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The expression or activity of RCAN1, rather than the RCAN1 copy number, may contribute to DS-associated congenital heart disease.
Study found that RCAN1 RNA expression was suppressed in glomeruli in human diabetic nephropathy, IgA nephropathy, and lupus nephritis, and in mouse models of HIV-associated nephropathy and diabetic nephropathy. Findings suggest that epigenetic suppression of RCAN1 aggravates podocyte injury in the setting of HIV infection and diabetic nephropathy.
A novel mutation of g.482G>T in RCAN1 may be related to congenital heart diseases by causing overexpression of RCAN1.
RCAN1.4 plays a novel role in regulating endothelial cell migration by establishing endothelial cell polarity in response to VEGF.
Lycopene inhibits RCAN1-mediated apoptosis by reducing ROS levels and by inhibiting NF-kappaB activation, Nucling induction, and the increase in apoptotic indices in neuronal cells.
Overexpression of RCAN1 markedly reduced glioma cells viability.
RCAN1.4 prevents cell proliferation, migration, and invasion in vitro; overexpressed RCAN1.4 in HCC cells prevents growth, angiogenesis, and metastases of xenograft tumors by inhibiting calcineurin activity and nuclear translocation of NFAT1.
elucidated a novel function of regulator of calcineurin 1 isoform 1 in mitochondria and provides a molecular basis for the regulator of calcineurin 1 isoform over-expression-induced mitochondrial dysfunctions and neuronal apoptosis
our research revealed that RCAN1 was involved in the development of small cell lung cancer, and it might be a cancer-inhibiting gene for the formation of bone metastases in small cell lung cancer
The results of the study indicate that RCAN1 is suppressed in endothelial cells of chronically inflamed periodontal tissues. During an acute infection, however, rcan1 seems to be upregulated in endothelial cells, indicating a modulating role in immune homeostasis of periodontal tissues.
mRNA expression levels of DSCR1 and VEGF-C, and microvessel density are increased in cancerous tissues, compared with paracancerous tissue in hypopharyngeal cancer.
The objective of this study was aimed to detect the association of Down syndrome critical region 1 (DSCR1) gene polymorphisms (rs149048873 and rs143081213) and congenital heart disease (CHD) susceptibility.
Results support overexpression of RCAN1 and particularly the RCAN1.1S isoform during aging as a pathogenic mechanism in both Down syndrome-related and sporadic Alzheimer's disease
RCAN1 can interact with IkappaBalpha and affect the phosphorylation of IkappaBalpha at tyrosine 42.
The sequence variations in RCAN1 promoter are not major genetic factors involved in sporadic CHD, at least in the current research population.
For DSCR1rs6517239, patients with an AA genotype had higher recurrence probability than patients carrying at least one allele G (37 +/- 4% SE vs. 15 +/- 6% SE) (HR: 0.51; 95% CI, 0.27-0.94; P = 0.027).
E4BP4 and BIM regulation correlated with that of RCAN1-1. A putative GRE and four EBPREs were identified within 1500bp upstream from the transcription start site of RCAN1-1
The transcriptional regulation of RCAN1.1 and RCAN1.4 by two alternative promoters, is reported.
Rcan1-1L may play a protective role in Ang II-treated cardiomyocytes through the induction of mitochondrial autophagy, and may be an alternative method of cardiac protection.
Results show that Rcan1 isoform 1L (Rcan1-1L) overexpression specifically activates mitophagy and increases cell survival under hypoxic conditions.
RCAN1 up-regulation enhanced mitochondrial fusion and conferred protection from myocardial reperfusion injury.
Regulator of Calcineurin 1 (RCAN1), a feedback inhibitor of the calcium-activated protein phosphatase calcineurin (CN), acts to suppress two distinctly different mechanisms of non-shivering thermogenesis.
Our results suggest that Rcan1 might act as endogenous negative modulator of COX-2 expression and activity by inhibiting calcineurin and NF-kB pathways to maintain normal contractility and vascular stiffness in aorta and small mesenteric arteries, respectively.
This study demonstrated that Rcan1 is regulated by oxidative stress and identified RCAN1 as a potential diagnostic marker of acute pancreatitis.
Conditional deletion of Rcan1 predisposes to hypertension-mediated intramural hematoma and subsequent aneurysm and aortic rupture.
These findings demonstrate a novel regulatory role of RCAN1 in TLR signaling, which differentially regulates MyD88 and TRIF pathways.
The expression of DSCR1-4 increased strongly at P16 after OIR. There was no change in messenger RNA (mRNA) expression of DSCR1-1 at P16 after oxygen-induced retinopathy. The increased DSCR1 was mainly located in the RGCs of avascular retina. In addition, DSCR1-4 expression was increased in primary RGCs after hypoxia exposure.
RCANs play critical roles in bone homeostasis by regulating both osteoclastogenesis and osteoblastogenesis, and they serve as inhibitors for calcineurin-NFATc1 signaling both in vivo and in vitro.
The present study demonstrates that RCAN1 deficiency protects against Salmonella intestinal infection by enhancing proinflammatory JNK signaling.
DSCR1 as a key protein that couples axon growth.
from amongst the myriad of gene expression changes occurring in Type 2 diabetes (T2D) b-cells where we had little knowledge of which changes cause b-cell dysfunction, we applied a trisomy 21 screening approach which linked RCAN1 to b-cell mitochondrial dysfunction in T2D.
These results uncover a critical link between calcineurin signalling, impaired neurotrophin trafficking and neurodevelopmental deficits in the peripheral nervous system in Down syndrome.
Data suggest that expression of Dscr1 in hippocampus can be regulated by dietary factors; supplementation of maternal diet and offspring diet with fish oil down-regulates Dscr1 in hippocampus of offspring; Dscr1 is a presumed target in Down syndrome.
inhibition of the calcineurin-nuclear factor of activated T cells pathway enhances the proliferation of granulocyte-monocyte progenitors both in vitro and in vivo
PACAP targets RCAN1 to control neuronal differentiation.
We also confirmed that overexpression of RCAN1-1L could inhibit the transcriptional activation of an NFAT-dependent promoter in response to PMA and ionomycin by inhibiting Calcineurin activity in HEK293T cells
found that RCAN1/3 interact with RAF kinases and CN in a non-exclusive manner. Our data suggests that the balance of RCAN interactions with CN and/or RAF kinases may influence T cell positive selection
Calcineurin and its regulator, RCAN1, confer time-of-day changes in susceptibility of the heart to ischemia/reperfusion.
Data indicate that neuron from Down syndrome candidate region 1 (DSCR1)-transgenic mice were more resistant than wild-type neurons to apoptotic cell death following 24 h of glucose deprivation.
RCAN1-regulated vascular branching which may play a role in the patterning of morphologically different vasculature.
The protein encoded by this gene interacts with calcineurin A and inhibits calcineurin-dependent signaling pathways, possibly affecting central nervous system development. This gene is located in the minimal candidate region for the Down syndrome phenotype, and is overexpressed in the brain of Down syndrome fetuses. Chronic overexpression of this gene may lead to neurofibrillary tangles such as those associated with Alzheimer disease. Three transcript variants encoding three different isoforms have been found for this gene.
Down syndrome candidate region 1
, Down syndrome critical region gene 1
, calcium and oxidant-inducible mRNA
, down syndrome critical region protein 1
, modulatory calcineurin-interacting protein 1
, myocyte-enriched calcineurin-interacting protein 1
, near DSCR proline-rich protein
, calcipressin 1
, down syndrome critical region protein 1 homolog
, regulator of calcineurin 1
, Down syndrome critical region homolog 1
, calcineurin inhibitor
, myocyte-enriched calcineurin interactin protein 1
, Down syndrome critical region protein 1 homolog
, Oxidative-induced protein Adapt78