CX3CR1 (Extracellular Loop) Peptide
- Known as:
- CX3CR1 (Extracellular Loop) Peptide
- Catalog number:
- 2201P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CX3CR1 (Extracellular Loop) Peptide
Related genes to: CX3CR1 (Extracellular Loop) Peptide
- 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 (Extracellular Loop) Peptide
Related articles to: CX3CR1 (Extracellular Loop) Peptide
- Microglia are innate immune cells of the central nervous system (CNS). They extend their processes and migrate toward injuries in vivo. However, how the fractalkine receptor (CX3CR1) influences microglial migration remains unknown. Label-free proteomic profiling predicted changes in Ras homology family (RHO)-signaling activity that hint at dysregulated cytoskeleton signaling in Cx3cr1-deficient murine cortex tissue. To further investigate microglial migration, we carried out two-photon in vivo imaging at 4-h intervals for 72 h after a laser lesion in the cortex. Cx3cr1-deficient microglia showed enhanced migration toward the lesion. Additionally, the length and velocity of microglial fine processes extending toward the lesion were increased in Cx3cr1-deficient microglia. Migration remained unchanged in Ccr2-deficient mice, indicating that monocyte-derived macrophages/microglia did not contribute to microglia accumulation around the lesion. These results demonstrate that CX3CR1 modulates microglia migration toward laser-induced CNS injury. Manipulating microglia migration via the CX3CR1 signaling axis is therefore a potential target for the treatment of CNS injury. - Source: PubMed
Wagner JensAntony HenrikeHoyer CorneliaLundgrén KristiinaSoliymani RabahCrux SophieJustus LenaKeppler KevinSteffen JuliaKurts ChristianEngel Daniel RHerms JochenŁałowski MaciejFuhrmann Martin - Neuroinflammation is a key mechanism underlying neuropathic pain, in which microglial cells play a central role. Poly(ADP-ribose) polymerase 12 (PARP12) is an interferon-stimulated gene (ISG) containing a predicted RNA-binding domain and may be involved in inflammatory regulation and RNA metabolism; however, its posttranscriptional regulatory functions in microglia remain to be fully elucidated. PARP12 was stably knocked down in BV2 microglial cells using lentiviral shRNA. Quantitative PCR confirmed a significant reduction in mRNA levels (knockdown efficiency 78.3%), but Western blot analysis showed no successful downregulation of PARP12 protein levels. Transcriptomic and alternative splicing changes were systematically analyzed using RNA sequencing (RNA-seq), and selected key genes were validated by RT-qPCR. Functional enrichment analysis was performed on differentially expressed genes (DEGs) and regulated alternative splicing events (RASEs). Expression changes of homeostatic microglial markers and classical polarization markers were analyzed from the existing RNA-seq data. Comparisons were made with public proinflammatory microglial signature gene sets. PARP12 mRNA knockdown led to substantial transcriptomic remodeling: 276 DEGs (107 upregulated and 169 downregulated) and 287 significant RASEs were identified. Downregulated DEGs were significantly enriched in inflammatory pathways such as NF-κB, TNF, and chemokine signaling; most core immune genes (including Ccl2, Ptgs2, and C3) showed coordinated downregulation, whereas a smaller subset (Ccl5, Cd81, and S1pr1) was upregulated. Homeostatic microglial markers (Tmem119, P2ry12, Cx3cr1, Sall1, etc.) did not differ significantly between shPARP12 and shNC cells. Splicing analysis revealed altered splicing of immune/metabolism-related genes such as Fyb, Tnfaip8, Lrch4, and Pkm, but changes in protein isoform ratios were not validated. The overall proinflammatory signature gene set was downregulated after PARP12 knockdown. PARP12 mRNA knockdown is closely associated with attenuation of the proinflammatory transcriptional program and widespread alternative splicing changes in BV2 microglial cells. However, given the unsuccessful knockdown at the protein level, the observed changes cannot be directly attributed to loss of PARP12 protein function. Further mechanistic studies combining CRISPR/Cas9 gene knockout and in vivo pathological models are warranted. - Source: PubMed
Publication date: 2026/08/15
Hu BangZhou WenLiChen HuaLi Feng - Marijuana (cannabis) and cannabinoids are getting global medical and recreational approvals in this era of the opioid epidemic. Both opiates and cannabis are often co-abused, and their use increases the risk of opioid and cannabis use disorders (OUDs and CUDs), and dependency. Opioid and cannabinoid systems share many neuromodulating and pharmacological effects by activating opioid and cannabinoid receptors, respectively. Inflammation is increasingly implicated in many diseases, and mu-opioid receptor (MOR) and CB2 cannabinoid receptor (CB2R) have been linked to neuroinflammation. The hypothesis that changes in MOR and CB2R mediated behavioral and cytokine alterations are associated with their roles in inflammation was tested here. Naïve male C57Bl/6J as wild type, MOR KO mice with deletion of MOR, DAT- cKO mice with deletion of CB2R from dopamine neurons and CX3Cr1- cKO mice with deletion of CB2R from microglia were used in the study. Nociception was assessed using tail-flick latency, followed by ELISA to quantify levels of cytokines and chemokines in the cerebellum and prefrontal cortex (PFC) regions of the animals. MOR KO, DAT-, and CX3Cr1- conditional knockout mice exhibited distinct behavioral and neuroimmune phenotypes, marked by genotype- and region-specific alterations in cytokines and chemokine. CX3Cr1- cKO mice had reduced tail-flick sensitivity compared to MOR KO, DAT- cKO, and wild-type controls. These findings suggest that MOR deletion and cell-specific loss of CB2Rs in dopamine neurons or microglia distinctly affect nociceptive functions, alongside immune signaling changes. Targeting components of the eCBome and opioid systems may offer novel therapeutic strategies for inflammation-linked chronic pain. - Source: PubMed
Publication date: 2026/07/29
Kibret BerhanuOnaivi Emmanuel SSharma Venkatanarayanan - Relapse is common in IgG4-related disease (IgG4-RD), but reliable predictors to identify high-risk patients remain limited. We sought to identify blood and tissue immune features at the initiation of remission induction therapy associated with subsequent relapse. - Source: PubMed
Publication date: 2026/08/12
Shimanuki KanakoAkiyama MitsuhiroSaito KoichiAlshehri WaleedMaruyama TakeruSasaki TakanoriYoshimoto KeikoSeki NoriyasuTsujimoto HidetoChiba KenjiKaneko Yuko - Gestational diabetes mellitus (GDM) may increase offspring susceptibility to neurodevelopmental stressors. Sevoflurane is widely used in pediatric anesthesia but carries potential neurotoxicity risks. This study investigated whether maternal GDM exacerbates sevoflurane-induced developmental neurotoxicity in offspring, and explored the underlying mechanisms related to neuroinflammation, microglial activation and mitochondrial dysfunction. - Source: PubMed
Publication date: 2026/08/10
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