- Probes for (1559217)
- Kits & Accessories (135)
- Support & Documents (0)
- Publications (7110)
- Image gallery (0)
Refine Probe List
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.
Diagnostics
2022 Feb 23
Ingravallo, G;Tamma, R;Opinto, G;Annese, T;Gaudio, F;Specchia, G;Perrone, T;Musto, P;Cazzato, G;Bellitti, E;Capodiferro, S;Maiorano, E;Ribatti, D;
| DOI: 10.3390/diagnostics12030573
Lymphomas are characteristic tumors surrounded by an inflammatory microenvironment. The cells of the microenvironment are essential for the growth and survival of neoplastic cells and are recruited through the effect of cytokines/chemokines. Lymphomas include heterogeneous groups of neoplasms infiltrating various lymphoid structures which may arise from B lymphocytes, T lymphocytes, and natural killer (NK) cells at various stages of their differentiation state. In this review article, we analyze the literature data concerning the involvement of the tumor microenvironment (TME) in the progression of lymphomas and the recent advances in the analysis of microenvironment components in the most common forms: some mature B cell lymphoma neoplasms and classic Hodgkin lymphomas. The complex crosstalk between the TME and tumor cells led to the discovery of many mechanisms usable as molecular-targeted therapy through the control of diverse elements of the TME, varying from inhibitors of angiogenic cytokines and their receptors to the regulation of cells’ activities and the novel immune checkpoint inhibitors.
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
ADAMTS18 is an orphan member of the ADAMTS family of metalloproteinase. ADAMTS18 mutation has been linked to developmental eye disorders, such as retinal dystrophies and ectopia lentis. Here, we report a new function of ADAMTS18 in modulating the lacrimal gland (LG) branching morphogenesis, and an association with dry eye in mice. Adamts18 mRNA was found to be enriched in the epithelium of branching tips of embryonic (E) LG, but its expression was barely detectable after 2 weeks of birth. Histological analyses of E16.5-E17.5 LG showed that ADAMTS18 deficiency resulted in a significant reduction of epithelial branching in embryonic LG. In vitro culture of E15.5 LG explants showed that the numbers of epithelial buds and branches in Adamts18 knockout (Adamts18-/-) LGs were significantly decreased when compared to those of wild type (Adamts18+/+) LGs after 0 h, 24 h, and 48 h of culture. Increased fibronectin deposition was detected in LG mesenchyme of E16.5 Adamts18-/- mice. At 14 months of age, Adamts18-/- mice manifested multiple LG pathological changes, including acinar atrophy and irregular duct ectasis with periductal fibrosis. The tear volume was significantly decreased in Adamts18-/- mice at 4 months of age, which corresponds to early adulthood in humans.
Pathology - Research and Practice
2022 Mar 01
Yoshizawa, T;Uehara, T;Iwaya, M;Asaka, S;Kobayashi, S;Nakajima, T;Kinugawa, Y;Nagaya, T;Kamakura, M;Shimizu, A;Kubota, K;Notake, T;Masuo, H;Hosoda, K;Sakai, H;Hayashi, H;Umemura, K;Kamachi, A;Goto, T;Tomida, H;Yamazaki, S;Ota, H;Soejima, Y;
| DOI: 10.1016/j.prp.2022.153832
Leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5) is a known cancer stem cell marker. However, there are no reported analyses of LGR5 mRNA expression in normal liver and liver cancer tissues. Here, we evaluated LGR5 expression by RNAscope, a newly developed RNA in situ hybridization technique, using a tissue microarray consisting of 25 samples of intrahepatic cholangiocarcinoma (ICC) selected from the medical archives at our hospital. LGR5 expression levels were divided into high and low expression groups by the five-grade scoring system, and clinicopathological features were analyzed. Low LGR5 expression was identified in some normal hepatocytes and bile duct cells. In addition, LGR5 expression was identified in all bile duct cancer samples except one case. Well-differentiated to moderately-differentiated adenocarcinoma tended to show higher LGR5 expression than poorly-differentiated adenocarcinoma (P=0.0561), and the large duct type showed significantly higher LGR5 expression levels than the small duct type (P=0.0225). Patients in the high LGR5 expression group tended to have good overall survival (OS) (P=0.0623). The Cox proportional hazard regression model revealed that the high LGR5 expression group showed independently better OS for ICC (P = 0.0285). High LGR5 expression is possibly a good prognosis factor in ICC. However, the detailed mechanism of LGR5 in this disease remains unclear, and further analysis is warranted.
PloS one
2022 Feb 10
Cline, C;Bell, TM;Facemire, P;Zeng, X;Briese, T;Lipkin, WI;Shamblin, JD;Esham, HL;Donnelly, GC;Johnson, JC;Hensley, LE;Honko, AN;Johnston, SC;
PMID: 35143571 | DOI: 10.1371/journal.pone.0263834
Disease associated with Nipah virus infection causes a devastating and often fatal spectrum of syndromes predominated by both respiratory and neurologic conditions. Additionally, neurologic sequelae may manifest months to years later after virus exposure or apparent recovery. In the two decades since this disease emerged, much work has been completed in an attempt to understand the pathogenesis and facilitate development of medical countermeasures. Here we provide detailed organ system-specific pathologic findings following exposure of four African green monkeys to 2.41×105 pfu of the Malaysian strain of Nipah virus. Our results further substantiate the African green monkey as a model of human Nipah virus disease, by demonstrating both the respiratory and neurologic components of disease. Additionally, we demonstrate that a chronic phase of disease exists in this model, that may provide an important opportunity to study the enigmatic late onset and relapse encephalitis as it is described in human disease.
The Journal of comparative neurology
2022 Feb 10
Bono, BS;Koziel Ly, NK;Miller, PA;Williams-Ikhenoba, J;Dumiaty, Y;Chee, MJ;
PMID: 35143049 | DOI: 10.1002/cne.25306
Beta-klotho (KLB) is a coreceptor required for endocrine fibroblast growth factor (FGF) 15/19 and FGF21 signaling in the brain. Klb is prominent within the hypothalamus, which is consistent with its metabolic functions, but diverse roles for Klb are now emerging. Central Klb expression is low but discrete and may govern FGF-targeted sites. However, given its low expression, it is unclear if Klb mRNA is more widespread. We performed in situ hybridization to label Klb mRNA to generate spatial maps capturing the distribution and levels of Klb within the mouse hypothalamus, hippocampal region, subiculum, and amygdala. Semiquantitative analysis revealed that Klb-labeled cells may express low, medium, or high levels of Klb mRNA. Hypothalamic Klb hybridization was heterogeneous and varied rostrocaudally within the same region. Most Klb-labeled cells were found in the lateral hypothalamic zone, but the periventricular hypothalamic region, including the suprachiasmatic nucleus, contained the greatest proportion of cells expressing medium or high Klb levels. We also found heterogeneous Klb hybridization in the amygdala and subiculum, where Klb was especially distinct within the central amygdalar nucleus and ventral subiculum, respectively. By contrast, Klb-labeled cells in the hippocampal region only expressed low levels of Klb and were typically found in the pyramidal layer of Ammon's horn or dentate gyrus. The Klb-labeled regions identified in this study are consistent with reported roles of Klb in metabolism, taste preference, and neuroprotection. However, additional identified sites, including within the hypothalamus and amygdala, may suggest novel roles for FGF15/19 or FGF21 signaling.
The Journal of comparative neurology
2022 Feb 08
Karthik, S;Huang, D;Delgado, Y;Laing, JJ;Peltekian, L;Iverson, GN;Grady, F;Miller, RL;McCann, CM;Fritzsch, B;Iskusnykh, IY;Chizhikov, VV;Geerling, JC;
PMID: 35134251 | DOI: 10.1002/cne.25307
Diverse neurons in the parabrachial nucleus (PB) communicate with widespread brain regions. Despite evidence linking them to a variety of homeostatic functions, it remains difficult to determine which PB neurons influence which functions because their subpopulations intermingle extensively. An improved framework for identifying these intermingled subpopulations would help advance our understanding of neural circuit functions linked to this region. Here, we present the foundation of a developmental-genetic ontology that classifies PB neurons based on their intrinsic, molecular features. By combining transcription factor labeling with Cre fate-mapping, we find that the PB is a blend of two, developmentally distinct macropopulations of glutamatergic neurons. Neurons in the first macropopulation express Lmx1b (and, to a lesser extent, Lmx1a) and are mutually exclusive with those in a second macropopulation, which derive from precursors expressing Atoh1. This second, Atoh1-derived macropopulation includes many Foxp2-expressing neurons, but Foxp2 also identifies a subset of Lmx1b-expressing neurons in the Kölliker-Fuse nucleus (KF) and a population of GABAergic neurons ventrolateral to the PB ("caudal KF"). Immediately ventral to the PB, Phox2b-expressing glutamatergic neurons (some coexpressing Lmx1b) occupy the KF, supratrigeminal nucleus, and reticular formation. We show that this molecular framework organizes subsidiary patterns of adult gene expression (including Satb2, Calca, Grp, and Pdyn) and predicts output projections to the amygdala (Lmx1b), hypothalamus (Atoh1), and hindbrain (Phox2b/Lmx1b). Using this molecular ontology to organize, interpret, and communicate PB-related information could accelerate the translation of experimental findings from animal models to human patients.
American journal of physiology. Renal physiology
2022 Feb 07
Douma, LG;Costello, HM;Crislip, GR;Cheng, KY;Lynch, IJ;Juffre, A;Barral, D;Masten, SH;Roig, E;Beguiristain, K;Li, W;Bratanatawira, P;Wingo, CS;Gumz, ML;
PMID: 35129370 | DOI: 10.1152/ajprenal.00385.2021
PER1 is a circadian clock transcription factor that is regulated by aldosterone, a hormone that increases blood volume and sodium retention to increase blood pressure. Male global Per1 knockout (KO) mice develop reduced night/day differences in sodium excretion in response to a high salt diet plus desoxycorticosterone pivalate treatment (HS+DOCP), a model of salt-sensitive hypertension. Additionally, global Per1 KO mice exhibit higher aldosterone levels on a normal salt diet. To determine the role of Per1 in the kidney, male kidney-specific Per1 KO (KS-Per1 KO) mice were generated using Ksp-cadherin Cre recombinase to remove exons 2-8 of Per1 in the distal nephron and collecting duct. Male KS-Per1 KO mice have increased sodium retention, but have normal diurnal differences in sodium excretion in response to HS+DOCP. The increased sodium retention is associated with altered expression of glucocorticoid and mineralocorticoid receptors, increased serum aldosterone, and increased medullary endothelin-1 compared to control (CNTL) mice. Adrenal gland gene expression analysis revealed that circadian clock and aldosterone synthesis genes have altered expression in the KS-Per1 KO mice compared to CNTL mice. These results emphasize the importance of the circadian clock, not only in maintaining rhythms of physiological functions but also for adaptability in response to environmental cues, such as HS+ DOCP, to maintain overall homeostasis. Given the prevalence of salt-sensitive hypertension in the general population, these findings have important implications for our understanding of how circadian clock proteins regulate homeostasis.
Diagnostic pathology
2022 Feb 05
Kamakura, M;Uehara, T;Iwaya, M;Asaka, S;Kobayashi, S;Nakajima, T;Kinugawa, Y;Nagaya, T;Yoshizawa, T;Shimizu, A;Ota, H;Umemura, T;
PMID: 35123536 | DOI: 10.1186/s13000-022-01203-w
Leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5) is a strong cancer stem cell marker in colorectal cancer; however, there are many unclear aspects of LGR5 expression in pancreatic cancer. It has been reported that the interaction between tumor cells and stroma at the fat infiltration site has a significant effect on pancreatic cancer prognosis. Therefore, we report a clinicopathological study of LGR5 expression at the fat invasion front in pancreatic cancer.LGR5 expression was analyzed in 40 pancreatic ductal adenocarcinoma cases with RNAscope, which is a newly developed high-sensitivity in situ hybridization method. Epithelial-mesenchymal transition (EMT) was analyzed by the expression of E-cadherin and vimentin via immunohistochemistry.LGR5-positive dots were identified in all cases, especially with glandular formation. In the fat invasion front, a high histological grade showed significantly reduced LGR5 expression compared with a low histological grade (p=0.0126). LGR5 expression was significantly higher in the non-EMT phenotype group than in EMT phenotype group (p=0.0003). Additionally, LGR5 expression was significantly lower in cases with high vascular invasion than in those with low vascular invasion (p=0.0244).These findings suggest that decreased LGR5 expression in the fat invasion front is associated with more aggressive biological behavior in pancreatic ductal adenocarcinoma, with higher tumor grade, EMT phenotype, and higher vascular invasion.
Journal of neurovirology
2022 Feb 09
Gumbs, SBH;Kübler, R;Gharu, L;Schipper, PJ;Borst, AL;Snijders, GJLJ;Ormel, PR;van Berlekom, AB;Wensing, AMJ;de Witte, LD;Nijhuis, M;
PMID: 35138593 | DOI: 10.1007/s13365-021-01049-w
HIV persistence in the CNS despite antiretroviral therapy may cause neurological disorders and poses a critical challenge for HIV cure. Understanding the pathobiology of HIV-infected microglia, the main viral CNS reservoir, is imperative. Here, we provide a comprehensive comparison of human microglial culture models: cultured primary microglia (pMG), microglial cell lines, monocyte-derived microglia (MDMi), stem cell-derived microglia (iPSC-MG), and microglia grown in 3D cerebral organoids (oMG) as potential model systems to advance HIV research on microglia. Functional characterization revealed phagocytic capabilities and responsiveness to LPS across all models. Microglial transcriptome profiles of uncultured pMG showed the highest similarity to cultured pMG and oMG, followed by iPSC-MG and then MDMi. Direct comparison of HIV infection showed a striking difference, with high levels of viral replication in cultured pMG and MDMi and relatively low levels in oMG resembling HIV infection observed in post-mortem biopsies, while the SV40 and HMC3 cell lines did not support HIV infection. Altogether, based on transcriptional similarities to uncultured pMG and susceptibility to HIV infection, MDMi may serve as a first screening tool, whereas oMG, cultured pMG, and iPSC-MG provide more representative microglial culture models for HIV research. The use of current human microglial cell lines (SV40, HMC3) is not recommended.
Archives of virology
2022 Mar 01
Zhang, J;Han, W;Xie, C;Gao, M;Wang, X;Hu, X;Zhang, W;Cao, S;Liu, X;Cheng, G;Gu, C;
PMID: 35119507 | DOI: 10.1007/s00705-021-05283-9
Japanese encephalitis (JE) is a zoonotic epidemic disease caused by Japanese encephalitis virus (JEV), and currently, no medicines are available to treat this disease. Autophagy modulators play an important role in the treatment of tumors, heart disease, and some viral diseases. The aim of this study was to investigate the effects of autophagy modulators on JEV infection and the host response in mice. The experimental mice were grouped as follows: DMEM (control), JEV, JEV+rapamycin (JEV+Rapa), JEV+wortmannin (JEV+Wort), JEV+chloroquine (JEV+CQ), Rapa, Wort, and CQ. The control group was treated with DMEM. The mice in other groups were infected with 105 PFU of JEV, and Rapa, Wort, and CQ were administered 2 h prior to JEV challenge and then administered daily for 10 consecutive days. All mice were monitored for neurological signs and survival. The damage of subcellular structures in the mouse brain was evaluated by transmission electron microscopy. The distribution of virus in the mouse brain was determined by RNAScope staining and immunohistochemical staining. The neuroinflammatory responses in the brain were examined via quantitative real-time PCR, and the signal pathways involved in neuroinflammation were identified by Western blot. The mice in the JEV+Wort and JEV+CQ groups showed milder neurological symptoms, less damage to the mitochondria in the brain tissue, and a higher survival rate than those in the JEV+Rapa and JEV groups. Compared with the JEV+Rapa and JEV groups, the distribution of JEV in the brain of mice in the JEV+Wort and JEV+CQ groups was lower, and the inflammatory response was weaker. No significant difference was observed in the expression of the PI3K/AKT/NF-κB pathway in mouse brain among the different groups. Our study suggests that the autophagy inhibitors Wort and CQ reduce JEV infection and weaken the inflammatory response, which does not depend on the PI3K/AKT/NF-κB pathway in mouse brain.
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
2022 Feb 22
Marella, M;Yao, X;Carreira, V;Bustamante, MF;Clark, HB;Jackson, CC;Zudaire, E;Schecter, JM;Glover, TD;Shenton, J;Cornax, I;
PMID: 35193424 | DOI: 10.1369/00221554221079579
B-cell maturation antigen (BCMA) is a target for the treatment of multiple myeloma with cytolytic therapies, such as chimeric antigen receptor T-cells or T-cell redirecting antibodies. To better understand the potential for "on-target/off-tumor" toxicity caused by BCMA-targeting cytolytic therapies in the brain, we investigated normal brain BCMA expression. An immunohistochemistry (IHC) assay using the E6D7B commercial monoclonal antibody was applied to 107 formalin-fixed, paraffin-embedded brain samples (cerebrum, basal ganglia, cerebellum, brainstem; 63 unique donors). Although immunoreactivity was observed in a small number of neurons in brain regions including the striatum, thalamus, midbrain, and medulla, this immunoreactivity was considered nonspecific and not reflective of BCMA expression because it was distinct from the membranous and Golgi-like pattern seen in positive control samples, was not replicated when a different IHC antibody (D6 clone) was used, and was not corroborated by in situ hybridization data. Analysis of RNA-sequencing data from 478 donors in the GTEx and Allen BrainSpan databases demonstrated low levels of BCMA RNA expression in the striatum of young donors with levels becoming negligible beyond 30 years of age. We concluded that BCMA protein is not present in normal adult human brain, and therefore on-target toxicity in the brain is unlikely.
Pages
X
| 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 | |
- Toll-free in the US and Canada
- +1877 576-3636
X
Contact Us
Complete one of the three forms below and we will get back to you.
For Quote Requests, please provide more details in the Contact Sales form below
Advanced Cell Diagnostics
Our new headquarters office starting May 2016:
7707 Gateway Blvd.
Newark, CA 94560
Toll Free: 1 (877) 576-3636
Phone: (510) 576-8800
Fax: (510) 576-8798
Bio-Techne
19 Barton Lane
Abingdon Science Park
Abingdon
OX14 3NB
United Kingdom
Phone 2: +44 1235 529449
Fax: +44 1235 533420
Advanced Cell Diagnostics China
20F, Tower 3,
Raffles City Changning Office,
1193 Changning Road, Shanghai 200051
021-52293200
info.cn@bio-techne.com
Web: www.acdbio.com/cn
For general information: Info.ACD@bio-techne.com
For place an order: order.ACD@bio-techne.com
For product support: support.ACD@bio-techne.com
For career opportunities: hr.ACD@bio-techne.com
×
You have already Quick ordered an Item in your cart . If you want to add a new item , Quick ordered Item will be removed form your cart. Do You want to continue?
OK Cancel