Magic™ Anti-LGALS3 polyclonal antibody [Biotin]

Context. Galectin-3, a 35 kDa protein, is the only known member of chimera type galectin family. A growing body of evidences demonstrated the pro-inflammatory role of galectin-3 in the pathogenesis of Rheumatoid arthritis (RA). Objectives. Keeping in view the pivotal role of galectin-3 in pathogenesis of RA, the present case-control study was designed for genotypic and phenotypic screening of galectin-3 in RA. Methods. A case-control association study recruited 200 RA patients and 200 age- as well as gender- matched (p >0.05) controls, after written informed consent. A total of eight SNPs were selected on the basis of in silico analysis, which were subjected to genetic analysis using different techniques. LD was calculated and different haplotypes were constructed. Results. Significant association of three SNPs i.e. rs1009977, rs4644, and rs74050921 along with elevated galectin-3 levels were observed with susceptibility towards RA. Further, high prevalence of TACGTAGC haplotype were observed in RA patients. In addition to the studied SNPs, eight novel variants were also identified in the CRD region of LGALS3. Genotype phenotype correlation indicated significant elevated galectin-3 levels among different genotypes in rs1009977 and rs74050921. Conclusion. The findings of the present study may indicate the role of galectin-3 and its variants in pathogenesis of RA. (C) 2019 IMSS. Published by Elsevier Inc.

Aim: This study evaluated the genesPNPLA3 and LGALS3 in patients who have undergone bariatric surgery. Methods: Individuals with NAFLD and NASH were evaluated, the DNA was extracted from total blood for genotyping of rs4644, rs4652 from LGALS3 and rs738409 from PNPLA3 genes, the total RNA was obtained from liver biopsy. For the detection of the molecular targets, real-time PCR through Taqman probes was used. Results: From a total of 46 collected patients, of those 21 (456%) were included as NASH and 25 (544%) as steatosis group. This groups showed significant difference to aspartate aminotransferase (AST), alanine aminotransferase (ALT) and Glutamyl transpeptidase (GGT) (p = 0.0108, p = 0.0090 and p = 0.0044). Regarding to gene expression in studied groups, hepatic steatosis vs NASH, we observed a higher expression of the LGALS3 gene in NASH (p = 0.0273). In addition, patients with C allele in homozygous for rs4644 and rs4652 of LGALS3 gene had higher expression, in NASH group (p = 0.0500 and p = 0.0242, respectively), furthermore for rs4644 both alleles in homozygous showed higher expression (AA/CC vs AC) (p = 0.0500), when analyzed PNPLA3 rs738409, NASH patients with G allele in homozygous had higher expression (p = 0.0494). Conclusions: Therefore, an increased expression of the LGALS3 gene in patients with NASH may be important in the etiopathogenesis of the disease, as well as the presence of rs4652 and rs4644 SNPs in the regulation of transcriptional levels of the gene in patients with NAFLD and NASH. (C) 2020 Published by Elsevier Ltd on behalf of Asia Oceania Association for the Study of Obesity.