The Ah receptor signaling pathway critically regulates cardiac development

2015 ◽  
Vol 238 (2) ◽  
pp. S278
Author(s):  
V. Carreira ◽  
Y. Fan ◽  
Q. Wang ◽  
X. Zhang ◽  
H. Kurita ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cardiac Development ◽  
Ah Receptor ◽  
Receptor Signaling ◽  
Receptor Signaling Pathway

Activation of the Ah Receptor Signaling Pathway by Prostaglandins

2001 ◽  
Vol 15 (4) ◽  
pp. 187-196 ◽  
Author(s):  
Shawn D. Seidel ◽  
Greg M. Winters ◽  
William J. Rogers ◽  
Michael H. Ziccardi ◽  
Violet Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Ah Receptor ◽  
Receptor Signaling ◽  
Receptor Signaling Pathway

scholarly journals A comprehensive contribution of genes for aryl hydrocarbon receptor signaling pathway to hypertension susceptibility

2017 ◽  
Vol 27 (2) ◽  
pp. 57-69 ◽  
Author(s):  
Alexey V. Polonikov ◽  
Olga Yu. Bushueva ◽  
Irina V. Bulgakova ◽  
Maxim B. Freidin ◽  
Mikhail I. Churnosov ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Signaling Pathway ◽  
Receptor Signaling ◽  
Aryl Hydrocarbon ◽  
Receptor Signaling Pathway

Cross-talk between an activator of nuclear receptors-mediated transcription and the D1 dopamine receptor signaling pathway

2005 ◽  
Vol 80 (3) ◽  
pp. 379-385 ◽  
Author(s):  
Azriel Schmidt ◽  
Robert Vogel ◽  
Su Jane Rutledge ◽  
Evan E. Opas ◽  
Gideon A. Rodan ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Dopamine Receptor ◽  
Nuclear Receptors ◽  
Cross Talk ◽  
Receptor Signaling ◽  
D1 Dopamine Receptor ◽  
Receptor Signaling Pathway

Neuromedin U-induced anorexigenic action is mediated by the corticotropin-releasing hormone receptor-signaling pathway in goldfish

Peptides ◽  
2009 ◽  
Vol 30 (12) ◽  
pp. 2483-2486 ◽  
Author(s):  
Keisuke Maruyama ◽  
Kohei Wada ◽  
Kotaro Ishiguro ◽  
Sei-Ichi Shimakura ◽  
Tatsuya Wakasugi ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hormone Receptor ◽  
Receptor Signaling ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Receptor Signaling Pathway

Zinc oxide nanoparticle disruption of store-operated calcium entry in a muscarinic receptor signaling pathway

2010 ◽  
Vol 24 (7) ◽  
pp. 1953-1961 ◽  
Author(s):  
Hsiu-Jen Wang ◽  
Anna C. Growcock ◽  
Tso-hao Tang ◽  
Jennifer O’Hara ◽  
Yue-wern Huang ◽  
...  
Keyword(s):  
Zinc Oxide ◽  
Signaling Pathway ◽  
Muscarinic Receptor ◽  
Calcium Entry ◽  
Receptor Signaling ◽  
Zinc Oxide Nanoparticle ◽  
Store Operated Calcium Entry ◽  
Receptor Signaling Pathway ◽  
Oxide Nanoparticle

scholarly journals Transcriptome Analysis for Genes Associated with Small Ruminant Lentiviruses Infection in Goats of Carpathian Breed

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2054
Author(s):  
Monika Olech ◽  
Katarzyna Ropka-Molik ◽  
Tomasz Szmatoła ◽  
Katarzyna Piórkowska ◽  
Jacek Kuźmak
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Proviral Load ◽  
Cytokine Production ◽  
Small Ruminant ◽  
Receptor Signaling ◽  
Toll Like Receptor ◽  
Receptor Signaling Pathway

Small ruminant lentiviruses (SRLV) are economically important viral pathogens of sheep and goats. SRLV infection may interfere in the innate and adaptive immunity of the host, and genes associated with resistance or susceptibility to infection with SRLV have not been fully recognized. The presence of animals with relatively high and low proviral load suggests that some host factors are involved in the control of virus replication. To better understand the role of the genes involved in the host response to SRLV infection, RNA sequencing (RNA-seq) method was used to compare whole gene expression profiles in goats carrying both a high (HPL) and low (LPL) proviral load of SRLV and uninfected animals. Data enabled the identification of 1130 significant differentially expressed genes (DEGs) between control and LPL groups: 411 between control and HPL groups and 1434 DEGs between HPL and LPL groups. DEGs detected between the control group and groups with a proviral load were found to be significantly enriched in several gene ontology (GO) terms, including an integral component of membrane, extracellular region, response to growth factor, inflammatory and innate immune response, transmembrane signaling receptor activity, myeloid differentiation primary response gene 88 (MyD88)-dependent toll-like receptor signaling pathway as well as regulation of cytokine secretion. Our results also demonstrated significant deregulation of selected pathways in response to viral infection. The presence of SRLV proviral load in blood resulted in the modification of gene expression belonging to the toll-like receptor signaling pathway, the tumor necrosis factor (TNF) signaling pathway, the cytokine-cytokine receptor interaction, the phagosome, the Ras signaling pathway, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) (PI3K-Akt) signaling pathway and rheumatoid arthritis. It is worth mentioning that the most predominant in all pathways were genes represented by toll-like receptors, tubulins, growth factors as well as interferon gamma receptors. DEGs detected between LPL and HPL groups were found to have significantly enriched regulation of signaling receptor activity, the response to toxic substances, nicotinamide adenine dinucleotide (NADH) dehydrogenase complex assembly, cytokine production, vesicle, and vacuole organization. In turn, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway tool classified DEGs that enrich molecular processes such as B and T-cell receptor signaling pathways, natural killer cell-mediated cytotoxicity, Fc gamma R-mediated phagocytosis, toll-like receptor signaling pathways, TNF, mammalian target of rapamycin (mTOR) signaling and forkhead box O (Foxo) signaling pathways, etc. Our data indicate that changes in SRLV proviral load induced altered expression of genes related to different biological processes such as immune response, inflammation, cell locomotion, and cytokine production. These findings provide significant insights into defense mechanisms against SRLV infection. Furthermore, these data can be useful to develop strategies against SRLV infection by selection of animals with reduced SRLV proviral concentration that may lead to a reduction in the spread of the virus.

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