Anti_Human, mab CXCL9 Source Mouse
- Known as:
- Anti_Human, mab CXCL9 Source Mouse
- Catalog number:
- 101-M359
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CXCL9 Source Mouse
Related genes to: Anti_Human, mab CXCL9 Source Mouse
- Gene:
- CXCL9 NIH gene
- Name:
- C-X-C motif chemokine ligand 9
- Previous symbol:
- CMK, MIG
- Synonyms:
- SCYB9, Humig, crg-10
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-05-28
- Date modifiied:
- 2016-10-05
Related products to: Anti_Human, mab CXCL9 Source Mouse
Related articles to: Anti_Human, mab CXCL9 Source Mouse
- Tuberculosis (TB) remains a major global health threat, underscoring the need for vaccines that surpass BCG efficacy. We developed QTAP-R, a novel mRNA-lipid nanoparticle (LNP) vaccine encoding Ag85B, Hsp70, and ESAT-6, to enhance immunity against Mycobacterium tuberculosis. QTAP efficiently encapsulated and delivered mRNA with high transfection efficiency and low cytotoxicity. In C57BL/6 mice, QTAP-R induced strong antigen-specific IgG and T-cell responses, including elevated CD4⁺ and CD8⁺ activation and increased polyfunctional cytokines (IFN-γ, TNF-α, IL-2, IL-17A). When combined with BCG (BCG + QTAP-R), the vaccine elicited enhanced immune memory, reduced bacterial burden in lungs and spleen, and minimized lung pathology following M. tuberculosis challenge. Subcutaneous QTAP-R (QTAP-SQ) provided partial protection under high-dose challenge, outperforming intranasal delivery. Transcriptomic profiling revealed upregulation of inflammatory cytokines (IL-1, IL-6, IL-12) and chemokines (CCL3, CCL4, CXCL9, CXCL10), indicating enhanced immune recruitment and activation. CD4⁺ T-cell depletion abolished protection, confirming their critical role in QTAP-R-mediated immunity. Overall, QTAP-R demonstrates potent immunogenicity and synergistic efficacy with BCG, positioning it as a promising mRNA-based TB vaccine candidate. - Source: PubMed
Publication date: 2026/05/02
Touray Bubacarr J BFaburay Alieu KMohamed Fakry FAbdelgayed Sherein STalaat Adel M - CXCL9 and CXCL11 are chemokine ligands that bind to the CXCR3 receptor. Their interaction mediates the recruitment, activation, and differentiation of immune cells, including T helper 1 (Th1) cells, CD8+ cytotoxic T lymphocytes (CTLs), and natural killer (NK) cells. Quantification of CXCL9, CXCL11, and CXCR3 offers a potential non-invasive approach for detecting allograft rejection. This study aims to elucidate the correlation between urinary and blood concentrations of CXCL9, CXCL11, and CXCR3 at both mRNA and protein levels in renal graft recipients. - Source: PubMed
Publication date: 2026/04/29
Akhgar NargesAfshari AfsoonYaghobi RaminNaeini Fatemeh HeidaryanJanfeshan Sahar - Protein epigenetic scores (EpiScores) are DNA methylation (DNAm)-based proxies for circulating protein levels and may provide insights into inflammation-cognition relationships. Although some EpiScores have been linked to cognitive decline, it remains unclear whether these proxies show similar associations in other cohorts, and whether their effects vary across distinct cognitive domains. We aimed to evaluate the associations between inflammatory proteins EpiScores and cognitive functions including specific domains in the Swedish Adoption/Twin Study of Aging (SATSA) cohort. We analyzed 1332 repeated measurements from 520 SATSA participants across up to six testing waves (1992-2014). Inflammatory protein EpiScores (N = 27) were generated using previously published CpG site-specific weights. Outcomes were a global cognitive function (GCF) score and four specific cognitive domains (verbal ability, spatial ability, memory, and perceptual speed). We applied marginal linear models within the generalized estimating equations (GEE) framework to estimate population-averaged longitudinal associations, controlling the false discovery rate (FDR) using the Benjamini-Hochberg (BH) procedure (q < 0.05 considered significant). Two EpiScores-C-X-C motif chemokine ligand 9 (CXCL9) and vascular cell adhesion molecule 1 (VCAM1)-showed significant positive associations with GCF. In domain-specific outcomes, VCAM1 demonstrated a positive association with spatial ability, whereas C-X-C motif chemokine ligand 11 (CXCL11) had a negative association with verbal ability. These associations were broadly consistent across multiple sensitivity analyses. Inflammation-related DNAm signatures of certain proteins were associated with cognitive performance in SATSA samples. Moreover, the associations differ by cognitive domain. Future longitudinal studies are warranted to clarify the causal implications of these EpiScore-cognition associations and to explore population differences in DNAm patterns. - Source: PubMed
Publication date: 2026/04/30
Ishihara KazuyukiHägg SaraLopes De Oliveira Thaís - Triple-negative breast cancer (TNBC) still poses an important clinical challenge due to its aggressiveness, notwithstanding the increasing amount of treatment options. While radiation therapy (RT) is important for TNBC management, dose-limiting side effects limit its efficacy. FLASH-RT, delivered with ultra-high dose rates, has shown anti-tumour effects comparable to conventional dose rate RT (CONV-RT) but with reduced normal tissue side effects, offering the potential of dose escalation to treat aggressive tumour subtypes such as TNBC. - Source: PubMed
Publication date: 2026/04/28
Arrigo AdrienBrants LouizeKramp LauraVanreusel VerdiStevens PietColijn ArnaudHermans ChristopheMeijnders PaulVerellen DirkPoortmans PhilipAudenaerde Jonas VanWouters AnGasparini AlessiaMontay-Gruel Pierre - Acquired resistance to Epidermal Growth Factor Receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as gefitinib, remains a major therapeutic challenge in EGFR-mutant non-small cell lung cancer (NSCLC). Here, we report that cepharanthine (CEP), a natural bisbenzylisoquinoline alkaloid, effectively reverses gefitinib resistance through concurrent suppression of the AKT/P70S6K survival axis and activation of the Stimulator of Interferon Genes (STING)-mediated innate immune pathway. In gefitinib-resistant H1975 cells (EGFR L858R/T790M), CEP monotherapy significantly inhibited proliferation and induced mitochondrial apoptosis. Notably, CEP synergized with gefitinib to enhance therapeutic efficacy. RNA sequencing and functional validation revealed that CEP activates the STING/TANK-Binding Kinase 1 (TBK1)/Interferon Regulatory Factor 3 (IRF3) signaling cascade, resulting in robust production of T-cell chemoattractants C-X-C Motif Chemokine Ligand 9 (CXCL9), C-X-C Motif Chemokine Ligand 10 (CXCL10), and C-C Motif Chemokine Ligand 5 (CCL5). Critically, the STING inhibitor H-151 abolished CEP's antitumor effects in vitro. Our findings reveal a novel dual mechanism action of CEP and nominate it as a potential candidate for overcoming TKI resistance in NSCLC. - Source: PubMed
Kang Li-PingChen Hui-HuiLv Tong-TongHuang Hua-JingHuang Dong-HuiChen Ying-QingJiang Ze-Bo