CXCL10 (IP_10) Whole Serum Human
- Known as:
- CXCL10 (IP_10) Serum Human
- Catalog number:
- RS-80CX10
- Product Quantity:
- 1.0 mL
- Category:
- -
- Supplier:
- ICL I.C.L
- Gene target:
- CXCL10 (IP_10) Whole Serum Human
Ask about this productRelated genes to: CXCL10 (IP_10) Whole Serum Human
- Gene:
- BBIP1 NIH gene
- Name:
- BBSome interacting protein 1
- Previous symbol:
- NCRNA00081
- Synonyms:
- bA348N5.3, BBIP10, BBS18
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-09-02
- Date modifiied:
- 2016-10-05
- Gene:
- CXCL10 NIH gene
- Name:
- C-X-C motif chemokine ligand 10
- Previous symbol:
- INP10, SCYB10
- Synonyms:
- IFI10, IP-10, crg-2, mob-1, C7, gIP-10
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-09
- Date modifiied:
- 2016-10-05
- Gene:
- CXCR3 NIH gene
- Name:
- C-X-C motif chemokine receptor 3
- Previous symbol:
- GPR9
- Synonyms:
- CKR-L2, CMKAR3, IP10-R, MigR, CD183
- Chromosome:
- Xq13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-01
- Date modifiied:
- 2016-10-05
- Gene:
- MED24 NIH gene
- Name:
- mediator complex subunit 24
- Previous symbol:
- THRAP4, CRSP4
- Synonyms:
- TRAP100, KIAA0130, DRIP100, CRSP100, MED5
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-30
- Date modifiied:
- 2016-10-05
- Gene:
- PPIAP10 NIH gene
- Name:
- peptidylprolyl isomerase A pseudogene 10
- Previous symbol:
- PPIAL2, PPIP10
- Synonyms:
- CRP
- Chromosome:
- 20q13.2
- Locus Type:
- pseudogene
- Date approved:
- 1998-10-12
- Date modifiied:
- 2017-08-21
Related products to: CXCL10 (IP_10) Whole Serum Human
Related articles to: CXCL10 (IP_10) Whole Serum Human
- Chronic ethanol exposure, a key feature of alcohol use disorder (AUD), can affect the nervous system, but its molecular impact on the olfactory bulb remains unclear. In this study, an intermittent two-bottle voluntary drinking model was established in male mice, and transcriptome sequencing was performed on olfactory bulb tissues. DESeq2 analysis identified 188 differentially expressed genes, including 68 upregulated and 120 downregulated genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome pathway database (Reactome) analyses indicated that ethanol-responsive genes were predominantly enriched in receptor-mediated signaling pathways, particularly those linked to G protein-coupled receptor (GPCR) signaling. Protein-protein interaction analysis further identified eight core GPCR-related genes. quantitative real-time PCR (qRT-PCR) validation revealed that Cxcl10, Grp, Pcp2, and Pdyn were markedly downregulated in the ethanol group. These results suggest that chronic ethanol exposure is associated with transcriptional alterations in the male mouse olfactory bulb and may selectively affect several GPCR-related signaling components. This study provides candidate molecular evidence for further investigation of ethanol-associated olfactory dysfunction. - Source: PubMed
Publication date: 2026/09/05
Peng YujingYu FengweiQi XunzhongZhu XiaofengSun Guangtao - Epidermolysis bullosa simplex (EBS) is a genetic skin disorder driven by dominant pathogenic variants in or genes, leading to cytoskeletal fragility in basal keratinocytes and intraepidermal blistering. No curative therapies are currently available, and the link between keratin mutations and disease mechanisms remains incompletely understood. To further investigate the inflammatory component of EBS, we used a model of hiPSC-derived keratinocytes carrying dominant variants, alongside a genetically corrected isogenic counterpart. This approach established a direct link between the variants and keratin aggregation, impaired proliferation, and an inflammatory phenotype. The inflammatory signature was confirmed by increased expression of IL1A and IL1B, consistent with previous observations in EBS, while CXCL10 and CXCL11 emerged as newly identified dysregulated chemokines. Their consistent increase across independent cell lines, elevated secretion, and normalization in the CRISPR-corrected isogenic cells indicate that variants trigger a keratinocyte-intrinsic CXCL10/CXCL11 inflammatory response. Pharmacological inhibition of the IFN-γ-JAK1/2-STAT1 pathway suppressed their secretion, supporting JAK inhibition as a potential therapeutic strategy to modulate EBS-associated inflammatory dysregulation. In conclusion, this study shows that beyond structural defects, variants establish a keratinocyte-intrinsic inflammatory phenotype in which the CXCL10 and CXCL11 axis emerges as a key disease-associated signature and a promising therapeutic target. - Source: PubMed
Publication date: 2026/08/21
Saidani ManoubiaMartineau SabrinaMahmoud MarwaDomingues SophieDoyen ManonEl Kassar LinaHadj-Rabia SmailBodemer ChristineAllouche JenniferBaldeschi ChristineHolic Nathalie - High plasma Epstein-Barr virus (EBV)-DNA load may be associated with host immune dysregulation and secondary infection in children, although the underlying mechanisms remain uncertain. This study analyzed peripheral blood samples from 34 children with high plasma EBV-DNA load and 31 children with low plasma EBV-DNA load using transcriptomic analysis, WGCNA, CIBERSORT-based deconvolution, LASSO regression, Random Forest, qPCR, ELISA, and flow cytometry to explore immune features associated with EBV-DNA load and secondary-infection status. A total of 459 differentially expressed genes were identified. In the high-load group, antiviral and inflammatory pathways were significantly upregulated, whereas adaptive immune pathways were suppressed, revealing a pattern of innate immune hyperactivation together with impaired adaptive cellular immunity. CIBERSORT analysis estimated higher neutrophil and monocyte proportions and lower CD8⁺ T-cell and NK-cell proportions in the high-load group; these deconvolution estimates should not be interpreted as direct cell counts. Multi-strategy integrative analysis prioritized , , and as candidate immune-related markers; their expression was positively associated with plasma EBV-DNA load and was higher in the secondary-infection group than in the non-infection group. Within this cohort, the combined three-gene model yielded an AUC of 0.85 for discriminating secondary-infection status and should be considered exploratory pending independent validation. Experimental validation was directionally consistent with the bioinformatic findings and supports an association between high plasma EBV-DNA load, circulating immune dysregulation, and secondary-infection status; it does not establish a causal mechanism. - Source: PubMed
Publication date: 2026/09/02
Dai ShashaWang PengCao Liming - The limited intrinsic repair capacity of articular cartilage impairs tissue regeneration in osteoarthritis (OA). Platelet-rich plasma (PRP) fibrin gels offer a viable autologous scaffold for cartilage repair but often promote fibrous tissue rather than native hyaline structures. Mesenchymal stromal cell-derived extracellular vesicles (MSC-EVs) can overcome this limitation by actively promoting hyaline cartilage formation and suppressing matrix degradation. This study describes and validates a protocol for embedding adipose-derived MSC (ASC)-EVs into PRP gels (PRP-EVs) and evaluates the protective efficacy in human pathologic chondrocytes and synoviocytes. - Source: PubMed
Ragni EnricoTaiana MichelaLandoni SimonaValli FedericoNebuloni Andrea MassimilianoDe Luca PaolaLazzari Lorenzade Girolamo LauraPeretti Giuseppe - Tazarotene-induced gene 2 (), also known as retinoic acid receptor responder 2 (), encodes the secreted protein TIG2, also known as chemerin, which is involved in immune regulation and metabolism. However, its role in melanoma remains unclear. - Source: PubMed
Wang Chun-HuaWang Lu-KaiTsai Fu-Ming