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Fig. 3 | BMC Research Notes

Fig. 3

From: Fanconi anemia core complex-dependent HES1 mono-ubiquitination regulates its transcriptional activity

Fig. 3

HES1 lysine 109 is required for HES1 transcriptional regulation. a Altered HES1 expression in FA mutant cells. FA-A cells were transfected with pHES1pro-Luc and plasmids carrying either the correcting gene FANCA or, as a negative control, FANCE; with the HES1 or the HES1K109E expression plasmid. b HES1 lysine 109 is required for FA complex-mediated regulation of HES1. COS-1 cells were transfected with pHES1pro-Luc and HES1 or HES1K109E expression vector with or without plasmids encoding the FA core complex (coFA) and in c with NICD expression plasmid. d Mutation of HES1 lysine 109 promotes FA complex-mediated p21CIP1/WAF1 repression. COS-1 cells were transiently transfected with p21pro-Luc reporter vector with HES1 or HES1K109E coding vectors, and either with FA complex members coding vectors. e FA complex-mediated repression of p21CIP1/WAF1 transcription is enhanced by HES1 K109E mutation. FA-A cells were transiently transfected with p21pro-Luc and either FANCA or FANCE (negative control) coding vectors, along with wildtype or K109E mutant HES1 coding vectors. All plasmids were transfected at equimolar ratios. Control indicates empty vectors. All experiments were done at least three times in duplicates. 2-way ANOVA with Bonferroni correction test, *p < 0.01, **p < 0.005, *** p < 0.0001, as compared to Empty; #p < 0.01, ##p < 0.001 and ###p < 0.0001, as compared to Control

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