Anti_Mouse, mab CX3CL1 Source Rat
- Known as:
- Anti_Mouse, mab CX3CL1 Source Rat
- Catalog number:
- 103-M352
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab CX3CL1 Source Rat
Related genes to: Anti_Mouse, mab CX3CL1 Source Rat
- 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: Anti_Mouse, mab CX3CL1 Source Rat
Related articles to: Anti_Mouse, mab CX3CL1 Source Rat
- Neurodegeneration is a leading cause of long-term disability and cognitive impairment, and the aberrant activation of the NOD-like receptor protein 3 (NLRP3) inflammasome is closely implicated in its pathogenesis. The NLRP3 inflammasome, as a central mediator of inflammatory cascades, can, when excessively activated, promote neuroinflammation and glial polarization, induce neuronal death, disrupt the blood-brain barrier, suppress angiogenesis and neurogenesis, impair synaptic plasticity, and induce inflammaging, ultimately leading to neurodegeneration. Exerkines, including neurotrophic factors, adipokines, myokines, hepatokines, enzymes/coenzymes, metabolites, and miRNAs, can target the aberrant activation of the NLRP3 inflammasome, exerting neuroprotective effects. Exercise has attracted increasing attention for its benefits to brain health, as it can modulate the release and expression of numerous exerkines (such as BDNF, NGF, GDNF, APN, Chemerin, Apelin, Irisin, CX3CL1, HSP90, IGF-1, LCN2, SAA, SIRT1, lactate, and exosomal miRNAs), which, through the activation of specific kinases and downstream signaling pathways in the brain, precisely target the excessive activation of the NLRP3 inflammasome and thereby ameliorate neurodegeneration. This review summarizes and critically evaluates recent advances in the mechanistic roles of the NLRP3 inflammasome in the onset and progression of neurodegeneration, as well as in the molecular mechanisms by which exerkines regulate the NLRP3 inflammasome to ameliorate neurodegeneration, and in exercise interventions, providing a theoretical basis for the precise and targeted application of exercise in the prevention and treatment of neurodegeneration. - Source: PubMed
Publication date: 2026/07/04
Tang ShaokaiGeng YuanwenLin QinqinTian Zhenjun - - Source: PubMed
Publication date: 2026/07/03
Yang ZhenyunWang XinFu YizhenWu WeijieHu ZiliLin QingyangPeng WeiPan YangxunWang JunchengChen JinbinHu DandanZhou ZhongguoXu LiZhang YaojunHou JiajieChen Minshan - miR-139 acts as a tumor suppressor in breast cancer cells, yet its role within the tumor immune microenvironment (TIME) remains unclear. This study explores the dual functions of miR-139 in both tumor and immune cells, particularly its effect on CD8 T cell function and chemokine-mediated immune recruitment. Bioinformatics analysis using TCGA and GEO data identified miR-139 as differentially expressed in breast cancer. Using samples from 32 patients, we detected elevated miR-139 levels in tumor-infiltrating CD8 T cells compared with adjacent normal tissues. Further experiments confirmed that miR-139 directly targets CD28, leading to its downregulation. Concurrently, increased expression of exhaustion markers PD-1 and TIGIT was observed. Moreover, tumors with high miR-139 expression showed upregulation of T-cell-recruiting chemokines CX3CL1, CXCL12, and CXCL14. These results demonstrate that miR-139 promotes CD8 T cell exhaustion via suppression of CD28 and facilitates chemokine-mediated T cell recruitment, highlighting its immunosuppressive role in breast cancer. - Source: PubMed
Publication date: 2026/06/23
Chen JianrongZhang HaiyongLv YantingLi XiufangHu Mengjun - Inflammaging, a term describing the chronic, low-grade inflammatory state associated with aging, is implicated in various age-related diseases. Inflammatory proteins are central to inflammaging and bone-muscle communication. This study sought to investigate the role of inflammatory proteins as potential myokines and osteokines in the context of sarcopenia-osteoporosis crosstalk using a convenient and efficient method, Mendelian Randomization (MR). - Source: PubMed
Publication date: 2026/06/29
Liu MingchongWang JiamingFu XiaoYang ChensongZhao JingleiSun Guixin - Renal-resident macrophages (RMs) are essential regulators of kidney homeostasis and repair, yet the mechanisms governing RM niche regeneration after acute depletion remain poorly defined. To overcome these limitations, we have developed an inducible human CD59- intermedilysin (hCD59-ILY) ablation system, enabling rapid, specific, and reversible depletion of targeted macrophage populations, and subsequent replenishment of RMs, followed by longitudinal scRNA-seq analysis of kidneys at baseline and days 1, 3, and 7 post-ablation. RM ablation triggered a rapid and sustained upregulation of , predominantly in proximal tubular epithelial cells (PTC1/PTC2), establishing a persistent chemotactic niche signal that coincided with macrophage repopulation. Regenerating RMs transitioned from inflammatory/stress-associated states toward metabolically active and proliferative phenotypes enriched in glycolysis, oxidative phosphorylation, MYC, and cell-cycle programs, with attenuation of canonical inflammatory pathways. Cell-cell communication analysis revealed an early burst of intercellular signaling at day 1, followed by progressive normalization, with fibronectin ), osteopontin (), chemokine (), and amyloid precursor protein () axes emerging as key mediators of niche restoration. Transcriptional network analysis identified a conserved regulatory module (, , , , , ) coordinating macrophage differentiation and regenerative programming, linking metabolic adaptation to lineage reconstitution. Sub-clustering revealed five dynamically shifting RM subsets with distinct inflammatory, remodeling, proliferative, and surveillance states, reflecting a hierarchical regeneration process. Functional validation using clodronate-mediated depletion in Secreted Phosphoprotein 1 (Opn)-deficient mice demonstrated impaired macrophage repopulation, establishing osteopontin as a critical regulator of RM regeneration. Together, these data define a coordinated epithelial-immune circuit in which Cx3cl1-driven chemotaxis, -dependent signaling, and a core transcriptional network orchestrate macrophage niche reconstitution and kidney repair following acute immune cell ablation. - Source: PubMed
Publication date: 2026/06/18
Islamuddin MohammadJi LixuanChen YilinSong KejingEllsworth Calder RRappaport JackWang ChenxiaoLiu ShumeiKolls JayXu XiaojiangQin Xuebin