Fractalkine CX3CL1, Human
- Known as:
- Fractalkine CX3CL1, Human
- Catalog number:
- Z02828-20
- Product Quantity:
- 20,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- Fractalkine CX3CL1 Human
Related genes to: Fractalkine CX3CL1, Human
- Gene:
- CX3CL1 NIH gene
- Name:
- C-X3-C motif chemokine ligand 1
- Previous symbol:
- SCYD1
- Synonyms:
- NTN, C3Xkine, ABCD-3, CXC3C, CXC3, fractalkine, neurotactin
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
Related products to: Fractalkine CX3CL1, Human
Related articles to: Fractalkine CX3CL1, Human
- Chronic pain acts as a potent driver of progressive cognitive impairment. Although microglial hyperactivation serves as a pivotal mechanistic bridge in this comorbidity, the intracellular molecular cascades coupling persistent nociception to cognitive decline remain largely elusive. Here, we identify a previously unrecognized microglial secretome remodeling axis, governed by CX3CL1-CX3CR1 signaling, that drives pain-associated cognitive impairment. Clinically, elevated cerebrospinal fluid (CSF) CX3CL1 correlates strongly with cognitive impairment in chronic pain patients. In murine models, pharmacological blockade of the microglial CX3CL1-CX3CR1 signaling attenuated chronic pain-induced memory deficits. Mechanistically, aberrant CX3CL1-CX3CR1 activation triggers a sequential p38 MAPK-NF-κB cascade to upregulate the kinesin motor KIFC2. This KIFC2 surge fundamentally reprograms microglial vesicular trafficking, driving the massive release of IL-17-enriched small exosomes (<100 nm) that subsequently induce synaptic deterioration and neuronal apoptosis manifested by PSD95 degradation, caspase-3 cleavage, and compromised cell viability. Crucially, this microglial p38 MAPK-NF-κB-KIFC2 cascade hyperactivation was validated in situ within the hippocampal slices of chronic pain models. Collectively, our findings delineate a comprehensive cascade spanning from receptor hyperactivation to KIFC2-dependent exosomal remodeling, elucidating a novel mechanism of microglia-mediated neurotoxicity. Targeting this CX3CL1-KIFC2 exosomal axis offers a potential therapeutic strategy to uncouple chronic pain from its debilitating cognitive comorbidities. - Source: PubMed
Publication date: 2026/07/15
Hu ChenZhang XinluZhao WeiKe WenjunMa HaoxiangSang WennaGao Qian - Psychological distress may be associated with systemic immune regulation through neuroendocrine-immune pathways. Emergency medical services (EMS) personnel represent a high-demand occupational group, but their circulating cytokine and chemokine profiles and their relationship with psychological distress remain poorly characterized. This exploratory cross-sectional study examined inflammatory and physiological markers in EMS personnel compared with matched controls, with particular attention to the association between cortisol and CXCL1 and exploratory sex-related patterns. - Source: PubMed
Publication date: 2026/07/10
Serrano-Ibáñez Elena RFlores-López MaríaMartín-Chaves LauraCorrás-Vázquez TaniaAntúnez-Muñoz InésSamper-Zapata JavierCarmona-Segovia Ada Del MarReviriego RaquelJiménez-Navarro ManuelRodríguez de Fonseca FernandoSerrano AntoniaPavón-Morón Francisco Javier - Microarray and Next Generation Sequencing studies offer insight into gene regulation in Parkinson's disease (PD). However, analysing vast numbers of genes can make the interpretation of data difficult when considering the platforms and techniques used across different studies. In this study, transcript expression, restricted to genes related to G-protein coupled receptors, activating agonists, agonist precursors, synthesis enzymes and transduction processes, as well as stress-related chaperones and solute carriers, was assessed across nine microarray platforms and two RNAseq studies of the substantia nigra (nigral volume). Changes in gene expression associated with PD were assessed by differential expression analysis while RNAseq studies were also used to calculate transcript per million values for each of the genes within the nigral volume. This analysis showed extensive changes in nigral volume signalling for several robustly expressed signal-related transcripts including tyrosine hydroxylase (TH), WNT signalling components (SFRP1, RSPO2 and DKK3), Kallikrein Related Peptidase 6 (KLK6), neurexins (NRXN1, NRXN3), prostaglandin synthases (PTGES2, PTGES3) and fractalkine (CX3CL1). The nigral volume signalling ligand data was then cross-referenced to the most abundant G-protein coupled receptor and signal transduction transcripts in the pigmented neurons using two RNAseq and two microarray studies. There were 32 significant changes in G-protein coupled receptor and associated signalling genes in pigmented neurons from PD tissue. Of these, 30 genes were upregulated. Analysis of the transcription factors likely regulating the 30 upregulated genes indicates a stimulation of cell stress pathways, particularly the JNK-MAP kinase pathway. Following this pathway back to changes in nigral signalling transcripts indicates that deficits in at least two autocrine/paracrine signalling systems; dopamine, via Gαo-coupled dopamine D2 receptors and Dickkopf-3 (DKK3) appear likely to contribute to pigmented neuron stress in PD. - Source: PubMed
Publication date: 2026/07/24
Haynes John M - To identify the cytokine genes influencing the formation of tertiary lymphoid structures (TLS) through CRISPR-Cas9 library screening, and to discover potential key regulatory molecules, providing new targets for enhancing the efficacy of bladder cancer immunotherapy. - Source: PubMed
Wang YongcunSong HongchenDU YiqingXu Tao - Ketamine, a non-competitive N-methyl-D-aspartate acid (NMDA) receptor antagonist, produces rapid and sustained antidepressant actions, but the underlying molecular mechanism remains unclear. The CXCL1/CXCR1 signaling is closely related to mood disorders, and this study aims to investigate its role in ketamine's antidepressant actions. We pharmacologically (AZD8797, a selective CXCR1 antagonist) and genetically (intra-mPFC microinjection with AAV-CXCR1-siRNA) manipulated the CXCL1/CXCR1 signaling and investigated their effects on ketamine's antidepressant-like effects in mice treated with corticosterone (Cort), and observed changes in synaptic plasticity in response to these manipulations. We found that 24 h after drug injection, ketamine (10 mg/kg, i.p.) significantly reversed the Cort-induced depression-like behaviors, and inhibited the overexpression of pro-inflammatory cytokines and microglial activation. Ketamine significantly improved the Cort-induced impairment in the dendritic complexity and spine densities. In addition, our ELISA results showed that ketamine significantly inhibited the activation of CXCL1/CXCR1 signaling, and ketamine attenuated the upregulation of CXCR1 and CXCL1 expression in Cort-treated HT22 and BV2 cells in vitro. Furthermore, pretreatment with AZD8797 (0.8 mg/kg, i.p., twice a week) completely blocked ketamine's antidepressant-like behavioral effects and eliminated ketamine-induced enhancement in the synaptic plasticity; intra-mPFC microinjection with AAV-CXCR1-siRNA also prevented ketamine's behavioral effects and beneficial effects on the synaptic plasticity. These findings demonstrated that CXCL1/CXCR1 signaling-mediated synaptic plasticity played essential roles in ketamine's antidepressant-like effects, which opened a new door to targeting chemokines to improve depression symptoms. - Source: PubMed
Publication date: 2026/07/20
Yin Yong-YuSun Si-RuiZhang Hui-YingBi Peng-WeiZhao Jia-NingCheng HaoLi Yun-Feng