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.
Elife. 2018 Oct 25;7.
2018 Oct 25
Teng CS, Ting MC, Farmer DT, Brockop M, Maxson RE, Crump JG.
PMID: 30375332 | DOI: 10.7554/eLife.37024
Dev Biol.
2018 Jul 05
Li J, Yuan Y, He J, Feng J, Han X, Jing J, Ho TV, Xu J, Chai Y.
PMID: 29981310 | DOI: 10.1016/j.ydbio.2018.07.003
Cleft palate is one of the most common craniofacial congenital defects in humans. It is associated with multiple genetic and environmental risk factors, including mutations in the genes encoding signaling molecules in the sonic hedgehog (Shh) pathway, which are risk factors for cleft palate in both humans and mice. However, the function of Shh signaling in the palatal epithelium during palatal fusion remains largely unknown. Although components of the Shh pathway are localized in the palatal epithelium, specific inhibition of Shh signaling in palatal epithelium does not affect palatogenesis. We therefore utilized a hedgehog (Hh) signaling gain-of-function mouse model, K14-Cre;R26SmoM2, to uncover the role of Shh signaling in the palatal epithelium during palatal fusion. In this study, we discovered that constitutive activation of Hh signaling in the palatal epithelium results in submucous cleft palate and persistence of the medial edge epithelium (MEE). Further investigation revealed that precise downregulation of Shh signaling is required at a specific time point in the MEE during palatal fusion. Upregulation of Hh signaling in the palatal epithelium maintains the proliferation of MEE cells. This may be due to a dysfunctional p63/Irf6 regulatory loop. The resistance of MEE cells to apoptosis is likely conferred by enhancement of a cell adhesion network through the maintenance of p63 expression. Collectively, our data illustrate that persistent Hh signaling in the palatal epithelium contributes to the etiology and pathogenesis of submucous cleft palate through its interaction with a p63/Irf6-dependent biological regulatory loop and through a p63-induced cell adhesion network.
Experimental eye research
2022 Feb 28
Wang, L;Sun, M;Zhang, Q;Dang, S;Zhang, W;
PMID: 35240198 | DOI: 10.1016/j.exer.2022.109020
Development (Cambridge, England)
2023 Jun 28
Imaimatsu, K;Hiramatsu, R;Tomita, A;Itabashi, H;Kanai, Y;
PMID: 37376880 | DOI: 10.1242/dev.201660
Reproductive biology
2021 Jul 13
Lin, X;Wang, C;Zhang, Q;Pan, YH;Dang, S;Zhang, W;
PMID: 34271244 | DOI: 10.1016/j.repbio.2021.100537
Biol Open.
2016 Sep 16
Ataca D, Caikovski M, Piersigilli A, Moulin A, Benarafa C, Earp SE, Guri Y, Kostic C, Arsenivic Y, Soininen R, Apte SS, Brisken C.
PMID: 27638769 | DOI: 10.1242/bio.019711
The ADAMTS family comprises 19 secreted metalloproteinases that cleave extracellular matrix components and have diverse functions in numerous disease and physiological contexts. A number of them remain 'orphan' proteases, among them ADAMTS18, which has been implicated in developmental eye disorders, platelet function and various malignancies. To assess in vivo function of ADAMTS18, we generated a mouse strain with inactivated Adamts18 alleles. In the C57Bl6/Ola background, Adamts18 deficient mice are born in a normal Mendelian ratio, and are viable but show a transient growth delay. Histological examination revealed a 100% penetrant eye defect resulting from leakage of lens material through the lens capsule occurring at embryonic day (E)13.5, when the lens grows rapidly. Adamts18 deficient lungs showed altered bronchiolar branching. Fifty percent of the mutant females are infertile because of vaginal obstruction due to either a dorsoventral vaginal septum or imperforate vagina. The incidence of ovarian rete is increased in the mutant mice. Thus, Adamts18 is essential in the development of distinct tissues and the new mouse strain is likely to be useful for investigating ADAMTS18 function in human disease, particularly in the contexts of infertility and carcinogenesis.
Neuroscience. 2018 Dec 21.
2018 Dec 21
Zhu R, Pan YH, Sun L, Zhang T, Wang C, Ye S, Yang N, Lu T, Wisniewski T, Dang S, Zhang W.
PMID: 30579834 | DOI: 10.1016/j.neuroscience.2018.12.025
Cancer Res.
2016 Aug 19
Sommer A, Kopitz C, Schatz CA, Nising CF, Mahlert C, Lerchen HG, Stelte-Ludwig B, Hammer S, Greven S, Schumacher J, Braun M, Zierz R, Wittemer-Rump S, Harrenga A, Dittmer F, Reetz F, Apeler H, Jautelat R, Huynh H, Ziegelbauer K, Kreft B.
PMID: 27543601 | DOI: 10.1158/0008-5472.CAN-16-0180
The fibroblast growth factor receptor FGFR2 is overexpressed in a variety of solid tumors, including breast, gastric and ovarian tumors, where it offers a potential therapeutic target. In this study, we present evidence of the preclinical efficacy of BAY 1187982, a novel antibody-drug conjugate (ADC). It consists of a fully human FGFR2 monoclonal antibody (mAb BAY 1179470), which is specific for the FGFR2 isoforms FGFR2-IIIb and FGFR2-IIIc, conjugated through a non-cleavable linker to a novel derivative of the microtubule-disrupting cytotoxic drug auristatin (FGFR2-ADC). In FGFR2-expressing cancer cell lines, this FGFR2-ADC exhibited potency in the low nM to sub-nM range and was more than 100-fold selective against FGFR2-negative cell lines. High expression levels of FGFR2 in cells correlated with efficient internalization, efficacy and cytotoxic effects in vitro. Pharmacokinetic analyses in mice bearing FGFR2-positive NCI-H716 tumors indicated that the toxophore metabolite of FGFR2-ADC was enriched more than 30-fold in tumors compared to healthy tissues. Efficacy studies demonstrated that FGFR2-ADC treatment leads to a significant tumor growth inhibition or tumor regression of cell line-based or patient-derived xenograft models of human gastric or breast cancer. Further, FGFR2 amplification or mRNA overexpression predicted high efficacy in both of these types of in vivo model systems. Taken together, our results strongly support the clinical evaluation of BAY 1187982 in cancer patients, and a Phase I study (NCT02368951) has been initiated.
Pathobiology.
2015 Oct 31
Han N, Kim MA, Lee HS, Kim WH.
PMID: 26516773 | DOI: -
Nature
2022 May 01
Chen, X;Du, Y;Broussard, GJ;Kislin, M;Yuede, CM;Zhang, S;Dietmann, S;Gabel, H;Zhao, G;Wang, SS;Zhang, X;Bonni, A;
PMID: 35545673 | DOI: 10.1038/s41586-022-04711-3
PLoS One.
2016 Nov 09
Topczewska JM, Shoela RA, Tomaszewski JP, Mirmira RB, Gosain AK.
PMID: 27829009 | DOI: 10.1371/journal.pone.0165775
Using morphological, histological, and TEM analyses of the cranium, we provide a detailed description of bone and suture growth in zebrafish. Based on expression patterns and localization, we identified osteoblasts at different degrees of maturation. Our data confirm that, unlike in humans, zebrafish cranial sutures maintain lifelong patency to sustain skull growth. The cranial vault develops in a coordinated manner resulting in a structure that protects the brain. The zebrafish cranial roof parallels that of higher vertebrates and contains five major bones: one pair of frontal bones, one pair of parietal bones, and the supraoccipital bone. Parietal and frontal bones are formed by intramembranous ossification within a layer of mesenchyme positioned between the dermal mesenchyme and meninges surrounding the brain. The supraoccipital bone has an endochondral origin. Cranial bones are separated by connective tissue with a distinctive architecture of osteogenic cells and collagen fibrils. Here we show RNA in situ hybridization for col1a1a, col2a1a, col10a1, bglap/osteocalcin, fgfr1a, fgfr1b, fgfr2, fgfr3, foxq1, twist2, twist3, runx2a, runx2b, sp7/osterix, and spp1/ osteopontin, indicating that the expression of genes involved in suture development in mammals is preserved in zebrafish. We also present methods for examining the cranium and its sutures, which permit the study of the mechanisms involved in suture patency as well as their pathological obliteration. The model we develop has implications for the study of human disorders, including craniosynostosis, which affects 1 in 2,500 live births.
Gene
2023 Jan 09
Nie, J;Zhang, W;
PMID: 36632911 | DOI: 10.1016/j.gene.2023.147169
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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