IL20RA (aa 159_175)
- Known as:
- IL20RA (aa 159_175)
- Catalog number:
- AP08451PU-N
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- IL20RA ( 159_175)
Related genes to: IL20RA (aa 159_175)
- Gene:
- IL20RA NIH gene
- Name:
- interleukin 20 receptor subunit alpha
- Previous symbol:
- -
- Synonyms:
- ZCYTOR7, IL-20R1
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2015-12-11
Related products to: IL20RA (aa 159_175)
0.2ml Thin Wall PCR Tubes0.2ml Thin Wall PCR Tubes Clear, Flat Cap0.2ml Thin Wall PCR Tubes Clear, Flat Cap1 x 175-225ml Bottle Adapters For 250ml Round Buckets14-3-3 tau Antibody14-3-3 tau Antibody.159
175
2,7_Diaza spiro[4.4] nonane _25bp DNA Ladder marker (5μl T) 25,50,75,100,125,150,175,200,225,250,275,300,325,350,375,400,450 ,2000bp25bp DNA Ladder marker (5μl/T) 25,50,75,100,125,150,175,200,225,250,275,300,325,350,375,400,450 ,2000bp4-bromo-1H-indazole, CAS Nr: 186407-74-95' TEXAS RED per 3' ECLIPSE, 10 - 20 nmol yield range Ex: 586 nm per Em: 610 nm5' TEXAS RED per 3' ECLIPSE, 20 - 30 nmol yield range Ex: 586 nm per Em: 610 nm5' TEXAS RED per 3' ECLIPSE, 30 - 50 nmol yield range Ex: 586 nm per Em: 610 nm Related articles to: IL20RA (aa 159_175)
- Type 2 diabetes (T2D) and its complications are linked to cognitive decline over time, accompanied by cortical abnormalities. The causality between T2D and cortical modifications, however, remains elusive. - Source: PubMed
Huang HongHuang HanyuGong YanlinZhou TengtengLiang YundanWang Yichao - Previous studies have found that circulating inflammatory proteins may play an essential role in the occurrence and development of neuropathic pain. However, the majority of existing evidence is derived from observational studies, which are prone to confounding factors and reverse causality, and the inflammatory profiles associated with different types of neuropathic pain remain poorly understood. Consequently, more robust methodologies are urgently required to elucidate the causal relationships between these variables. Therefore, a bidirectional Mendelian randomization analysis was performed to assess the causal relationship between inflammatory proteins and neuropathic pain, specifically focusing on neuralgia and neuritis, including glossopharyngeal neuralgia, phantom limb syndrome with pain,small fiber neuropathy, and unspecified neuralgia. - Source: PubMed
Publication date: 2026/02/17
Zhong JiajunLi HuanminHuang ChongboZhang PengfeiPang XiaoyuLuo ZimengLi Chunguang - The Republic of Korea is the global leading producer of olive flounder (Paralichthys olivaceus), accounting for approximately 49% of national aquaculture production. Acute low-temperature stress poses a major challenge to this industry, causing substantial economic losses through impaired growth, increased mortality, and compromised immune function. This study aimed to identify genetic markers associated with acute low-temperature stress tolerance using a genome-wide association study (GWAS) and determine optimal genomic prediction parameters. A total of 576 healthy olive flounders (average weight 419.57 ± 9.56 g) were subjected to acute low-temperature stress at 9 °C for 20 min. Serum cortisol levels were measured and caudal fin samples were collected from 384 individuals for genomic DNA isolation. Genotyping using a 70 K single-nucleotide polymorphism (SNP) chip yielded 57,638 high-quality SNPs from 375 individuals, which were analyzed using a linear mixed model. Eighteen putative SNPs exhibiting suggestive significance level (p < 1 × 10) were identified on chromosomes 8, 20, and 21; however, none surpassed the Bonferroni-corrected genome-wide significance threshold (p < 8.6 × 10). These suggestive associations, therefore, require validation in independent populations. Among them, SNPs AX-419197258 and AX-419200963 explained 3.44% and 3.25% of the phenotypic variance, respectively. Functional annotation indicated that putative candidate genes, including gbe1, serta, lpgat1, and il20ra, are involved in key biological and immune-related pathways. Genomic prediction analyses demonstrated that the random forest model achieved the highest accuracy for predicting serum cortisol levels. Moreover, GWAS-based marker selection outperformed random marker selection, with approximately 1000 markers identified as optimal for reliable prediction. Collectively, these findings provide insights into the genetic architecture of low-temperature stress tolerance in olive flounder and support the application of genomic approaches in selective breeding programs to enhance resilience and sustainability in aquaculture. - Source: PubMed
Publication date: 2026/02/05
Hanchapola H A C RKim GaeunOmeka W K MGong PoLiyanage D SUdayantha H M VKodagoda Yasara KavindiDilshan M A HRodrigo D C GGanepola G A N PiyumikaJo YuhwanLee JeongyongMassault CecileJerry Dean RLee JihunKim JeongeunLee Jehee - Deep skin wounds demand tightly coordinated communication across diverse tissue systems, yet knowledge of the molecular logic governing organ-scale injury response remains incomplete. Existing wound atlases profile fragments of this process, capturing limited tissue groups and healing phases, obscuring how whole organs synchronize repair. Here, we present the Organ-Scale Wound Healing Atlas (OWHA), a 4D multimodal omnibus that integrates snRNA-seq, scRNA-seq, CITE-seq and high-definition spatial transcriptomics to reconstruct the complete spatial and temporal choreography of mammalian wound healing at single cell resolution. OWHA profiles over 725,000 murine single-cell and spatial transcriptomes encompassing the entire wound healing process from early to late healing phases across the vast skin microanatomical tissue niches. This omnibus overcomes long-standing technical limitations, enabling robust resolution of adipocytes, Schwann cells, fragile epithelial intermediates, and over 100 precisely annotated cell states, including populations missed in prior wound databases. This revealed that wound repair proceeds through sharp transcriptional and cellular inflection points driven by Central Orchestrator populations that coordinate healing via synchronized transcriptional activation and direct cross-tissue signaling. Key among these is a keratinocyte subpopulation (Basal IV), detectable only through snRNA-seq but entirely missed by conventional wound atlasing. After injury, Basal IV cells deviate from canonical differentiation programs and adopt a neurovasculogenic signaling state during the proliferation phase, forming a transient spatially privileged regulatory hub at the wound edge. This epithelial-anchored niche spatially aligns Basal IV keratinocytes with proliferative endothelial cells, Pericytes, and Repair Schwann Cells, synchronizing re-epithelialization, angiogenesis, and neurite guidance. Mechanistically, this is orchestrated by a conserved Sema3C-Nrp1/Nrp2 axis that coordinates epithelial-vascular-neuronal crosstalk at the wound site. Cross-species integration confirms that the Basal IV/SEMA3C axis is conserved in human skin, yet undetected by conventional scRNA-seq human atlases due to dissociation-induced artifacts - underscoring the critical need for multimodal atlasing to accurately capture organ-scale physiology. Notably, the Basal IV/SEMA3C circuitry is selectively disrupted in human diabetic wounds, but topical Sema3C treatments restores peri-wound angiogenic sprouting and accelerates re-epithelialization of diabetic ulcers . OWHA establishes the first 4D, organ-scale molecular blueprint of mammalian wound healing, creating a foundational platform for decoding systems-level principles of repair and regeneration for tissue wounds. - Source: PubMed
Publication date: 2026/01/16
Cheong Jonathan ChinVan Deursen SimonAmador DreytonHiner ShannonWoappi Yvon - Both osteochondrosis and osteomalacia are metabolic disorders that are impacted by a combination of genetic and environmental factors. The objective of this research is to explore the potential causal connection between plasma metabolomics and the development of osteochondrosis and osteomalacia, with a focus on inflammatory factors. Summary statistics were collected for 91 inflammatory cytokine traits, 1400 plasma metabolite traits, and osteochondrosis and osteomalacia traits from publicly accessible genome-wide association studies. Causality was evaluated through two-sample Mendelian randomization analyses, which included methods such as inverse variance weighting, Mendelian randomization-Egger, weighted median, weighted mode, and simple mode analyses. Extensive sensitivity analyses were conducted to evaluate the reliability, diversity, and identification of horizontal pleiotropy in the results. The results of our study indicate that 4 cytokines play a significant causal role in osteochondrosis: C-X-C motif chemokine 5 (P = .029, OR = 0.864, 95% CI = 0.758-0.985), interleukin-20 receptor subunit alpha (P = .041, OR = 1.244, 95% CI = 1.009-1.534), interleukin-33 (P = .009, OR = 0.786, 95% CI = 0.657-0.941), and macrophage inflammatory protein 1a (P = .021, OR = 0.829, 95% CI = 0.707-0.971). Furthermore, we identified an association between inflammatory cytokines and osteomalacia, specifically with tumor necrosis factor receptor superfamily member 9 (P = .010, OR = 1.820, 95% CI = 1.157-2.863). Subsequent screening of metabolites related to osteochondral (X-12798 levels, P = 9.95E-05) and osteomalacia (adenosine 5'-monophosphate to glutamate ratio, P = 1.27E-04) was conducted based on these inflammatory factors. The research indicates that IL-33, CXCL5, IL-20RA, and MIP-1α could potentially play crucial roles as upstream factors influencing the development of osteochondrosis, while metabolites like X-12798 may serve as promising biomarkers in this context. Furthermore, TNFRSF9 is suggested as an upstream determinant of osteomalacia, with the AMP to glutamate ratio identified as a potential biomarker. These results underscore the importance of utilizing these cytokines and metabolites in clinical practice for distinguishing between osteochondrosis and osteomalacia, as well as for exploring potential therapeutic interventions. - Source: PubMed
Chen JiahaoLiu YiChen JialuWu HengWu LeiHuang YanfengZhang Chi