Mouse CXCL10 ELISA Kit
- Known as:
- Mouse CXCL10 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 55r-1745
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- Mouse CXCL10 ELISA Kit
Related genes to: Mouse CXCL10 ELISA Kit
- 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
Related products to: Mouse CXCL10 ELISA Kit
Related articles to: Mouse CXCL10 ELISA Kit
- Vestibular migraine (VM) is characterized by recurrent episodes of headache and vertigo, and its pathogenesis is closely associated with neuroinflammation and central sensitization. C-X-C motif chemokine ligand 10 (CXCL10) plays a critical role in neuroinflammation and pain modulation; however, its specific involvement in VM remains unclear. - Source: PubMed
Publication date: 2026/06/26
Song Mao-MeiCoppola GianlucaGao Ying-JieSong Shi-NaLi Chang-XinXu Sui-Yi - Adult-onset dermatomyositis (DM) is an autoimmune inflammatory myopathy with distinct cutaneous manifestations and a strong association with malignancy. Through comparative analysis with cutaneous lupus erythematosus (CLE), our integrated spatial and single-cell transcriptomics analysis reveals unique immune and stromal niches associated with DM subtypes. We find that cancer-associated DM skin lesions are distinguished by the presence of dispersed immune infiltrates enriched with macrophages or organized lymphoid aggregates with dense B cell cores surrounded by CD4 + /CD8 + T cells, accompanied by preserved vascular architecture. In contrast, non-cancer-associated DM skin is characterized by dense myeloid cell infiltrates, harbouring elevated expression of IL1B and CXCL10 localizing near injured vascular endothelia. Cytokines produced by these myeloid infiltrates, together with local tissue hypoxia, trigger dramatic stromal remodelling, leading to loss of vascular-associated fibroblasts. In addition to the CXCL10+ myeloid signature, non-cancer-associated DM skin is characterized by specific cellular pairs: PD-L1-expressing mature dendritic cells enriched in immunoregulatory molecules (mregDC) and activated regulatory T cells (Treg) expressing NFKB2 and TNF receptors. While both DM and CLE show strong interferon signatures, DM uniquely displays IFNβ expression. Together, our study provides a comprehensive spatial mapping of immune and stromal cells in adult-onset DM. - Source: PubMed
Publication date: 2026/06/26
Anufrieva Ksenia SShahriari NedaGao CeYiu Stephanie Pei TungKazerounian ShidehCastillo Rochelle LLiu JessicaPrell Sean ABhamidipati KartikAfshari KhashayarParmelee LindsayKazakova Anastasia NTheisen ErinBowman TeresaLaChance AveryCrisler William JHashemi KimberlyKorsunsky IlyaJiang SizunRashighi MehdiVleugels Ruth AnnWei Kevin - - Source: PubMed
Publication date: 2026/06/26
Ni ZhexinZhao QianqianLi YangshuoMei ShanshanYu JinDing JieLiang XiaolanSun ShuaiWang YuqingCheng WenZhou WeiYu Chaoqin - Steatohepatitis integrates metabolic stress and mitochondrial damage, but single-node interventions often incompletely quell inflammation and fibrosis. We tested a dual-node strategy that reduces the trigger and blocks the adaptor of the mtDNA-cGAS-STING pathway in a high-fat diet plus streptozotocin mouse model. Male C57BL/6 J mice with steatohepatitis (SH) received urolithin A (UA; mitophagy enhancer), C176 (murine STING inhibitor), or their combination. Endpoints included liver injury (ALT/AST), lipids (serum and hepatic triglycerides, cholesterol), glycemia/insulin resistance (fasting glucose, insulin, HOMA-IR), cGAS-STING/type-I interferon signaling (Ifnb1, Cxcl10, IFN-β, CXCL10; p-STING, p-TBK1, p-IRF3), mitochondrial damage signals (cytosolic mtDNA, mtTFA), autophagy/mitophagy (LC3-II/I, cleaved-PINK1, p-PARKIN, p62), inflammasome/cytokines (NLRP3, IL-1β, TNF-α), and fibrosis (hydroxyproline, Col1a1, Tgfb1/TGF-β1). Compared with SH, UA or C176 monotherapy improved injury, lipid, interferon, and fibrotic readouts, with UA preferentially lowering mtDNA/mtTFA and C176 more strongly suppressing p-STING-TBK1-IRF3 and IFN-β/CXCL10. The combination produced the largest, pathway-concordant effects across domains, frequently approaching CTRL. Formal combination analysis on fractional inhibition showed predominant synergistic activity (ΔBliss and ΔHSA > 0 for most endpoints). A precision-weighted correlation map linked insulin resistance, mitochondrial stress, cGAS-STING activation, and fibrosis, while mitophagy restoration markers correlated inversely. By pairing a mitophagy enhancer with a STING inhibitor, we provide first evidence in this model that coordinated upstream and downstream targeting of the mtDNA-cGAS-STING axis yields superior, multi-domain control of disease biology and is immediately translatable via IFN-β/CXCL10, cell-free mtDNA, and imaging readouts. - Source: PubMed
Publication date: 2026/06/24
Hamad Rabab SMohammed Sura AkramHasan Waseem AliAbuoHashish Norhan AhmedEl Afify Sherin RefatAli Mohamed A MMohamed Alaa Eldin AhmedEl-Kott Attalla FAlShehri Mohammed AMorsy KareemFarrag Alshaimaa ASalem Karem MohamedMorsy Nesreen ElsayedElmowafy RashaElmetwally Ahmed Abdel-MonemAhmed Walid Mostafa SayedJamil LubnaShata AhmedChaudhary Anis AhmadEissa HananSaber Sameh - Nasopharyngeal carcinoma (NPC) is characterized by aggressive progression, frequent metastasis, and heterogeneous therapeutic responses. Through integrated bulk transcriptomic datasets, single-cell analysis, clinical specimens, and NPC cell lines, we identified SLC44A4, a member of the choline transporter-like family, as a significantly downregulated gene in NPC. Transcriptomic analyses revealed that SLC44A4 expression was negatively associated with oxidative phosphorylation-related genes, DNA damage repair pathways, and malignant transcriptional programs related to proliferation, invasion, and metastasis. Moreover, SLC44A4-high tumors exhibited increased B-cell infiltration and enrichment of TLS-related transcriptional signatures. In vitro, SLC44A4 overexpression in NPC cells suppressed proliferation, colony formation, migration, and invasion, induced G0/G1 cell-cycle arrest, reduced expression of oxidative phosphorylation-related proteins, and selectively upregulated CXCL10. SLC44A4 overexpression also increased sensitivity to DNA-damaging agents, including temozolomide, doxorubicin, cisplatin, olaparib, and etoposide, while decreasing sensitivity to 5-fluorouracil. Together, these findings identify SLC44A4 as a potential tumor-suppressive factor in NPC and suggest that SLC44A4 may serve as a biomarker for metabolic state, B-cell/TLS-associated immune features, and vulnerability to DNA damage-based therapies. - Source: PubMed
Publication date: 2026/06/26
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