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Receptors, psoralen

Photochemically reactive molecules have often been used as labels for specific sites in proteins and nucleic acids. Psoralen derivatives serve as relatively nonspecific photochemically activated crosslinking agents for DNA and double-stranded RNA.195 Aryl azides are converted by light to aryl nitrenes, which react in a variety of ways including insertion into C-H bonds (Eq. 23-27).200 201 In some cases UV irradiation can be used to join natural substrates to enzymes or hormones to receptors. For example, progesterone, testosterone, and other steroids have been used for direct photoaffinity labeling of their receptors.202 Synthetic benzophenones have also been used widely as photoactivated probes.203... [Pg.1297]

In psoriasis, PUVA therapy (psoralen and UVA) leads to an inhibition of abnormally high rates of epidermal cell growth associated with the disease [297]. It has been shown that photoactivated psoralens are also potent inhibitors of epidermal cell growth in vitro. There are several lines of evidence that indicate the psoralen receptor is not associated with the DNA [298]. Studies on the distribution of compounds in cells based on their fluorescence properties demonstrated that psoralen (2) was present in the cytoplasm and cell surface membranes [299]. When cell membrane Auction of HeLa cells were prepared, psoralen receptor binding could be detected [297]. Using [3H]-8-MOP (methoxypsoralen), the cellular distribution of covalently bound psoralen in HeLa cells was also examined [300]. In these experiments, cells were treated with [3H]-8-MOP, then pulsed with UV light. It was indicated that labeled 8-MOP was distributed in cytoplasm and membrane finctions. These results have been repeated in several laboratories and all of them implicate targets outside of the nucleus... [Pg.379]

The compounds psoralen and isopsoralen were selective ER-a agonists in a HeLa cell assay. These compounds promoted proliferation of estrogen receptor-positive breast cancer cells (MCF-7). Other compounds in psoralea were ER-P agonists (Xin et al. 2010). [Pg.284]

Decreased epidermal proliferation is considered to be the main mechanism of action of PUVA in the treatment of psoriasis. Once excited by UVA, psoralens can react with molecular oxygen, producing reactive oxygen species that cause mitochondrial dysfunction and lead to apoptosis of skin Langerhans cells, keratinocytes, and lymphocytes [134]. PUVA further decreases epidermal cell proliferation by noncompetitively binding to epidermal growth factor receptors and directly altering the cell surface membrane. [Pg.176]

Psoralen Receptors Interaction with Ionic Channels... [Pg.2751]

Laskin et al. identified cellular protein as a target for the psoralen molecules linked to cell growth regulation. Subcellular fractionation studies revealed that this receptor is located in membranes and the cytoplasmic fractions of various ceU types, in particular, melanocytes and keratinocytes. ... [Pg.2760]

Mermelstein, F.H., Abidi, T.R, and Laskin, J.D., Inhibition of epidermal growth factor receptor tyrosine kinase activity in A431 human epidermoid ceUs foUowing psoralen/ultraviolet Ught treatment, Mol. Pharmacol., 36, 848, 1989. [Pg.2766]


See other pages where Receptors, psoralen is mentioned: [Pg.143]    [Pg.143]    [Pg.7]    [Pg.305]    [Pg.28]    [Pg.522]    [Pg.499]    [Pg.380]    [Pg.34]    [Pg.2760]    [Pg.2761]    [Pg.2761]    [Pg.33]   


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