CX3CR1 Antibody
- Known as:
- CX3CR1 Antibody
- Catalog number:
- XW-7725
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CX3CR1 Antibody
Related genes to: CX3CR1 Antibody
- Gene:
- CX3CR1 NIH gene
- Name:
- C-X3-C motif chemokine receptor 1
- Previous symbol:
- GPR13, CMKBRL1
- Synonyms:
- CMKDR1, V28, CCRL1
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-12
- Date modifiied:
- 2016-10-05
Related products to: CX3CR1 Antibody
Related articles to: CX3CR1 Antibody
- Bisphenol A (BPA) is a widely distributed environmental contaminant; however, its potential role in modulating ischemic neurovascular injury remains unclear. We applied an integrative approach combining network toxicology, Mendelian randomization, molecular docking, and single-cell transcriptomics to identify BPA-responsive targets relevant to ischemic stroke. CX3CL1 was prioritized based on network centrality, genetic association with stroke risk, and endothelial enrichment in post-ischemic brain tissue. Functional validation was performed in bEnd.3 brain endothelial cells and an endothelial-astrocyte Transwell blood-brain barrier (BBB) co-culture model subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). Under normoxic conditions, BPA (50 and 100 μM) did not markedly reduce cell viability; however, it significantly aggravated OGD/R-induced injury. BPA increased endothelial apoptosis (10.1% and 21.2% vs. 4.6% under OGD/R alone), elevated CX3CL1 protein expression (1.71- and 2.28-fold vs. control), increased BAX, and reduced Bcl-2 levels. Tight junction proteins were substantially decreased (claudin-5: 0.49 and 0.24; ZO-1: 0.46 and 0.23 relative to control), accompanied by reduced transendothelial electrical resistance and increased FITC-dextran permeability. Pharmacological inhibition of CX3CR1 using AZD8797 (0.5 μM) partially attenuated BPA-exacerbated apoptosis, tight junction loss, and barrier hyperpermeability without significantly altering CX3CL1 expression. Collectively, these findings suggest that BPA potentiates ischemia-reperfusion-associated endothelial and barrier dysfunction, accompanied by changes in CX3CL1-CX3CR1-related signaling, and support a potential role for environmental toxicants as modifiers of ischemic neurovascular vulnerability. - Source: PubMed
Publication date: 2026/05/04
Zhou KeguiZhu HongLi LongxuanLi Qiang - Microglia contribute to the pathogenesis of multiple sclerosis (MS) by promoting inflammatory cascades, mediating demyelination and regulating autoimmune responses, however, the molecular mechanisms connecting cellular stress to microglia-mediated immune responses in MS remain elusive. Stress granules (SGs) serve as an adaptive response of cells to various stressors such as viral infection and oxidative stress. In this study, we found that microglial T-cell intracellular antigen 1 (TIA1), a core SG component, was upregulated in MS patients and experimental autoimmune encephalomyelitis (EAE) mice. The neuroinflammation, demyelination and clinical deficits were exacerbated in Tia1-CKO (TIA1 knockout in microglia and monocyte-derived macrophages) EAE mice. Furthermore, TIA1 microglia exhibited the heightened activation characterized by increased proliferation, enhanced phagocytic activity, and a sustained polarization toward a pro-inflammatory phenotype. Notably, in an in vitro model of NaAsO-induced stress, TIA1 deficiency in BV2 cells and primary cultured microglia resulted in both enhanced phagocytic capacity and a pro-inflammatory phenotypic shift. Mechanistically, upon to stresses, microglial TIA1-mediated SGs formation was enhanced, leading to sequester ApoE mRNA into SGs to reduce ApoE expression, which in turn prevented excessive activation of microglia and inhibited demyelination in EAE mice. These findings uncover a previously unrecognized neuroprotective mechanism wherein TIA1-mediated SGs in microglia dynamically restrain neuroinflammation via post-transcriptional control of ApoE, revealing a new therapeutic avenue for MS. - Source: PubMed
Publication date: 2026/05/04
Fu QinjiaoLiu YanzhuLi FangfangWang YanjiaoYue JuanqingChen YingyiWu ShufangZhang JingjingJia MengxianHe YaozhiWang JiaweiHuang ZhihuiWang Ying - Retinal ischemia-reperfusion (IR) elicits microglia-driven neuroinflammation and mitochondrial failure that led to retinal ganglion cell (RGCs) loss, yet effective disease-modifying therapies remain limited. Acarbose (ACA), an α-glucosidase inhibitor widely used for diabetes, has recently been recognized for its dual regulatory potential on immune metabolism and aging-associated neurodegeneration. Here, we demonstrate that intravitreal ACA administration attenuates retinal inflammation and improves RGCs survival following IR injury. Single-cell RNA sequencing revealed extensive inflammatory activation and metabolic reprogramming across the retina, characterized by enhanced nicotinamide adenine dinucleotide (NAD) catabolism, particularly in microglia. ACA treatment was associated with reversal of these alterations, replenished NAD levels, and restored mitochondrial integrity. Integrative proteomic and biochemical analyses identified pyruvate kinase, muscle-type 2 (Pkm2) as a candidate regulatory node affected by ACA. Intravitreal delivery of siPkm2 partially protected against IR injury, and co-administration with ACA produced an additive trend in neuroprotection. Mechanistically, ACA upregulated sirtuin 1 (Sirt1) and reduced Pkm2 acetylation at lysine 270 (K270), which was linked to pro-inflammatory microglial activation. Structure-based virtual screening further identified HY-113082, a small molecule targeting Pkm2-K270, which synergized with ACA to suppress inflammation and enhance retinal protection. Moreover, Pkm2Cx3cr1-Cre mice conferred partial resistance to IR injury, but blunted the additional benefit of HY-113082 when combined with ACA, consistent with on-target engagement. Our findings support that ACA exerts retinal protection through the Sirt1-Pkm2-NAD axis, suggesting a metabolic checkpoint that integrates immune and mitochondrial regulation. This study provides mechanistic insight into ACA's dual immunometabolic and neuroprotective actions, holding promise for therapeutic insights into neuroinflammation. - Source: PubMed
Publication date: 2026/05/02
Wen YuwenDou Ya-NanChen XiaohongLiu XiuxingYang ZhenlanZhu YingtingLi ZhidongDeng CaibinDeng YeSu WenruZhuo Yehong - CD4 T cells play key roles in regulating immune responses during pregnancy; therefore, we aimed to understand the CD4 T-cell surface proteome and transcriptome during pregnancy. - Source: PubMed
Publication date: 2026/04/28
Habel Jennifer RNguyen Thi H Ode Alwis NatashaAllen E KaitlynnLi ShihanSkinner Morgan JJuno Jennifer AKent Stephen JBond KatherineWilliamson Deborah ALappas MarthaHannan Natalie JWalker SusanSchroeder JanCrawford Jeremy ChaseThomas Paul GKedzierska KatherineRowntree Louise C - Rheumatoid arthritis-related depression (RAD) is a major depressive disorder with high morbidity and disability rate. Our previous studies have shown that FKN/CX3CR1 signal axis led to observable depressive-like behaviors in RAD rats. Emerging evidence indicates that abnormal activated NMDA receptors and failed resilience of hippocampal plasticity contribute to the onset of depression. However, the underlying neural mechanisms of RAD remain unclear. We hypothesized that RAD might be associated with the hippocampal synaptic dysfunction, triggered by FKN-CX3CR1-NR signal pathway. To test this hypothesis, here we employed RAD model in vivo and in vitro and found that RAD rats exhibited a FKN level elevation with obvious features of rheumatoid arthritis and depressive-like behaviors. In addition, RAD modeling markedly destroyed the brain microvascular and activated microglia, eventually leading to hippocampal synaptic dysfunction and monoamine neurotransmitter deficiency via abnormal CX3CR1-NR signal pathway. Further in vitro study also indicated that the simulated RAD conditions resulted in synaptic damage of hippocampal neuron with abnormal levels of FKN and monoamine neurotransmitter, and then the activated CX3CR1-NR signal pathway caused microglia activation followed by hippocampal neuron synaptic dysfunction. Interestingly, both CX3CR1 receptor agonist (fractalkine) and NR receptor agonist (NMDA) aggravated the hippocampal synaptic dysfunction and monoamine neurotransmitter deficiency in RAD rats and in simulated RAD conditions. In contrast, both CX3CR1 receptor blocker (AZD8797) and NR receptor blocker (MK-801) ameliorated the FKN-CX3CR1-NR signal-driven microglia activation, hippocampal synaptic dysfunction and depressive-like behaviors in RAD rats. Collectively, these findings unveiled that the microglia activation-driven hippocampal synaptic dysfunction, triggered by abnormal FKN-CX3CR1-NR signal pathway, is responsible for depressive-like behaviors in RAD rats. The current results provide promising molecular targets and strategy for the treatment of RAD. - Source: PubMed
Publication date: 2026/04/28
Yao Shu-XiaLuo Shuang-YangZhao Hong-QingTan HuLiu Ping-AnLiu Jian