Protein and fat intake interacts with the haplotype of PTPN11_rs11066325, RPH3A_rs886477, and OAS3_rs2072134 to modulate serum HDL concentrations in middle-aged people.
<i>In vitro</i> expression of the TRAF6 protein, phosphorylated transcription factor p65 and phosphorylated p100 in myeloma cell lines was induced by MSCs from patients with MM.
Polymorphisms in the OAS1 SNPs (rs1131454), OAS2 SNPs (rs1293762, rs15895 and rs1732778) and OAS3 SNPs (rs2285932 and rs2072136) genes were studied using PCR followed by restriction fragment length polymorphism methods in 30 patients for dengue infection and 40 control group who have no documented evidence of symptomatic dengue.
The two locus haplotype of OAS2 G-G was significantly higher in all patient groups [DEN vs. HCs, P=0.0041, P corrected (Pc)=0.012, Odds ratio (OR) 1.73 95% CI 1.16-2.59] while the four locus haplotype of OAS3-OAS2 C-G-A-G was significantly lower in all dengue patient groups [DEN vs. HCs, P=0.0054, Pc=0.0486, OR 0.09, 95% CI 0.00-0.64] compared to controls.
The molecular mechanism of p100 degradation has implications in multiple myeloma, a disease with constitutive activation of the noncanonical NF-κB pathway.
Thus, OAS1 p42/p46 and OAS3 p100 are likely to contribute to host defense against DEN infection and play a role in determining the outcomes of DEN disease severity.
C-terminal truncations of the NFKB2 p100 gene product have been observed in a number of cases of human cutaneous T cell lymphomas, as well as human B-cell lymphomas and myelomas.
The rates of change in the absence of optic neuritis (ON) for minimal VEP intervals of ≥3 months between baseline and last follow-up were +1.951 ms/y (n = 101 eyes; SD = 6.274; <i>p</i> = 0.012) for the P100 latencies and -2.149 µV/y (n = 64 eyes; SD = 5.013; <i>p</i> = 0.005) for the P100-N140 amplitudes.
In a multivariable regression model, age and P100 latency were significant parameters for affecting AA in patients with MS (<i>p</i> < .001 and <i>p</i> = .001).
To examine the thiol-disulphide homeostasis during an optic neuritis episode in patients with multiple sclerosis and the relationship between this homeostasis and P100 wave latency.
To examine the thiol-disulphide homeostasis during an optic neuritis episode in patients with multiple sclerosis and the relationship between this homeostasis and P100 wave latency.
Genetic polymorphism in OAS3 gene has been reported to be a susceptibility factor in many infected diseases, but evidence of its effect on enterovirus 71 (EV71) infection is still lacking.
Previous work has identified that following viral infection, type I IFN signaling induces the production of the 2'-5'-oligoadenylate synthetase (OAS) family, which include OAS1, OAS2, OAS3, and OAS-like (OASL) protein.
Together, these findings identify specific roles for p100 and p105 signaling in defining DLBCL molecular subtypes and posit MYD88/p100 signaling as a regulator for B-cell activation.