CXL11_MOUSE I-TAC ELISA tesk kit
- Known as:
- CXL11_MOUSE I-TAC Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen14750
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CXL11_MOUSE I-TAC ELISA tesk kit
Related genes to: CXL11_MOUSE I-TAC ELISA tesk kit
- Gene:
- SDCBP2 NIH gene
- Name:
- syndecan binding protein 2
- Previous symbol:
- -
- Synonyms:
- ST-2, SITAC18
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-17
- Date modifiied:
- 2015-12-16
Related products to: CXL11_MOUSE I-TAC ELISA tesk kit
Related articles to: CXL11_MOUSE I-TAC ELISA tesk kit
- Porokeratosis (PK) encompasses genetically heterogeneous keratinization disorders, with disseminated superficial actinic porokeratosis (DSAP) and porokeratosis ptychotropica (PPt) as distinct subtypes. Although MVK is a known causative gene, how different variants drive distinct phenotypes remains unclear. Through whole-exome sequencing of two DSAP patients, we identified an MVK variant (c.439G > A, p.Ala147Thr) cataloged as likely pathogenic in ClinVar yet uncharacterized functionally in DSAP keratinocytes. A previously reported PPt-associated variant (c.64G > A) was included for comparison. We established HaCaT cells stably overexpressing each mutant via lentiviral transduction and validated expression by qPCR and Western blot. Integrated transcriptomic and proteomic analyses identified differentially expressed genes (DEGs) and proteins (DEPs) across MVK439 versus control, MVK64 versus control, and MVK439 versus MVK64 groups, followed by GO and KEGG enrichment. Transcriptomic profiling revealed 231, 1,849, and 2,329 DEGs in the respective comparisons. Proteomic screening identified 2,673 DEPs, with 42 shared across all groups, 77 specifically associated with c.439G > A, and 832 linked to c.64G > A. Integrated analysis suggested IL12A and pIgR as potential contributors to c.439G > A-driven DSAP, while CXCL11, CXCL9, and TNFRSF12A may mediate c.64G > A-induced PPt. These findings offer new insights into MVK function and PK pathogenesis, warranting validation in larger cohorts. - Source: PubMed
Publication date: 2026/06/03
Lai ShuqinZhu WenjieLin ChunliGuo ZimengChen ShiqiXie LangLiu JieZeng ZhaolinYou CongLi Longnian - Vitiligo is a skin disease characterized by the loss of skin melanocytes, featuring the dual pathology of melanocyte damage due to oxidative stress and immune-mediated inflammation, which ultimately classifies it as an autoimmune condition. Sappanone A (SA), isolated from Caesalpinia sappan L., exhibits notable anti-oxidative stress and anti-inflammatory activity in various diseases. However, its potential effects and mechanisms in vitiligo remain uninvestigated. This study was designed to investigate the effects of SA on melanocytes and keratinocytes under oxidative stress and to evaluate its therapeutic potential in the monobenzone-induced vitiligo model. In vitro, SA protected PIG1 cells from HO-induced cytotoxicity and suppressed HMGB1 expression, nuclear export, and extracellular release. Furthermore, SA reduced HMGB1-induced overexpression of inflammatory cytokines in HaCaT cells, including CXCL8, CXCL9, CXCL10, CXCL11, and TNF-α. In vivo, SA administration alleviated monobenzone-induced depigmentation and CD8 T-cell infiltration in C57BL/6 mice. Transcriptomic analysis, protein-protein interaction network construction, and molecular docking revealed that Wnt5a may be a potential target of SA, and SA significantly reversed monobenzone-induced Wnt5a expression and activation of noncanonical Wnt signaling. Overall, SA effectively attenuated the HMGB1-mediated inflammatory response in keratinocytes. Furthermore, it exerted repigmentation effects in monobenzone-induced vitiligo mice via inhibiting the Wnt5a-mediated noncanonical Wnt signaling pathway. These results suggest that SA is a promising therapeutic candidate for vitiligo. - Source: PubMed
Publication date: 2026/06/02
Xu MingmingDing MeilinLi RuiZhang HejuanRen FeifeiLi HongyangZhang Wei - Parkinson's disease (PD) is a progressive neurodegenerative disorder lacking established clinical biomarkers. We performed an exploratory multi‑omics analysis of transcriptome and proteome data from small PD and control cohorts at Huaihe Hospital of Henan University. Using two local datasets, we identified 124 differentially expressed genes (DEGs) and 28 proteins, then performed protein‑protein interaction (PPI) and gene set variation analysis (GSVA). After intersecting with 2,964 DEGs from Gene Expression Omnibus (GEO) Dataset 3, we obtained a 28‑gene panel. Potential markers were prioritized via random forest (RF), support vector machine (SVM) and principal component analysis (PCA), and evaluated in external GEO data, clinical serum samples and a 1‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine (MPTP)‑induced PD mouse model. PPI highlighted C‑X‑C motif chemokine ligand 1 (CXCL1), C‑X‑C chemokine receptor type 4 (CXCR4), S100 calcium‑binding protein A12 (S100A12) and C‑X‑C motif chemokine ligand 11 (CXCL11) as hub genes. GSVA indicated upregulated cardiac muscle contraction and oxidative phosphorylation (OXPHOS). C‑C motif chemokine ligand 4 (CCL4), CKLF like MARVEL transmembrane domain containing 2 (CMTM2), tudor domain containing 6 (TDRD6), potassium voltage‑gated channel subfamily S member 1 (KCNS1) and member RAS oncogene family (RAB15) were identified as candidate markers. They showed consistent expression changes in clinical samples and mice. Immune infiltration differed in B cells, CD8 + T cells and natural killer (NK) cells. LY‑303511 and HC‑toxin were predicted as candidate compounds. These five genes represent preliminary candidate biomarkers for PD; however, further validation in larger independent cohorts is warranted for clinical translation. - Source: PubMed
Publication date: 2026/06/01
Liu TingtingCao SongqiangLiang HuiminWei Jianshe - African swine fever (ASF) remains a persistent threat to global pig production, with no licensed vaccines or effective treatments available. Observations of surviving individuals within low-virulence infected herds suggest that host genetic resistance plays a crucial role. Here, we present a multi-dimensional integrative analysis to uncover host genomic variants associated with ASF resistance. Combining genome-wide association studies (GWAS), genetic differentiation, and functional genomic approaches, including TWAS, SMR, colocalization, and Bayesian network GWAS, we prioritized 135 high-priority candidate resistance genes from an initial gene set of 1,102 candidates. These prioritized genes are enriched in immune-related pathways, such as chemokine signaling and IL-15-mediated activation. Heritability enrichment and transcriptomic analyses further revealed tissue- and cell-type-specific expression patterns, particularly in peripheral immune organs and pulmonary alveolar macrophages. Dynamic infection-responsive genes, including CXCL10, CXCL11 and IL15, exhibited robust antiviral signatures, which highlighted Mac_CD163 as key cellular mediators in the immune response to ASF. Moreover, multiple genes (such as SOS1, FCGR2B, FCGR3) converged on the PI3K-AKT and Fcγ receptor signaling axes pathways, underscoring their functional importance. Finally, we developed a polygenic resistance score using 40 prioritized independent SNPs, which effectively discriminates phenotypic outcomes and showed a positive correlation with health traits such as platelet distribution width. These findings provided a genomic foundation for the precision breeding of ASF-resistant pigs and inform host-targeted disease control strategies. - Source: PubMed
Publication date: 2026/05/30
Ye XiaoweiXie QinqinCao CaiyunLiu ShuangSun WenboZhang ZheWang QishanPan YuchunWang Zhen - Epstein-Barr virus (EBV)-associated infectious mononucleosis (IM) elicits a robust cellular immune response; however, systemic chemokine profiles in pediatric IM and their diagnostic relevance remain insufficiently characterized. This study evaluated proinflammatory chemokine expression in children with acute EBV-associated IM and its relationship with disease presence and severity. - Source: PubMed
Publication date: 2026/05/01
Nikčević AndreaRadmanić Matotek LeonaŠiftar SilvaStemberger Marić LornaTešović GoranZidovec-Lepej Snjezana