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.
Journal of Toxicologic Pathology
2021 Apr 17
SANO, T;YASUNO, H;WATANABE, T;
| DOI: 10.1293/tox.2020-0089
Biophysical Journal
2023 Feb 01
Bogdanov, V;Soltisz, A;Beard, C;Hernandez Orengo, B;Sakuta, G;Veeraraghavan, R;Davis, J;Gyorke, S;
| DOI: 10.1016/j.bpj.2022.11.1389
J Clin Invest.
2016 Jul 25
Lesina M, Wörmann SM, Morton J, Diakopoulos KN, Korneeva O, Wimmer M, Einwächter H, Sperveslage J, Demir IE, Kehl T, Saur D, Sipos B, Heikenwälder M, Steiner JM, Wang TC, Sansom OJ, Schmid RM, Algül H.
PMID: 27454298 | DOI: 10.1172/JCI86477
Tumor suppression that is mediated by oncogene-induced senescence (OIS) is considered to function as a safeguard during development ofpancreatic ductal adenocarcinoma (PDAC). However, the mechanisms that regulate OIS in PDAC are poorly understood. Here, we have determined that nuclear RelA reinforces OIS to inhibit carcinogenesis in the Kras mouse model of PDAC. Inactivation of RelA acceleratedpancreatic lesion formation in Kras mice by abrogating the senescence-associated secretory phenotype (SASP) gene transcription signature. Using genetic and pharmacological tools, we determined that RelA activation promotes OIS via elevation of the SASP factor CXCL1 (also known as KC), which activates CXCR2, during pancreatic carcinogenesis. In Kras mice, pancreas-specific inactivation of CXCR2 prevented OIS and was correlated with increased tumor proliferation and decreased survival. Moreover, reductions in CXCR2 levels were associated with advanced neoplastic lesions in tissue from human pancreatic specimens. Genetically disabling OIS in Kras mice caused RelA to promote tumor proliferation, suggesting a dual role for RelA signaling in pancreatic carcinogenesis. Taken together, our data suggest a pivotal role for RelA in regulating OIS in preneoplastic lesions and implicate the RelA/CXCL1/CXCR2 axis as an essential mechanism of tumor surveillance in PDAC.
Gut. 2014 Sep 10.
Masterson JC, McNamee EN, Fillon SA, Hosford L, Harris R, Fernando SD, Jedlicka P, Iwamoto R, Jacobsen E, Protheroe C, Eltzschig HK, Colgan SP, Arita M, Lee JJ, Furuta GT.
PMID: 25209655 | DOI: 10.1136/gutjnl-2014-306998.
Mov Disord.
2019 Apr 19
Steece-Collier K, Stancati JA, Collier NJ, Sandoval IM, Mercado NM, Sortwell CE, Collier TJ, Manfredsson FP.
PMID: 31002755 | DOI: 10.1002/mds.27695
Abstract
BACKGROUND:
Levodopa-induced dyskinesias are an often debilitating side effect of levodopa therapy in Parkinson's disease. Although up to 90% of individuals with PD develop this side effect, uniformly effective and well-tolerated antidyskinetic treatment remains a significant unmet need. The pathognomonic loss of striatal dopamine in PD results in dysregulation and disinhibition of striatal CaV1.3 calcium channels, leading to synaptopathology that appears to be involved in levodopa-induced dyskinesias. Although there are clinically available drugs that can inhibit CaV1.3 channels, they are not adequately potent and have only partial and transient impact on levodopa-induced dyskinesias.
METHODS:
To provide unequivocal target validation, free of pharmacological limitations, we developed a CaV1.3 shRNA to provide high-potency, target-selective, mRNA-level silencing of striatal CaV1.3 channels and examined its ability to impact levodopa-induced dyskinesias in severely parkinsonian rats.
RESULTS:
We demonstrate that vector-mediated silencing of striatal CaV1.3 expression in severely parkinsonian rats prior to the introduction of levodopa can uniformly and completely prevent induction of levodopa-induced dyskinesias, and this antidyskinetic benefit persists long term and with high-dose levodopa. In addition, this approach is capable of ameliorating preexisting severe levodopa-induced dyskinesias. Importantly, motoric responses to low-dose levodopa remained intact in the presence of striatal CaV1.3 silencing, indicating preservation of levodopa benefit without dyskinesia liability.
DISCUSSION:
The current data provide some of the most profound antidyskinetic benefit reported to date and suggest that genetic silencing of striatal CaV1.3 channels has the potential to transform treatment of individuals with PD by allowing maintenance of motor benefit of levodopa in the absence of the debilitating levodopa-induced dyskinesia side effect.
Biophysical Journal
2023 Feb 01
Medvedev, R;Turner, D;Gorelik, J;Alvarado, F;Bondarenko, V;Glukhov, A;
| DOI: 10.1016/j.bpj.2022.11.1392
Nature medicine
2022 Apr 01
Monteiro, C;Miarka, L;Perea-García, M;Priego, N;García-Gómez, P;Álvaro-Espinosa, L;de Pablos-Aragoneses, A;Yebra, N;Retana, D;Baena, P;Fustero-Torre, C;Graña-Castro, O;Troulé, K;Caleiras, E;Tezanos, P;Muela, P;Cintado, E;Trejo, JL;Sepúlveda, JM;González-León, P;Jiménez-Roldán, L;Moreno, LM;Esteban, O;Pérez-Núñez, Á;Hernández-Lain, A;Mazarico Gallego, J;Ferrer, I;Suárez, R;Garrido-Martín, EM;Paz-Ares, L;Dalmasso, C;Cohen-Jonathan Moyal, E;Siegfried, A;Hegarty, A;Keelan, S;Varešlija, D;Young, LS;Mohme, M;Goy, Y;Wikman, H;Fernández-Alén, J;Blasco, G;Alcázar, L;Cabañuz, C;Grivennikov, SI;Ianus, A;Shemesh, N;Faria, CC;Lee, R;Lorigan, P;Le Rhun, E;Weller, M;Soffietti, R;Bertero, L;Ricardi, U;Bosch-Barrera, J;Sais, E;Teixidor, E;Hernández-Martínez, A;Calvo, A;Aristu, J;Martin, SM;Gonzalez, A;Adler, O;Erez, N;RENACER, ;Valiente, M;
PMID: 35411077 | DOI: 10.1038/s41591-022-01749-8
The EMBO journal
2021 Mar 25
Lagnado, A;Leslie, J;Ruchaud-Sparagano, MH;Victorelli, S;Hirsova, P;Ogrodnik, M;Collins, AL;Vizioli, MG;Habiballa, L;Saretzki, G;Evans, SA;Salmonowicz, H;Hruby, A;Geh, D;Pavelko, KD;Dolan, D;Reeves, HL;Grellscheid, S;Wilson, CH;Pandanaboyana, S;Doolittle, M;von Zglinicki, T;Oakley, F;Gallage, S;Wilson, CL;Birch, J;Carroll, B;Chapman, J;Heikenwalder, M;Neretti, N;Khosla, S;Masuda, CA;Tchkonia, T;Kirkland, JL;Jurk, D;Mann, DA;Passos, JF;
PMID: 33764576 | DOI: 10.15252/embj.2020106048
Biophysical Journal
2023 Feb 01
Ramlow, L;Falcke, M;Lindner, B;
| DOI: 10.1016/j.bpj.2022.11.1390
Cell reports
2022 Dec 27
An, HW;Seok, SH;Kwon, JW;Choudhury, AD;Oh, JS;Voon, DC;Kim, DY;Park, JW;
PMID: 36577366 | DOI: 10.1016/j.celrep.2022.111878
Cell Metab. 2018 Dec 28.
2019 Jan 03
Ogrodnik M, Zhu Y, Langhi LGP, Tchkonia T, Krüger P, Fielder E, Victorelli S, Ruswhandi RA, Giorgadze N, Pirtskhalava T, Podgorni O, Enikolopov G, Johnson KO, Xu M, Inman C, Schafer M, Weigl M, Ikeno Y, Burns TC, Passos JF, von Zglinicki T, Kirkland JL, Jurk D.
PMID: 30612898 | DOI: 10.1016/j.cmet.2018.12.008
J Immunol.
2018 Mar 12
Zheng X, O'Connell CM, Zhong W, Nagarajan UM, Tripathy M, Lee D, Russell AN, Wiesenfeld H, Hillier S, Darville T.
PMID: 29531169 | DOI: 10.4049/jimmunol.1701658
Sexually transmitted infections with Chlamydia trachomatis and/or Neisseria gonorrhoeae and rates of pelvic inflammatory disease (PID) in women continue to rise, with reinfection being common because of poor adaptive immunity. Diagnosis remains imprecise, and pathogenesis data are derived primarily from monoinfection of mice with C. trachomatis or N. gonorrhoeae By comparing blood mRNA responses of women with C. trachomatis- and/or N. gonorrhoeae-induced PID and histologic endometritis with those from women with C. trachomatisand/or N. gonorrhoeae infection limited to their cervix and asymptomatic uninfected women determined via microarray, we discovered important pathogenic mechanisms in PID and response differences that provide a pathway to biomarker discovery. Women with N. gonorrhoeae- and/or C. trachomatis-induced PID exhibit overexpression of myeloid cell genes and suppression of protein synthesis, mitochondrial oxidative phosphorylation, and T cell-specific genes. Coinfected women exhibited the greatest activation of cell death pathways and suppression of responses essential for adaptive immunity. Women solely infected with C. trachomatis expressed elevated levels of type I and type II IFN genes, and enhanced type I IFN-induced chemokines in cervical secretions were associated with ascension of C. trachomatisto the endometrium. Blood microarrays reveal discrete pathobiological endotypes in women with PID that are driven by pathogen invasion of the upper genital tract.
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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