Anti-CD79A (N-terminal) polyclonal antibody

Soybean [Glycine max (L.) Merr.] is an important crop for oil and protein resources worldwide, and its farming is impacted by increasing soil salinity levels. In Arabidopsis the gene EARLY FLOWERING 3 (ELF3), increased salt tolerance by suppressing salt stress response pathways. J is the ortholog of AtELF3 in soybean, and loss-of-function J-alleles greatly prolong soybean maturity and enhance grain yield. The exact role of J in abiotic stress response in soybean, however, remains unclear. In this study, we showed that J expression was induced by NaCl treatment and that the J protein was located in the nucleus. Compared to NIL-J, tolerance to NaCl was significantly lower in the NIL-j mutant. We also demonstrated that overexpression of J increased NaCl tolerance in transgenic soybean hairy roots. J positively regulated expression of downstream salt stress response genes, including GmWRKY12, GmWRKY27, GmWRKY54, GmNAC, and GmSIN1. Our study disclosed a mechanism in soybean for regulation of the salt stress response. Manipulation of these genes should facilitate improvements in salt tolerance in soybean.

A recent study characterized the long non-coding RNA (lncRNA) ELF3-antisense RNA 1 (ELF3-AS1) as an oncogenic lncRNA in bladder cancer. The present study aimed to investigate the role of ELF3-AS1 in osteosarcoma (OS). It was found that ELF3-AS1 was upregulated in OS tissues, and ELF3-AS1 expression level increased with increasing clinical stage. In OS tissues, Kruppel-like factor 12 (KLF12) was positively correlated with ELF3-AS1, while microRNA (miR)-205 was negatively correlated with ELF3-AS1. ELF3-AS1 overexpression resulted in the upregulation of KLF12, but the downregulation of miR-205. Overexpression of miR-205 caused downregulation of KLF12, but had no significant effects on ELF3-AS1 expression. Overexpression of KLF12 showed no significant impact on ELF3-AS1 and miR-205. ELF3-AS1 and KLF12 overexpression resulted in an increased proliferation rate in OS cells, while miR-205 played an opposite role and attenuated the effects of ELF3-AS1 overexpression. ELF3-AS1 overexpression promoted the methylation of the miR-205 gene. Therefore, ELF3-AS1 may promote OS cell proliferation by upregulating KLF12 through the methylation of the miR-205 gene.