CXCL9 (MIG) Whole Serum Human
- Known as:
- CXCL9 (MIG) Serum Human
- Catalog number:
- RS-80CX9
- Product Quantity:
- 1.0 mL
- Category:
- -
- Supplier:
- ICL I.C.L
- Gene target:
- CXCL9 (MIG) Whole Serum Human
Related genes to: CXCL9 (MIG) Whole Serum Human
- Gene:
- AMIGO1 NIH gene
- Name:
- adhesion molecule with Ig like domain 1
- Previous symbol:
- -
- Synonyms:
- AMIGO, KIAA1163
- Chromosome:
- 1p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-23
- Date modifiied:
- 2016-07-04
- Gene:
- C17orf80 NIH gene
- Name:
- chromosome 17 open reading frame 80
- Previous symbol:
- -
- Synonyms:
- HLC-8, MIG3, FLJ20721, SPEP1
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-13
- Date modifiied:
- 2016-09-30
- 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
- Gene:
- DHPS NIH gene
- Name:
- deoxyhypusine synthase
- Previous symbol:
- -
- Synonyms:
- MIG13
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1995-12-12
- Date modifiied:
- 2016-10-05
- Gene:
- ERRFI1 NIH gene
- Name:
- ERBB receptor feedback inhibitor 1
- Previous symbol:
- -
- Synonyms:
- MIG-6, GENE-33, RALT
- Chromosome:
- 1p36.23
- Locus Type:
- gene with protein product
- Date approved:
- 2005-08-23
- Date modifiied:
- 2014-11-19
Related products to: CXCL9 (MIG) Whole Serum Human
Related articles to: CXCL9 (MIG) Whole Serum Human
- Traumatic brain injury (TBI) is a major cause of neurological dysfunction and long-term neurodegeneration, yet the intrinsic neuronal contributions to TBI pathophysiology remain incompletely defined. Here, we present a novel microfluidic platform that can be used to mechanically injure mature human prefrontal cortex neurons (hPFCs) embedded in three-dimensional (3D) hydrogels, enabling the study of injury responses in pure neuronal cultures. We assessed real-time calcium dynamics across 13 metrics of single-cell and network activity, revealing a biphasic injury response: an early phase (0.5-24 hr) characterized by excitotoxicity, hyper-synchronized bursting, and network collapse; and a late phase (8 d) marked by sustained depolarization and structural remodeling. Secretome profiling uncovered progressive elevations in extracellular pT181 and total Tau from days 1 to 5 post-injury. Cytokine analyses identified early (24 hr) elevations in IP-10, IL-10, IFNα2, and NCAM, and late increases (8 d) in CXCL9 and MPO, linking neuronal activity changes to stage-specific inflammatory signaling. Immunocytochemistry and immunoblotting confirmed temporally ordered upregulation of calpain-1 and active caspase-3 (days 1-3), phosphorylated Tau (AT8+, days 5-8), and neurofibrillary tangle-like Tau aggregates (NFT+, day 8). These findings establish our platform as a scalable microphysiological model for probing the dynamic cellular and molecular sequelae of neuronal response to injury, offering insights into neurodegeneration and opportunities for therapeutic discovery. - Source: PubMed
Publication date: 2026/07/05
Tang RuipingLatchoumane Charles-FrancoisChopra AviSarkar Md MarzanKim ChunkiGonsalves NathanWu Hsueh-FuSentmanat John CLiu AlanMhatre-Winters IshaMishra AdityaFedorov Andrei GPatel Jay MZeltner NadjaStice Steven LRichardson Jason RKarumbaiah Lohitash - Longer asthma duration predicts non-remission in Type-2 (T2) biologic-treated severe asthma, but underlying mechanisms remain unclear. We investigated associations between asthma duration and inflammatory biomarkers that may explain differential biologic response. - Source: PubMed
Publication date: 2026/07/09
Yang FredaSeo SujinHasegawa TakehiroBloom Chloe IZounemat-Kermani NazaninBhavsar Pankaj KRaby KatieAdcock Ian MWon SunghoKim Tae-BumChung Kian Fan - Diabetes and obesity are associated with poorer outcomes after ischemic stroke; however, it remains unclear whether this results from increased neuronal susceptibility to injury or from vascular dysfunction induced by metabolic syndrome. To minimize the contribution of vascular factors, we used a model of photoinduced thrombosis (PT) in cortical vessels, which generates lesions of reproducible size and is less dependent on collateral blood flow. PT was induced in wild-type (WT) mice, as well as in / (leptin-deficient) and / (leptin receptor-deficient) mice. Magnetic resonance imaging (MRI) revealed that PT produced comparable infarct volumes in all mouse groups. Several genes associated with inflammation and activation of microglia and macroglia in the peri-infarct area , , , ) exhibited similar expression patterns across all three mouse strains, while transcriptional response to cerebral ischemia of , , , , , and genes depended on the genotype. Overall, despite individual differences in the expression profiles of certain genes, disruption of leptin signaling (whether due to leptin deficiency or leptin receptor deficiency) caused no genotype-specific exacerbation of stroke-induced injury. Assessment of post-stroke neurological deficits revealed substantial differences in absolute scores between WT and / or / mice, attributable to baseline disparities in body weight and motor activity. In / mice, normalization of post-stroke neurological status scores to pre-injury values revealed a more pronounced relative functional decline compared to / mice, suggesting impairments in early compensatory mechanisms and an important role of leptin signaling in neuroplasticity rather than in the extent of acute neuronal damage. Thus, under conditions that minimize vascular complications, neither leptin deficiency nor leptin receptor deficiency exacerbated acute ischemic brain damage or neuroinflammation. - Source: PubMed
Bocharnikov Alexey DAbramicheva Polina AYakupova Elmira IAverina Olga AGrigoryeva Olga OPriymak Anastasia VGarmash Svetlana APermyakov Oleg APevzner Irina BBrezgunova Anna AAndrianova Nadezda VSergiev Petr VPlotnikov Egor Y - - Source: PubMed
Publication date: 2026/07/08
Assis de Souza AlvaroPeeters AnnemiekBost DouglasBaan CarlaBoer KarinHesselink Dennis A - Acral vitiligo responds less well to NB-UVB than non-acral disease, but site-specific immunologic changes during therapy are incompletely defined. The objective of this study was to compare NB-UVB-associated changes in T cell subsets and soluble mediators in acral versus non-acral vitiligo. Thirty patients with non-segmental vitiligo were enrolled. Ten underwent paired biopsies (acral and non-acral) before and after 6 months of NB-UVB for flow cytometry (Tregs, CD8+ T cells, CD8+CD45RO+ memory T cells, CD8+CD69+CD103+ TRM). Suction-blister fluid ELISA assessed IFN-γ-axis mediators (CXCR3, CXCL9, CXCL10, IFN-γ, IL-1β) in two separate groups: 10 treatment-naïve patients and 10 patients who had completed 6 months of NB-UVB therapy. Non-parametric tests used Benjamini-Hochberg FDR correction (pFDR). In paired biopsies (n = 10; CD8 n = 9), memory T cells decreased after NB-UVB in acral (4.38 [3.47-5.98] to 1.38 [0.73-2.21]; pFDR = 0.041) and non-acral lesions (5.23 [4.27-6.75] to 1.08 [0.48-2.54]; pFDR = 0.0039). TRM declined in acral (5.95 [3.17-7.41] to 0.65 [0.15-1.15]; pFDR = 0.0039) and non-acral sites (4.12 [2.50-5.57] to 0.69 [0.28-1.19]; pFDR = 0.0039). Tregs showed a site-divergent pattern: acral Tregs decreased (0.56 [0.41-0.75] to 0.08 [0.03-0.23]; pFDR = 0.0067) while non-acral Tregs increased (0.40 [0.24-0.61] to 0.95 [0.41-1.59]; pFDR = 0.0039). CD8+ T cells showed no change after correction. CXCL9 showed a non-significant decreasing trend (pFDR = 0.249); no ELISA marker remained significant after FDR correction. NB-UVB exerts a pronounced effect on cellular immunity (reductions in TRM and memory T cells) with limited cytokine suppression, with site-divergent Treg pattern. - Source: PubMed
Vinay KeshavamurthyMehta HitaishiThind AnishKaushik HitaishiKumaran Muthu SendhilParsad DavinderKumar Vinod