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Recombinant Mouse Interleukin-1 Alpha (IL-1α)
(Cat. No.: C041)
IL-1α is distinct from the other agonist member of the IL-1 family, IL-1β. Although IL-1α triggers the same IL-1 receptor and although many of the biological effects of IL-1α are similar to those of IL-1α, in humans IL-1α is predominantly an intracellular molecule. In fact, there is evidence that IL-1α has both intracellular functions as a precursor molecule due to a nuclear localization sequence. IL-1α as an unprocessed precursor is biologically as active as the processed form. IL-1α is also found constitutively in epithelial cells, whereas constitutive expression of IL-1β is rare. In many ways, IL-1α appears to be closer to the fibroblast growth factor family than the secreted IL-1β form. Therapeutic stratiegies for blocking IL-1β predominate over those for blocking IL-1α. Many humans
have circulating neutralizing antibodies to IL-1α but not IL-1β.
Recombinant Mouse IL-1 alpha produced in E. coli is a non-glycosylated polypeptide chain containing 156 amino acids and having a molecular mass of 18000 Dalton.
Biological activity: The ED50 as determined by the dose-dependant stimulation of mouse D10S cells was found to be less than 0.01 ng/ml, corresponding to a Specific Activity of 1.0 x 108 IU/mg.
Purity:Greater than 98% as determined by
(a) Analysis by RP-HPLC.
(b) Anion-exchange FPLC.
(c) Analysis by reducing and non-reducing SDS-PAGE Silver Stained gel..
Amino-Acid Sequence: The sequence of the first five N-terminal amino acids was determined and was found to be Ser-Ala-Pro-Tyr-Thr.
Endotoxin: Less than 0.1ng/µg (1 IEU/µg) of IL-1α.
Mouse IL-1α was lyophilized after extensive dialysis against PBS.
Lyophilized rmIL-1α although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. Upon reconstitution rmIL-1α should be stored at 4°C between 2-7 days and for future use below -18°C. For long-term storage it is recommended to add a carrier protein (0.1% HSA or BSA).
Please avoid freeze-thaw cycles.
It is recommended to reconstitute the lyophilized rmIL-1α in sterile 18MΩ-cm H2O not less than 100µg/ml, which can then be further diluted to other aqueous solutions.
1: Mol Hum Reprod 2009 Jan;
Proinflammatory cytokine polymorphisms and the risk of preterm birth and low birth weight in a Japanese population.
[Abstract] Pregnancy and parturition involve a complex and poorly understood molecular and biological interplay between mother and fetus. Inflammatory cytokines have been reported to be associated with fetal growth and parturition. The aim of this study was to examine whether common proinflammatory cytokine polymorphisms are associated with preterm birth (PTB), low birth weight (LBW) or intrauterine growth restriction (IUGR) in a Japanese population. We assessed a consecutive series of 414 women who had singleton deliveries in Sapporo, Japan between 2001 and 2005. Genotyping of IL1A -889C/T, +4845G/T (A114S), IL1B -511C/T, -31C/T, IL2 -384T/G and IL6 -634C/G polymorphisms was determined by an allelic discrimination assay. The risk of PTB significantly increased in women
carrying the IL1A -889T allele (CC genotype [reference]; CT genotype, OR: 2.5; 95% CI: 1.4-4.8; CT+TT genotypes [dominant genotype model], OR: 2.5, 95% CI: 1.3-4.6). Similarly, the risk of PTB significantly increased in women carrying the IL1A +4845T allele (GG genotype [reference]; GT genotype, OR: 2.4, 95% CI: 1.3-4.4; GT+TT genotypes [dominant genotype model], OR: 2.3, 95% CI: 1.2-4.2). The frequency of the IL1A TT haplotype in mothers with PTB was significantly higher than in mothers who had a term birth (TB) (p<0.001), whereas the frequency of the IL1A CG haplotype in mothers who had a PTB was significantly lower (p<0.001). Our findings suggest that the polymorphisms and haplotypes in the IL1A gene are associated with preterm birth in Japanese women.
2: Cancer Res 2008
Genetic variants in apoptosis and immunoregulation-related genes are associated with risk of chronic lymphocytic leukemia.
[Abstract] To identify low-penetrance susceptibility alleles for chronic lymphocytic leukemia (CLL), we performed a case-control study genotyping 768 single-nucleotide polymorphisms (SNP) in 692 cases of CLL and 738 controls. We investigated nonsynonymous SNPs, SNPs with potential functional effect, and tag SNPs in regulatory gene regions in a total of 172 genes involved in cancer biology. After adjustment for multiple testing, we found a strong association between CLL risk and six genetic variants: CCNH (rs2266690, V270A), APAF1 (rs17028658, 3'region), IL16 (rs4505265, first intron), CASP8 (rs1045485, D302H), NOS2A (rs2779251, promoter), and CCR7 (rs3136687, intron 1). We found association with CLL susceptibility and 22 haplotypes in APAF1, IL6, TNFRSF13B, IL16, CASP3,
CCR7, LTA/TNF, BAX, BCL2, CXCL12, CASP10/CASP8, CASP1, CCL2, BAK1, and IL1A candidate genes. Finally, we evaluated using public data sets the potential functional effect on gene expression levels of the CLL associated genetic variants detected in regulatory regions. Minor alleles for APAF1 and IL16 were associated with lower mRNA levels; no expression differences were observed for CCR7, whereas NOS2A could not be assessed. This study suggests that common genetic variation in apoptosis- and immunoregulation-related genes is associated with the CLL risk.
3: Mol Vis 2008 ;Vol 14
Association of -31T>C and -511 C>T polymorphisms in the interleukin 1 beta (IL1B) promoter in Korean keratoconus patients.
[Abstract] PURPOSE: To investigate the genetic association between unrelated Korean keratoconus patients and interleukin 1 alpha (IL1A), interleukin 1 beta (IL1B), and IL1 receptor antagonist (IL1RN) gene polymorphisms. METHODS: We investigated the association between IL1A (rs1800587, rs2071376, and rs17561), IL1B (rs1143627, rs16944, rs1143634, and rs1143633), and IL1RN (rs419598, rs423904, rs424078, and rs315952, variable number tandem repeat [VNTR]) polymorphisms in 100 unrelated Korean keratoconus patients. One hundred control individuals without any corneal disease were selected from the general population. Polymerase chain reaction (PCR) - restriction fragment length polymorphism (RFLP) analysis and direct sequencing were used to screen for genetic variations in
the IL1 gene cluster. Haplotypes for the IL1 gene cluster were constructed using Haploview version 4.0. RESULTS: We analyzed a total of 12 polymorphic sites in the IL1 gene cluster. Among them, the -511 (rs16944) and -31 (rs1143627) positions in the promoter region of IL1B were significantly different between patient and control groups. The C allele of rs16944 (-511C>T, p=0.022, odds ratio of risk [OR]=1.46, 95% confidence intervals [CI] 0.94<2.27) and the T allele of rs1143627 (-31T>C, p=0.025, OR=1.43, 95% CI 0.92<2.22) were associated with a significantly increased risk of keratoconus in Korean patients. Linkage of the two alleles, -31*C and -511*T, was associated with an increased risk for keratoconus with OR=2.38 (p=0.012, 95% CI=1.116-5.046). The *C/*A genotype of rs2071376 in IL1A
intron 6 was significantly different between the keratoconus patients and control subjects (p=0.034, OR=0.59, 95% CI 0.32<1.11). Other polymorphisms did not show an association with keratoconus risk. CONCLUSIONS: This is the first report of IL1 gene cluster mutation screening in Korean keratoconus patients. Significant differences in allelic frequency of IL1B between keratoconus patients and the control group suggest that IL1B polymorphisms may play a role in the susceptibility of unrelated Koreans to develop keratoconus.
4: Osteoarthritis Cartilage 2008
Attempt to replicate published genetic associations in a large, well-defined osteoarthritis case-control population (the GOAL study).
[Abstract] OBJECTIVE: Published studies have tested over 90 genes for association with osteoarthritis (OA), but few positives reported have been independently replicated. Using a new case-control study, our aim was to attempt the replication of findings from 12 genes reported to have significant genetic association with OA and to further examine the role of genetic variation in six of these genes. METHODS: A case-control study was undertaken in Nottingham, UK. Hospital-referred index cases with symptomatic, radiographic OA (ROA) of the knee (n=1040) or hip (n=1004) were recruited. Asymptomatic controls (n=1123) were recruited from intravenous urography waiting lists and screened for radiographic hip and knee OA. Sixty-eight polymorphisms were genotyped in IL1A, IL1B,
IL1RN, IL4R, IL6, COL2A1, ADAM12, ASPN, IGF1, TGFB1, ESR1 and VDR. Statistical analysis compared allele or genotype frequencies of these polymorphisms in all asymptomatic controls and the subset of controls without ROA vs all OA, knee OA and hip OA. The analyses were adjusted for age, gender and body mass index. RESULTS: We were unable to replicate any of the published genetic associations investigated. Our extended exploratory analyses identified some associations between polymorphisms in TGFB1, IGF1 and IL1RN and OA; but the strength of evidence varied with the control group used. CONCLUSION: Lack of replication is common and could be due to differences in study design, phenotype, populations examined or the occurrence of false positives in the initial study. Variants within TGFB1, IGF1
and IL1RN could have a role in OA susceptibility; however, replication of these findings is required in an independent study.
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