Molekulaarbioloogia praksi kontrolltöö vastused
thyroid hormone receptors, a family of proteins that function as ligand-dependent
transcription factors, suggests that the morphogenetic functions of RA may result at least
in part, from activation of developmentally regulated genes by RA receptor (RAR)
complexes. An additional feature of retinoid physiology is the existence of a distinct class
of molecules, the cellular retinol- and RA-binding proteins (CRBPs and CRABPs), which
may modulate the accessibility of RA to the receptors. Representatives of each binding
protein also show spatially restricted patterns of expression in the embryo. The
complexity of retinoid action was demonstrated further by the recent finding that specific
interactions between RARs and other nuclear proteins, including the thyroid hormone
receptors and AP-1 transcription factor, can modulate their transcriptional activity.
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