IL1F10, 1-152aa, Human, E.coli
- Known as:
- IL1F10, 1-152aa, Human, E.coli
- Catalog number:
- ATGP3044
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- IL1F10 1-152aa Human .coli
Related genes to: IL1F10, 1-152aa, Human, E.coli
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
- Gene:
- IL1F10 NIH gene
- Name:
- interleukin 1 family member 10
- Previous symbol:
- -
- Synonyms:
- FKSG75, IL-1HY2, IL-1F10, IL1-theta, MGC11983, MGC119832, MGC119833
- Chromosome:
- 2q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-02
- Date modifiied:
- 2017-08-07
Related products to: IL1F10, 1-152aa, Human, E.coli
Related articles to: IL1F10, 1-152aa, Human, E.coli
- Acute lymphoblastic leukemia (ALL) is a hematological malignancy of two main types, B-ALL and T-ALL, with B-ALL being the most common. Growing evidence suggests that B-ALL pathophysiology is linked to immune system dysfunction in which cytokines play a pivotal role. Interleukin (IL)-37, IL-38, and IL-40, encoded by IL37, IL1F10, and C17orf99 genes, respectively, are novel cytokines involved in regulating immune functions and are proposed to influence cancer pathogenesis. However, these cytokines have not been studied in B-ALL, either genetically or phenotypically. Therefore, this research aimed to evaluate gene expression of IL37, IL1F10, and C17orf99 to explore their association with B-ALL. - Source: PubMed
Publication date: 2026/06/10
Kadhim Noor TAbed Reema M - Gastric cancer (GC) is a highly heterogeneous malignancy with poor prognosis. Current prognostic models for GC rely on invasive tissue-based high-throughput sequencing. Secreted proteins, detectable non-invasively and involved in tumor microenvironment (TME) remodeling, offer promising biomarkers. We aimed to develop a non-invasive prognostic signature based on secreted protein-coding genes (SPCGs) to stratify GC patients and predict TME characteristics. - Source: PubMed
Publication date: 2026/01/13
Liu QiuxiaYin HaofengWang ZimingShen QianlongZhao JianguoXie Xianhe - Trained immunity is a long-lasting innate immune cell phenotype with benefits in infection control and recognized anti-cancer effects. Conversely, inappropriately induced trained immunity contributes to pathological inflammation, warranting the exploration of regulatory pathways. We explore interleukin-38 (IL-38) as a regulator of trained immunity in a cohort of 325 healthy adults vaccinated with Bacillus Calmette-Guérin (BCG). Using multi-omics profiling, we find that IL-38 is negatively associated with trained immunity on metabolic and epigenetic level. Genetic variants in , encoding for IL-38, further link IL-38 to diminished training responses. These associations were validated in human and murine models. We confirmed that IL-38 functionally impairs anti-microbial traits of trained immunity in trained immunity-infection models (IL-38KO mice) and (human monocytes). Our study therefore suggests that IL-38 endogenously regulates the induction of trained immunity in humans . - Source: PubMed
Publication date: 2025/10/14
Teufel Lisa UMatzaraki VasilikiFolkman Lukasde Graaf Dennis MHorst Rob TerMoorlag Simone J C F MDos Santos Jéssica CMulders-Manders Catharina MKrausgruber ThomasDinarello CharlesNetea Mihai GJoosten Leo A BArts Rob J W - Interleukin (IL)-37 and IL-38 are anti-inflammatory cytokines encoded by IL37 and IL1F10 genes, respectively. Recently, it has been proposed that missense single nucleotide polymorphisms (SNPs) of IL37 (rs3811046 G/T and rs3811047 A/G) and 5'-untranslated region SNPs of IL1F10 (rs3811050 C/T and rs3811051 T/G) may influence susceptibility to some inflammatory disorders. Inflammation has also been shown to play a key role in pathogenesis of acute myeloid leukemia (AML). Therefore, it is reasonable to hypothesize that rs3811046, rs3811047, rs3811050, and rs3811051 may have a role in susceptibility to AML. A case-control study was conducted on 131 AML patients and 169 controls to investigate the association of these SNPs with AML risk. SNP genotypes were determined using TaqMan allelic discrimination, a real-time PCR-based method. Results revealed that mutant alleles (T, G, and T) and corresponding homozygous genotypes (TT, GG, and TT) of rs3811046, rs3811047, and rs3811050, respectively, were significantly associated with an increased risk of AML, while rs3811051 showed no association. Four-locus haplotype analysis (rs3811046-rs3811047-rs3811050-rs3811051) demonstrated that T-A-C-G haplotype was associated a 2.47-fold increased risk of AML. SNP-SNP interaction analysis showed significant genetic interactions between rs3811046 and rs3811047, rs3811046 and rs3811050, and rs3811047 and rs3811050. Rs3811046 and rs3811047 did not affect IL37 gene expression. Some laboratory and clinical variables of AML may be influenced by IL37 and IL1F10 SNPs. In conclusion, rs3811046, rs3811047, and rs3811050 were associated with AML susceptibility in terms of allele, genotype, and haplotype, while rs3811051 showed no association. Three SNPs (rs3811046, rs3811047, and rs3811050) showed a significant gene-gene interaction. - Source: PubMed
Publication date: 2025/05/25
Bashi Mustafa AAd'hiah Ali H - Gout is caused by the response of the innate immune system to monosodium urate (MSU) crystals. A recent gout GWAS identified a signal of genetic association at a locus encompassing IL1RN-IL1F10. Colocalisation analysis using Genotype Tissue Expression Database (GTEx) eQTL data showed that the signal overlaps with genetic control of IL1RN/IL1F10 gene expression. We assess the functional implications of IL1RN rs9973741, the lead gout-associated variant. - Source: PubMed
Publication date: 2024/11/20
Gaal Orsolya ILeask MeganNica ValentinCabău GeorgianaBadii MedeeaHotea Ioanade Graaf Dennis MZhang ZhenhuaLi YangPamfil CristinaRednic SimonaMerriman Tony RCrișan Tania OJoosten Leo A B