sensitive and specific marker for detection of clear cell renal cell carcinoma (CRCC), papillary renal cell carcinoma (PRCC), and ovarian clear cell carcinoma (OCCC). Its use was limited to a few surgical pathology laboratories because this specific antibody to hKIM-1 was not commercially available. We investigated the diagnostic utility of RNA in situ hybridization/RNAscope in the detection of hKIM-1 in tumors from various organs. RNAscope for hKIM-1 was performed on 1,252 cases on tissue microarray sections, including CRCC (n = 185), PRCC (n = 59), chromophobe renal cell carcinoma (n = 18), oncocytoma (n = 12), OCCC (n = 27), and metastatic CRCC (n = 46). Fifty-nine (100%) of 59 PRCCs, 94 (95%) of 99 low-grade CRCCs, 83 (96%) of 86 high-grade CRCCs, and 24 (89%) of 27 OCCCs, and 44 (96%) of 46 metastatic CRCCs were positive for hKIM-1. In contrast, hKIM-1 expression was not seen in normal renal tubules or in most nonrenal tumors. Low-level expression could be seen in a small percentage of urothelial, hepatocellular, and colon carcinomas. hKIM-1 is a sensitive and relatively specific marker (1) for diagnosing PRCC, CRCC, and OCCC when working on a tumor of unknown origin and (2) for differentiating CRCC from chromophobe renal cell carcinoma and oncocytoma.
Nature medicine
2023 Jun 01
Magen, A;Hamon, P;Fiaschi, N;Soong, BY;Park, MD;Mattiuz, R;Humblin, E;Troncoso, L;D'souza, D;Dawson, T;Kim, J;Hamel, S;Buckup, M;Chang, C;Tabachnikova, A;Schwartz, H;Malissen, N;Lavin, Y;Soares-Schanoski, A;Giotti, B;Hegde, S;Ioannou, G;Gonzalez-Kozlova, E;Hennequin, C;Le Berichel, J;Zhao, Z;Ward, SC;Fiel, I;Kou, B;Dobosz, M;Li, L;Adler, C;Ni, M;Wei, Y;Wang, W;Atwal, GS;Kundu, K;Cygan, KJ;Tsankov, AM;Rahman, A;Price, C;Fernandez, N;He, J;Gupta, NT;Kim-Schulze, S;Gnjatic, S;Kenigsberg, E;Deering, RP;Schwartz, M;Marron, TU;Thurston, G;Kamphorst, AO;Merad, M;
PMID: 37322116 | DOI: 10.1038/s41591-023-02345-0
Despite no apparent defects in T cell priming and recruitment to tumors, a large subset of T cell rich tumors fail to respond to immune checkpoint blockade (ICB). We leveraged a neoadjuvant anti-PD-1 trial in patients with hepatocellular carcinoma (HCC), as well as additional samples collected from patients treated off-label, to explore correlates of response to ICB within T cell-rich tumors. We show that ICB response correlated with the clonal expansion of intratumoral CXCL13+CH25H+IL-21+PD-1+CD4+ T helper cells ("CXCL13+ TH") and Granzyme K+ PD-1+ effector-like CD8+ T cells, whereas terminally exhausted CD39hiTOXhiPD-1hiCD8+ T cells dominated in nonresponders. CD4+ and CD8+ T cell clones that expanded post-treatment were found in pretreatment biopsies. Notably, PD-1+TCF-1+ (Progenitor-exhausted) CD8+ T cells shared clones mainly with effector-like cells in responders or terminally exhausted cells in nonresponders, suggesting that local CD8+ T cell differentiation occurs upon ICB. We found that these Progenitor CD8+ T cells interact with CXCL13+ TH within cellular triads around dendritic cells enriched in maturation and regulatory molecules, or "mregDC". These results suggest that discrete intratumoral niches that include mregDC and CXCL13+ TH control the differentiation of tumor-specific Progenitor exhasuted CD8+ T cells following ICB.
ChemRxiv Analytical Chemistry
2023 Apr 28
Robles-Remacho*, A;Sanchez-Martin, R;Diaz-Mochon*, J;
| DOI: 10.26434/chemrxiv-2023-n20f0
Spatial transcriptomics technologies are providing new insights to study gene expression, allowing researchers to investigate the spatial organization of transcriptomes in cells and tissues. This approach enables the creation of high-resolution maps of gene expression patterns within their native spatial context, adding an extra layer of information to bulk sequencing data. Spatial transcriptomics has expanded significantly in recent years and is making a notable impact on a range of fields, including tissue architecture, developmental biology, cancer, neurodegenerative and infectious diseases. The latest advancements in spatial transcriptomics have resulted in the development of highly multiplexed methods, transcriptomic-wide analysis, and single-cell resolution, utilizing diverse technological approaches. In this perspective, we provide a detailed analysis of the molecular foundations behind the main spatial transcriptomics technologies, including methods based on microdissection, in situ sequencing, single-molecule FISH, spatial capturing, selection of regions of interest and single-cell or nuclei dissociation. We contextualize the detection and capturing efficiency, strengths, limitations, tissue compatibility, and applications of these techniques, as well as provide information on data analysis. In addition, this perspective discusses future directions and potential applications of spatial transcriptomics, highlighting the importance of the continued development to promote widespread adoption of these techniques within the research community.
Vectorology for Optogenetics and Chemogenetics
2023 Feb 07
Bohlen, M;Tremblay, S;
| DOI: 10.1007/978-1-0716-2918-5_16
The development of new genetic tools has revolutionized our ability to study the functional role of specific neuronal populations and circuits generating behavior. Although this revolution has already taken place in small animal models such as mice, adoption of these techniques has been relatively slow for animals more closely related to humans, such as nonhuman primates. Current challenges include effective delivery to much larger structural targets in the primate brain, cell-type specific transduction, and immunological responses. In this chapter, we will review some of the challenges and considerations that are specific to using these viral technologies in the nonhuman primate brain. Ultimately, these challenges can be met with new advances in surgical technique and gene therapy that will spin out new viral vectors with enhanced features able to compensate for the limitations of current vectors. As the existing challenges are circumvented, this will lead to a revolution in primate neuroscientific research and a greater understanding of the functional role circuits play in complex behaviors relevant to human neurological and psychiatric diseases.
Molecular cell
2022 Dec 15
Plaza-Jennings, AL;Valada, A;O'Shea, C;Iskhakova, M;Hu, B;Javidfar, B;Ben Hutta, G;Lambert, TY;Murray, J;Kassim, B;Chandrasekaran, S;Chen, BK;Morgello, S;Won, H;Akbarian, S;
PMID: 36525955 | DOI: 10.1016/j.molcel.2022.11.016
To explore genome organization and function in the HIV-infected brain, we applied single-nuclei transcriptomics, cell-type-specific chromosomal conformation mapping, and viral integration site sequencing (IS-seq) to frontal cortex from individuals with encephalitis (HIVE) and without (HIV+). Derepressive changes in 3D genomic compartment structures in HIVE microglia were linked to the transcriptional activation of interferon (IFN) signaling and cell migratory pathways, while transcriptional downregulation and repressive compartmentalization of neuronal health and signaling genes occurred in both HIVE and HIV+ microglia. IS-seq recovered 1,221 brain integration sites showing distinct genomic patterns compared with peripheral lymphocytes, with enrichment for sequences newly mobilized into a permissive chromatin environment after infection. Viral transcription occurred in a subset of highly activated microglia comprising 0.33% of all nuclei in HIVE brain. Our findings point to disrupted microglia-neuronal interactions in HIV and link retroviral integration to remodeling of the microglial 3D genome during infection.
Cell reports
2022 Nov 22
Bakker, W;Imbernon, M;Salinas, CG;Moro Chao, DH;Hassouna, R;Morel, C;Martin, C;Leger, C;Denis, RGP;Castel, J;Peter, A;Heni, M;Maetzler, W;Nielsen, HS;Duquenne, M;Schwaninger, M;Lundh, S;Johan Hogendorf, WF;Gangarossa, G;Secher, A;Hecksher-Sørensen, J;Pedersen, TÅ;Prevot, V;Luquet, S;
PMID: 36417883 | DOI: 10.1016/j.celrep.2022.111698
Therapies based on glucagon-like peptide-1 (GLP-1) long-acting analogs and insulin are often used in the treatment of metabolic diseases. Both insulin and GLP-1 receptors are expressed in metabolically relevant brain regions, suggesting a cooperative action. However, the mechanisms underlying the synergistic actions of insulin and GLP-1R agonists remain elusive. In this study, we show that insulin-induced hypoglycemia enhances GLP-1R agonists entry in hypothalamic and area, leading to enhanced whole-body fat oxidation. Mechanistically, this phenomenon relies on the release of tanycyctic vascular endothelial growth factor A, which is selectively impaired after calorie-rich diet exposure. In humans, low blood glucose also correlates with enhanced blood-to-brain passage of insulin, suggesting that blood glucose gates the passage other energy-related signals in the brain. This study implies that the preventing hyperglycemia is important to harnessing the full benefit of GLP-1R agonist entry in the brain and action onto lipid mobilization and body weight loss.
Developmental biology
2022 May 26
Clayton, SW;Angermeier, A;Halbrooks, JE;McCardell, R;Serra, R;
PMID: 35644252 | DOI: 10.1016/j.ydbio.2022.05.013
We previously showed the importance of TGFβ signaling in development of the mouse axial skeleton. Here, we provide the first direct evidence that TGFβ signaling is required for resegmentation of the sclerotome using chick embryos. Lipophilic fluorescent tracers, DiO and DiD, were microinjected into adjacent somites of embryos treated with or without TGFβRI inhibitors, SB431542, SB525334 or SD208, at developmental day E2.5 (HH16). Lineage tracing of labeled cells was observed over the course of 4 days until the completion of resegmentation at E6.5 (HH32). Vertebrae were malformed and intervertebral discs were small and misshapen in inhibitor injected embryos. Hypaxial myofibers were also increased in thickness after treatment with the inhibitor. Inhibition of TGFβ signaling resulted in alterations in resegmentation that ranged between full, partial, and slanted shifts in distribution of DiO or DiD labeled cells within vertebrae. Patterning of rostro-caudal markers within sclerotome was disrupted at E3.5 after treatment with TGFβRI inhibitor with rostral domains expressing both rostral and caudal markers. We propose that TGFβ signaling regulates rostro-caudal polarity and subsequent resegmentation in sclerotome during spinal column development.
Scientific reports
2022 Mar 08
Scheff, NN;Wall, IM;Nicholson, S;Williams, H;Chen, E;Tu, NH;Dolan, JC;Liu, CZ;Janal, MN;Bunnett, NW;Schmidt, BL;
PMID: 35260737 | DOI: 10.1038/s41598-022-08005-6
Oral cancer patients report sensitivity to spicy foods and liquids. The mechanism responsible for chemosensitivity induced by oral cancer is not known. We simulate oral cancer-induced chemosensitivity in a xenograft oral cancer mouse model using two-bottle choice drinking and conditioned place aversion assays. An anatomic basis of chemosensitivity is shown in increased expression of TRPV1 in anatomically relevant trigeminal ganglion (TG) neurons in both the xenograft and a carcinogen (4-nitroquinoline 1-oxide)-induced oral cancer mouse models. The percent of retrograde labeled TG neurons that respond to TRPV1 agonist, capsaicin, is increased along with the magnitude of response as measured by calcium influx, in neurons from the cancer models. To address the possible mechanism of TRPV1 sensitivity in tongue afferents, we study the role of PAR2, which can sensitize the TRPV1 channel. We show co-expression of TRPV1 and PAR2 on tongue afferents and using a conditioned place aversion assay, demonstrate that PAR2 mediates oral cancer-induced, TRPV1-evoked sensitivity in an oral cancer mouse model. The findings provide insight into oral cancer-mediated chemosensitivity.
Molecular therapy : the journal of the American Society of Gene Therapy
2022 Jan 31
Fang, F;Zhuang, P;Feng, X;Liu, P;Liu, D;Huang, H;Li, L;Chen, W;Liu, L;Sun, Y;Jiang, H;Ye, J;Hu, Y;
PMID: 35114390 | DOI: 10.1016/j.ymthe.2022.01.035
The lack of neuroprotective treatments for retinal ganglion cells (RGCs) and optic nerve (ON) is a central challenge for glaucoma management. Emerging evidence suggests that redox factor NAD+ decline is a hallmark of aging and neurodegenerative diseases. Supplementation with NAD+ precursors and overexpression of NMNAT1, the key enzyme in the NAD+ biosynthetic process, have significant neuroprotective effects. We first profile the translatomes of RGCs in naive mice and mice with silicone oil-induced ocular hypertension (SOHU)/glaucoma by RiboTag mRNA sequencing. Intriguingly, only NMNAT2, but not NMNAT1 or NMNAT3, is significantly decreased in SOHU glaucomatous RGCs, which we confirm by in situ hybridization. We next demonstrate that AAV2 intravitreal injection-mediated overexpression of long half-life NMNAT2 mutant driven by RGC-specific mouse γ-synuclein (mSncg) promoter restores decreased NAD+ levels in glaucomatous RGCs and ONs. Moreover, this RGC-specific gene therapy strategy delivers significant neuroprotection of both RGC soma and axon and preservation of visual function in the traumatic ON crush model and the SOHU glaucoma model. Collectively, our studies suggest that the weakening of NMNAT2 expression in glaucomatous RGCs contributes to a deleterious NAD+ decline, and that modulating RGC-intrinsic NMNAT2 levels by AAV2-mSncg vector is a promising gene therapy for glaucomatous neurodegeneration.
British journal of cancer
2022 Feb 16
Patel, M;Pennel, KAF;Quinn, JA;Hood, H;Chang, DK;Biankin, AV;Rebus, S;Roseweir, AK;Park, JH;Horgan, PG;McMillan, DC;Edwards, J;
PMID: 35173303 | DOI: 10.1038/s41416-022-01729-2
To understand the relationship between key non-canonical NF-κB kinase IKK-alpha(α), tumour mutational profile and survival in primary colorectal cancer.Immunohistochemical expression of IKKα was assessed in a cohort of 1030 patients who had undergone surgery for colorectal cancer using immunohistochemistry. Mutational tumour profile was examined using a customised gene panel. Immunofluorescence was used to identify the cellular location of punctate IKKα expression.Two patterns of IKKα expression were observed; firstly, in the tumour cell cytoplasm and secondly as discrete 'punctate' areas in a juxtanuclear position. Although cytoplasmic expression of IKKα was not associated with survival, high 'punctate' IKKα expression was associated with significantly reduced cancer-specific survival on multivariate analysis. High punctate expression of IKKα was associated with mutations in KRAS and PDGFRA. Dual immunofluorescence suggested punctate IKKα expression was co-located with the Golgi apparatus.These results suggest the spatial expression of IKKα is a potential biomarker in colorectal cancer. This is associated with a differential mutational profile highlighting possible distinct signalling roles for IKKα in the context of colorectal cancer as well as potential implications for future treatment strategies using IKKα inhibitors.
Brain
2021 Sep 30
Steinkellner, T;Conrad, WS;Kovacs, I;Rissman, RA;
| DOI: 10.1093/brain/awab373
Loss of midbrain dopamine neurons causes the cardinal symptoms of Parkinson’s disease. However, not all dopamine neurons are equally vulnerable and a better understanding of the cell-type specific properties relating to selective dopamine neuron degeneration is needed. Most midbrain dopamine neurons express the vesicular glutamate transporter VGLUT2 during development and a subset continue to express low levels of VGLUT2 in adulthood, enabling the co-release of glutamate. Moreover, VGLUT2 expression in dopamine neurons can be neuroprotective since its genetic disruption was shown to sensitize dopamine neurons to neurotoxins. Here, we show that in response to toxic insult, and in two distinct models of alpha-synuclein stress, VGLUT2 dopamine neurons were resilient to degeneration. Dopamine neurons expressing VGLUT2 were enriched whether or not insult induced dopamine neuron loss, suggesting that while VGLUT2 dopamine neurons are more resilient, VGLUT2 expression can also be transcriptionally upregulated by injury. Finally, we observed that VGLUT2 expression was enhanced in surviving DA neurons from postmortem Parkinson’s disease subjects. These data indicate that emergence of a glutamatergic identity in dopamine neurons may be part of a neuroprotective response in Parkinson’s disease.
Obstetrics and gynecology
2021 Nov 02
Girardi, G;Bremer, AA;
PMID: 34727554 | DOI: 10.1097/AOG.0000000000004636
Three coronavirus disease 2019 (COVID-19) vaccines have been authorized for use in the United States; specifically, the Pfizer-BioNTech, Moderna, and Johnson & Johnson-Janssen COVID-19 vaccines were granted emergency use authorization by the U.S. Food and Drug Administration in late 2020 and early 2021. Vaccination coverage and intent among adults are lowest among those aged 18-39 years and among females in particular. In females of reproductive age, enthusiasm for receiving a COVID-19 vaccine may be negatively affected by claims currently circulating widely on diverse social media platforms regarding the vaccines adversely affecting fertility and pregnancy. Yet it is important to note that these claims are anecdotal in nature and not supported by the available scientific evidence. It is also imperative that the effects of COVID-19 vaccine on reproductive health are clarified. Herein, we discuss the existing scientific data supporting COVID-19 vaccine safety and efficacy in people who are planning to conceive or who are pregnant or lactating and highlight the importance of COVID-19 vaccination in females of reproductive age.
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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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