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We found that common variants of the CX3CR1 gene influence amyotrophic lateral sclerosis survival. Our data provide further evidence for the role of neuroinflammation in amyotrophic lateral sclerosis
CX3CR1 genetic variants represent new modifying factors of pathology progression and age of onset in late-onset Alzheimer's disease.
Study demonstrated that CX3CL1/CX3CR1 was overexpressed in prostate cancer tissues with spinal metastasis compared with primary tumors. Overexpression of CX3CR1 increased cell proliferation, migration and invasion. Also, study observed that EGFR/Src/FAK pathway was activated by CX3CL1/CX3CR1.
CX3CR1 major allele carriers V249 and T280 are significantly associated with an increased total arterial blood volume of the whole brain, especially around the bilateral precuneus, left posterior cingulate cortex, and left posterior parietal cortex.
investigated the association of CX3CR1 839C/T, CX3CR1 745G/A, polymorphisms with Age-Related Macular Degeneration (AMD) risk. These associated with an increased AMD risk (CX3CR1 839C/T, additive model: aOR=2.682, 95% CI=1.119-5.709, P=0.022, recessive model: aOR=2.729, 95% CI=1.141-6.048, P=0.010; CX3CR1 745G/A, additive model: aOR=2.614, 95% CI=1.231-6.012, P=0.020, recessive model: aOR=2.340, 95% CI=1.227-5.993, P=0.011
CX3CR1 regulated chondrocyte proliferation.
We detected a statistically significant association between the variant Ala55Thr in CX3CR1 with schizophrenia and autism spectrum disorder phenotypes
This study shown that CX3CR1 expression in both Microglia and Astrocytes in hippocampus in affected by stroke, Alzheimer's disease, and Lewy body dementia.
The US28 gene product has maintained the function of the ancestral gene and has the ability to bind and signal in response to human CX3CL1, the natural ligand for CX3CR1.
Our findings demonstrate that motility, invasion, and contact-independent growth of PDAC cells all increase following CX3CL1 exposure, and that antagonism of CX3CR1 by the inhibitor JMS-17-2 reduces each of these phenotypes and correlates with a downregulation of AKT phosphorylation.
in Crohn's disease patients, a missense mutation in the gene encoding CX3CR1 was identified and found to be associated with impaired antifungal responses
CX3CL1/CX3CR1 axis plays a key role in the development of ischemia-induced oligodendrocyte injury via p38MAPK signaling pathway.
Soluble FKN that was efficiently shed from the surface of LPS-activated ECs in response to binding of CD16(+) monocytes to ECs, diminished monocyte adhesion in down-regulating CX3CR1 expression on the surface of CD16(+) monocytes resulting in decreased TNF-secretion.
CX3CR1 genetic variants were not associated with risk of atherosclerotic coronary heart disease and glucometabolic traits in European ancestry cohort. In a South Asian cohort, identified CX3CR1 SNP associated with myocardial infarction and type II diabetes mellitus.
FKN and CX3CR1 expression was significantly increased in pancreatic ductal adenocarcinoma (PDAC) tissues, especially in the metastatic samples, and was highly-correlated with severity of PDAC. Ectopic expression of FKN promoted the proliferation and migration of PDAC, while knockdown of CX3CR1 reversed the function of FKN.
CX3CL1 is upregulated in both human and murine tumors following VEGF signaling blockade, resulting in recruitment of CX3CR1+Ly6Clo monocytes into the tumor
The fractalkine functions on the activation of the AKT/NF-kappaB/p65 signalling cascade and regulation of the antiapoptosis process in pancreatic cancer cells.
High expression of CX3CR1 correlates with significantly shorter survival, specifically in post-menopausal patients with advanced and terminal stages of the disease. Taken together, this support a key regulatory role for the fractalkine axis in advanced and relapsed peritoneal metastasis in epithelial ovarian carcinoma.
rs3732378 and rs3732379 susceptibility loci for developmental dysplasia of the hip
V249I genotype of the fractalkine receptor showed a protector role in patients with type 2 diabetes. The T280M genotype is associated with increased carotid intima-media thickness in Mexican individuals with or without type 2 diabetes
CXCR1 mediates neuronal apoptotic cell death in ischemia.
These data implicate sex differences in microglial activation in the modulation of energy homeostasis and identify CX3CR1 signalling as a potential therapeutic target for the treatment of obesity.
Using the Theiler's virus model of encephalitis in C57BL/6 mice study shows that CCR2 as well as CX3CR1 plays a key role in the accumulation of myeloid cells in the CNS and activation of hippocampal myeloid cells upon infection.
Ang II up-regulates CX3CR1 expression in VSMCs via NADPH oxidase/ROS/p38 MAPK pathway and the CX3CL1/CX3CR1 axis contributes to the proliferative and pro-inflammatory effects of Ang II in VSMCs.
CX3CR1 ablation enhanced the neurotrophic action of microglia in Mecp2KO mice
These findings indicate that emotional and cognitive stress resilience involves CX3CR1-dependent basal and stress-induced alterations in hippocampal transcription
The effect of CX3CR1 deletion on murine acetabular development provides suggestive evidence of a susceptibility inducing role of the CX3CR1 gene on developmental dysplasia of the hip.
In Cx3cr1(-/-) mice, adult-born-granule-cells exhibited reduced spine density, dynamics and size, concomitantly with reduced contacts between Cx3cr1-deficient microglia and adult-born-granule-cells' dendritic shafts, along with increased proportion of microglia-contacted spines.
reveal CX3CR1 as a novel target for the clearance of extracellular Tau
These findings suggest that fractalkine receptor is not a universal regulator of synaptic plasticity, but rather has heterogeneous roles in specific brain regions and life stages.
Although CCR2 and CX3CR1 may synergistically impact inflammatory phenotypes, their joint deficiency did not influence the metabolic effects of a 45% high-fat diet-induced obesity in these model conditions.
that CX3CL1-CX3CR1 signaling is a molecular mechanism capable of modulating microglial-mediated degeneration
Increased fractalkine and its receptor CX3CR1 may cause a cross-talk between activated glial cells and neurons, playing an important role in the development of neuroinflammation in fructose-fed mice.
CX3CR1 deficiency accelerates the development of vascular pathology in diabetic retinopathy.
CX3CR1(-/-) mice did not become anhedonic in the "two hit" chronic stress paradigm, confirming resistance of these animals to chronic stress-induced mood alterations. However, there was no difference in stress hormone levels, open field performance and hypothalamic microglia distribution between the genotypes. Energy expenditure was increased in CX3CR1(-/-) mice, which may be related to their active coping behavior.
Inflammatory Osteoclasts Prime TNFalpha-Producing CD4(+) T Cells and Express CX3 CR1
our study demonstrates that macrophages expressing a functional CX3CR1 receptor have an important and non-redundant role in controlling the abnormal intestinal inflammation that may lead to tissue damage.
These results highlight the importance of fractalkine-CX3CR1 interaction in recruitment of macrophages into the brown adipose tissue of obese mice.
Results indicate that deletion of CX3CR1 from microglia under resting conditions modifies brain areas with elevated cellular turnover independent of CX3CL1.
Fractalkine is a transmembrane protein and chemokine involved in the adhesion and migration of leukocytes. The protein encoded by this gene is a receptor for fractalkine. The encoded protein also is a coreceptor for HIV-1, and some variations in this gene lead to increased susceptibility to HIV-1 infection and rapid progression to AIDS. Four transcript variants encoding two different isoforms have been found for this gene.
, CX3C chemokine receptor 1
, G protein-coupled receptor 13
, G-protein coupled receptor 13
, beta chemokine receptor-like 1
, chemokine (C-C) receptor-like 1
, chemokine (C-X3-C) receptor 1
, fractalkine receptor
, CX3C chemokine receptor 1-like
, Fractalkine receptor
, chemokine receptor 1
, chemokine (C-X3-C motif) receptor 1