Goat anti Human α2 Macroglobulin polyclonal antibody

We have cloned the mouse gene coding for alpha(2)-macro-globulin in overlapping lambda clones and have analyzed its structure. The gene contains 36 exons, coding for the 4.8-kb cDNA that we cloned previously. Including putative control elements in the 5' flanking region, the gene covers about 45 kb. A region of 3.8 kb, stretching from 835 bases upstream of the cDNA start site to exon 4, including all intervening sequences, was sequenced completely. The analysis demonstrated that the putative promoter region of the mouse A2M gene differed considerably from the known promoter sequences of the human A2M gene and of the rat acute-phase A2M gene. Comparison of the exon-intron structure of all known genes of the A2M family confirmed that the rat acute phase A2M gene is more closely related to the human gene than to the mouse A2M gene. To generate mice with the A2M gene inactivated, an insertion type of construct containing 7.5 kb of genomic DNA of the mouse strain 129/J, encompassing exons 16 to 19, was synthesized. A hygromycin marker gene was embedded in intron 17. After electroporation, 198 hygromycin-resistant ES cell lines were isolated and analyzed by Southern blotting. Five ES cell lines were obtained with one allele of the mouse A2M gene targeted by this insertion construct, demonstrating that the position and the characteristics of the vector served the intended goal. (C) 1994 Academic Press, Inc.

Background: This study focuses on the identification of conserved genes involved in myocardial infarction (MI), and then analyzed the differentially expressed genes (DEGs) between the incident and recurrent events to identify MI-recurrent biomarkers. Methods: Gene expression data of MI peripheral blood were downloaded from GSE97320 and GSE66360 datasets. We identified the common DEGs in these two datasets by functional enrichment analysis and protein-protein interaction (PPI) network analysis. GSE48060 was further analyzed to validate the conserved genes in MI and to compare the DEGs between the incident and recurrent MI. Results: A total of 477 conserved genes were identified in the comparison between MI and control. Protein-protein interaction (PPI) network showed hub genes, such as MAPK14, STAT3, and MAPKAPK2. Part of those conserved genes was validated in the analysis of GSE48060. The DEGs in the incident and recurrent MI showed significant differences, including RNASE2 and A2M-AS1 as the potential biomarkers of MI recurrence. Conclusions: The conserved genes in the pathogenesis of MI were identified, benefit for target therapy. Meanwhile, some specific genes may be used as markers for the prediction of recurrent MI.