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Canonical Wnt signaling is important for organogenesis, including kidney development. During this process, an appropriate concentration of retinoic acid (RA) is essential for the proper differentiation of cap mesenchyme and ureteric bud cells into glomeruli and renal vesicles, respectively. The differential expression pattern of ALDH1A2 and cytochrome P450 family 26 subfamily A/B/C member 1 is a crucial factor in regulating the local availability and concentration of RA.

ALDH1A2 antibody for research our study, we showed that b-catenin and TCF4 interact with the ALDH1A2 promoter in 293T cells to activate its expression. Moreover, we identified an enhancer element within the first intron of ALDH1A2 (intron1G) that is essential for its expression in mouse embryonic kidney stromal cells.

A ChIP assay showed that b-catenin directly binds to the ALDH1A2 intron1G region and recruits acetyl-histone 3 and RNA polymerase II. In addition, the Aldh1a2 intron1G DNA region partially overlapped with a luciferase reporter gene driven by the wild-type ALDH1A2 promoter and a mutated version of it.

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A luciferase assay showed that ectopic expression of the ALDH1A2 intron1G element in the wild-type ALDH1A2 plasmid results in a decrease of luciferase activity, whereas the mutated intron1G DNA region represses ALDH1A2 luciferase activity. The intron1G DNA element is therefore essential for the regulation of ALDH1A2 expression in fetal kidney stromal cells, which in turn determines the availability and local concentration of RA during ureteric bud formation. CHIR99021, a potent and selective inhibitor of b-catenin/TCF4 signaling, also reduces the level of ALDH1A2 mRNA and protein in WiT49 cells.