Immunological and functional quantitation of nuclear retinoid X (RXR) and retinoic acid (RAR) receptor proteins in human epidermis in vivo: High levels of RXRS and RAR-γ, low levels of RAR-α, and absence of RAR-β

Ultraviolet Irradiation Blocks Cellular Responses to Transforming Growth Factor-β by Down-regulating Its Type-II Receptor and Inducing Smad7

“…Western Analysis-Nuclear extracts were prepared as described previously (31). Membrane fractions were prepared according to a method previously described (32) with slight modification.…”

Keratinocyte differentiation induced by calcium, phorbol ester or interferon-γ elicits distinct changes in the retinoid signalling pathways

“…The expression of CRABPII is readily inducible by RA and has been used as a marker for retinoid activity in keratinocytes [6,7]. Several of the retinoid receptors known so far have been recognized in human epidermal keratinocytes [8][9][10][11]. In falling order of abundance, the major forms expressed are RXRα, RARγ and RARα [11], thus making RARγ/RXRα the predominant heterodimer.…”

“…Several of the retinoid receptors known so far have been recognized in human epidermal keratinocytes [8][9][10][11]. In falling order of abundance, the major forms expressed are RXRα, RARγ and RARα [11], thus making RARγ/RXRα the predominant heterodimer. According to some studies, these receptors are expressed mainly by cells in the upper (differentiated) cell layers of normal epidermis [9,10] suggesting that they are involved in the process of terminal differentiation.…”

Synthetic Retinoids and Their Nuclear Receptors

“…For these reasons, major efforts have been expended on identifying retinoids that are selective for one of the three RAR subtypes in the effort to improve therapeutic indices by eliminating any of the adverse reactions that would be caused by the other subtypes [14,15,17,[62][63][64][65]. This strategy was considered feasible because of the diversity in the retinoid response pathways with the RAR subtypes functioning as heterodimers with the RXR subtypes [7][8][9][10], complexing with various modulatory proteins (transcriptional coactivators and corepressors) [9,66], binding to various responsive elements (REs) in the promoter regions of retinoid-modulated genes [10,67], and having tissue distribution patterns that varied with cell type and differentiation state [68][69][70][71][72][73][74][75]. Generally, in normal epithelial cells, from which many cancers arise, only RARα and RARγ are expressed or predominate [72,73], whereas RARβ is absent or present at very low levels [72,75].…”