Fig 1: Examples of genes potentially regulated by RBM3 and a model for RBM3-mediated 3′UTR shortening. (A–C) Left: Schematic of RBM3 motifs adjacent to PAS sequences in ATP6V0A2 (A), PSMD11 (B) and LEPROTL1 (C) genes. Right: 3′RACE showing favoring of pPAS versus dPAS at 8 h of costimulation. (D) Top: 3′RACE of LEPROTL1 in 293T cells transfected with cDNA expressing hnRNP C (control) or RBM3 or vector alone. Asterisks mark products observed only in 293T cells. Bottom: Western blot expression of RBM3, hnRNP C and hnRNP L (loading control) in the same cells as top experiment. Expression of hnRNP C causes a small increase in endogenous RBM3. (E) Model for 3′UTR shortening by RBM3, showing the suggested competitive binding between RBM3 and the cleavage and polyadenylation machinery (CPSF complex).
Fig 2: RBM3 increases at 8 h of costimulation of primary human T cells and has its binding motif is enriched around dPAS that are repressed at 8 h. (A) Log2 fold changes of proteins that have been implicated in APA regulation. (B) Western blot analysis of RBM3 and hnRNP A3 protein following 8 h of CD3/CD28 costimulation of CD4+ human T cells. (C) Presence of RBM3 binding motifs around pPAS and dPAS elements for events that exhibit shortening at 8 h versus 48 h or show no change.
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