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.
Aging cell
2022 Apr 01
Chandra, A;Lagnado, AB;Farr, JN;Doolittle, M;Tchkonia, T;Kirkland, JL;LeBrasseur, NK;Robbins, PD;Niedernhofer, LJ;Ikeno, Y;Passos, JF;Monroe, DG;Pignolo, RJ;Khosla, S;
PMID: 35363946 | DOI: 10.1111/acel.13602
J Neurosci.
2016 Jun 22
Warren BL, Mendoza MP, Cruz FC, Leao RM, Caprioli D, Rubio FJ, Whitaker LR, McPherson KB, Bossert JM, Shaham Y, Hope BT.
PMID: 27335401 | DOI: 10.1523/JNEUROSCI.0140-16.2016
Front Mol Neurosci.
2018 Jun 19
Lee S, Lee E, Kim R, Kim J, Lee S, Park H, Yang E, Kim H, Kim E.
PMID: 29970987 | DOI: 10.3389/fnmol.2018.00209
Shank2 is an abundant postsynaptic scaffolding protein implicated in neurodevelopmental and psychiatric disorders, including autism spectrum disorders (ASD). Deletion of Shank2 in mice has been shown to induce social deficits, repetitive behaviors, and hyperactivity, but the identity of the cell types that contribute to these phenotypes has remained unclear. Here, we report a conditional mouse line with a Shank2 deletion restricted to parvalbumin (PV)-positive neurons (Pv-Cre;Shank2fl/fl mice). These mice display moderate hyperactivity in both novel and familiar environments and enhanced self-grooming in novel, but not familiar, environments. In contrast, they showed normal levels of social interaction, anxiety-like behavior, and learning and memory. Basal brain rhythms in Pv-Cre;Shank2fl/fl mice, measured by electroencephalography, were normal, but susceptibility to pentylenetetrazole (PTZ)-induced seizures was decreased. These results suggest that Shank2 deletion in PV-positive neurons leads to hyperactivity, enhanced self-grooming and suppressed brain excitation.
Nature communications
2022 Sep 26
Matson, KJE;Russ, DE;Kathe, C;Hua, I;Maric, D;Ding, Y;Krynitsky, J;Pursley, R;Sathyamurthy, A;Squair, JW;Levi, BP;Courtine, G;Levine, AJ;
PMID: 36163250 | DOI: 10.1038/s41467-022-33184-1
Elife.
2018 Mar 20
Niquille M, Limoni G, Markopoulos F, Cadilhac C, Prados J, Holtmaat A, Dayer A.
PMID: 29557780 | DOI: 10.7554/eLife.32017
Delineating the basic cellular components of cortical inhibitory circuits remains a fundamental issue in order to understand their specific contributions to microcircuit function. It is still unclear how current classifications of cortical interneuron subtypes relate to biological processes such as their developmental specification. Here we identified the developmental trajectory of neurogliaform cells (NGCs), the main effectors of a powerful inhibitory motif recruited by long-range connections. Using in vivo genetic lineage-tracing in mice, we report that NGCs originate from a specific pool of 5-HT3AR-expressing Hmx3+ cells located in the preoptic area (POA). Hmx3-derived 5-HT3AR+ cortical interneurons (INs) expressed the transcription factors PROX1, NR2F2, the marker reelin but not VIP and exhibited the molecular, morphological and electrophysiological profile of NGCs. Overall, these results indicate that NGCs are a distinct class of INs with a unique developmental trajectory and open the possibility to study their specific functional contribution to cortical inhibitory microcircuit motifs.
Cell reports methods
2022 Apr 25
Wu, Y;Xu, W;Ma, L;Yu, Z;Wang, Y;Yu, CR;
PMID: 35497500 | DOI: 10.1016/j.crmeth.2022.100201
Cell
2022 Jan 20
Cheng, S;Butrus, S;Tan, L;Xu, R;Sagireddy, S;Trachtenberg, JT;Shekhar, K;Zipursky, SL;
PMID: 35063073 | DOI: 10.1016/j.cell.2021.12.022
The Journal of investigative dermatology
2021 Jul 17
Zhu, X;Leboeuf, M;Liu, F;Grachtchouk, M;Seykora, JT;Morrisey, EE;Dlugosz, AA;Millar, SE;
PMID: 34284046 | DOI: 10.1016/j.jid.2021.05.026
Nature.
2018 Aug 08
La Manno G, Soldatov R, Zeisel A, Braun E, Hochgerner H, Petukhov V, Lidschreiber K, Kastriti ME, Lönnerberg P, Furlan A, Fan J, Borm LE, Liu Z, van Bruggen D, Guo J, He X, Barker R, Sundström E, Castelo-Branco G, Cramer P, Adameyko I, Linnarsson S, Kharc
PMID: 30089906 | DOI: 10.1038/s41586-018-0414-6
RNA abundance is a powerful indicator of the state of individual cells. Single-cell RNA sequencing can reveal RNA abundance with high quantitative accuracy, sensitivity and throughput1. However, this approach captures only a static snapshot at a point in time, posing a challenge for the analysis of time-resolved phenomena such as embryogenesis or tissue regeneration. Here we show that RNA velocity-the time derivative of the gene expression state-can be directly estimated by distinguishing between unspliced and spliced mRNAs in common single-cell RNA sequencing protocols. RNA velocity is a high-dimensional vector that predicts the future state of individual cells on a timescale of hours. We validate its accuracy in the neural crest lineage, demonstrate its use on multiple published datasets and technical platforms, reveal the branching lineage tree of the developing mouse hippocampus, and examine the kinetics of transcription in human embryonic brain. We expect RNA velocity to greatly aid the analysis of developmental lineages and cellular dynamics, particularly in humans.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
2023 Mar 24
Yi, T;Wang, N;Huang, J;Wang, Y;Ren, S;Hu, Y;Xia, J;Liao, Y;Li, X;Luo, F;Ouyang, Q;Li, Y;Zheng, Z;Xiao, Q;Ren, R;Yao, Z;Tang, X;Wang, Y;Chen, X;He, C;Li, H;Hu, Z;
PMID: 36961096 | DOI: 10.1002/advs.202300189
Cell reports
2021 Sep 21
Weyrer, C;Turecek, J;Harrison, B;Regehr, WG;
PMID: 34551307 | DOI: 10.1016/j.celrep.2021.109719
J Hepatol.
2019 Mar 29
Aronson SJ, Bakker RS, Shi X, Duijst S, ten Bloemendaal L, de Waart DR, Verheij J, Elferink RPO, Beuers U, Paulusma CC, Bosma PJ.
PMID: 30935993 | DOI: 10.1016/j.jhep.2019.03.021
Abstract
BACKGROUND:
Progressive familial intrahepatic cholestasis type 3 (PFIC3) often leads to end-stage liver disease before adulthood with limited therapeutic options, due to impaired ABCB4 dependent phospholipid transport to bile. To restore ABCB4 function we propose adeno-associated virus serotype 8 (AAV8)-mediated gene therapy directed to the liver, although achieving stable transgene expression in hyperproliferative tissue is challenging. By restoring the phospholipid content in bile to levels that prevent liver damage, this study aims for stable hepatic ABCB4 expression and long-term correction of the phenotype in a murine model of PFIC3.
METHODS:
Ten weeks old Abcb4-/- mice received a single dose of AAV8-hABCB4 (n=10) or AAV8-GFP (n=7) under control of a liver specific promoter via tail vein injection. Animals were sacrificed either 10 or 26 weeks after vector administration to assess transgene persistence, after being challenged with a 0.1% cholate diet for 2 weeks. Periodic evaluation of plasma cholestatic markers was performed and bile duct cannulation enabled analysis of biliary phospholipids. Liver fibrosis and the Ki67 proliferation index were assessed by (immuno-)histochemistry.
RESULTS:
Stable transgene expression was achieved in all animals that received AAV8-hABCB4 up to 26 weeks after administration, which restored biliary phospholipid excretion to levels that ameliorate liver damage. This resulted in normalization of plasma cholestatic markers, prevented progressive liver fibrosis and reduced hepatocyte proliferation for the duration of the study.
CONCLUSION:
Liver-directed gene therapy provides stable hepatic ABCB4 expression and long-term correction of the phenotype in a murine model of PFIC3, encouraging translational studies to verify clinical feasibility.
LAY SUMMARY:
Progressive familial intrahepatic cholestasis type 3 (PFIC3) is a severe genetic liver disease that results from impaired transport of lipids to bile, which makes the bile toxic to liver cells. Because therapeutic options are currently limited, this study aims to evaluate gene therapy to correct the underlying genetic defect in a mouse model of this disease. By introducing a functional copy of the missing gene in liver cells of mice, we were able to restore lipid transport to bile and strongly reduce damage to the liver. Also proliferation of liver cells was reduced, which contributes to long term correction of the phenotype. Limitations of the mouse model requires further studies to evaluate if this approach can be applied in PFIC3 patients.
Description | ||
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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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