SLC19A1 and folate deficiency: By ectopically expressing hRFC constructs in hRFC-null HeLa cells under control of a constitutive CMV promoter and culturing cells under well-defined conditions of folate deficiency or repletion, we were able to dissociate the effects of cellular folate status on steady-state hRFC transcripts and total cellular hRFC proteins from those involving hRFC transcription from endogenous promoters.