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EGF suppresses specifically CAR signaling mainly through transcriptional regulation and drives the xenobiotic response toward a pregnane X receptor (PXR)-mediated mechanism.
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The results pf this study demonstrated that CAR is expressed by mature neurons throughout the brain. In addition, we propose divergent roles for CAR in immature neurons, during neurogenesis, and at the mature synapse.
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data indicate that glycosylation of the extracellular CAR domain has only minor importance for the function of CAR as Coxsackievirus B3 (CVB3) receptor and that the D2 domain is not essential per se but contributes to receptor function by promoting the exposure of the D1 domain on the cell surface
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CAR expression has potential as a marker for monitoring and/or predicting the outcome of gene therapy, and increasing its expression levels may contribute to the upregulation of cellular sensitivity towards adenovirus infection.
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Membrane Dynamics and Signaling of the Coxsackievirus and Adenovirus Receptor.
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Combining CAR activation with limited beta-catenin activation induces tumorigenesis, and the tumours share a conserved gene expression signature with beta-catenin-positive human hepatocellular carcinoma.
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Glycan microarray, flow cytometry, surface plasmon resonance and ELISA analyses reveal that the terminal knob domain of the long fiber (52LFK) binds to CAR, and the knob domain of the short fiber (52SFK) binds to sialylated glycoproteins.
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Lovastatin enhances adenovirus-mediated TRAIL induced apoptosis by depleting cholesterol of lipid rafts and affecting CAR and death receptor expression of prostate cancer cells.
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Suggest that distinct forms of CAR play different roles in the undifferentiated state and tight junction formation of human embryos and embryonic stem cells.
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CAR might play a role in adipose tissue dysfunction, given its dual associations with adipogenic and inflammatory genes.
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Subsequent experiments also proved that both the rno-miR-466d and the human hsa-miR-466, which are orthologs of the miR-467 gene family, could effectively down-regulate the levels of rat and human CAR protein expression, respectively
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This study shows for the first time that lovastatin reduces the expression of CAR and subsequently the replication of CVB3 in human umbilical vein endothelial cells.
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CAR regulates epithelial cell junction stability through control of E-cadherin trafficking.
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Kinetic analyses show that the apparent first-order rate constant for the inactivation of coxsackievirus B3 by soluble CAR (sCAR) at physiological temperatures varies nonlinearly with sCAR concentration.
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CAR substantially impacts the growth and survival of oral squamous cell carcinoma cells as a negative regulator of ROCK in vitro and in vivo.
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novel modifier of ventricular conduction and arrhythmia vulnerability in the setting of myocardial ischemia
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CAR belongs to the increasing list of cell surface molecules that undergo ectodomain shedding and that are substrates for -secretase-mediated RIP.
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The expression of CAR was detected in all normal organs, except in the brain. In malignancies, a high degree of variability was notable, ranging from significantly elevated CAR expression to decreased CAR expression.
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CAR expression in tumor tissues was significantly higher than that in normal lung tissues. CAR expression had a correlation with the histological grade of lung squamous cell carcinoma.
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CAR and ASIC3 co-immunoprecipitate only when co-expressed with PSD-95.