Sandbox Reserved 428: Difference between revisions
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It has been shown that VDR has an effect on the hair folicle cycle through the elimination of the receptor. In null-VDR mice, it has been shown that with normal mineral ion levels that the mice result in alopecia, disease inducing hair loss [2]. VDR is expressed in the hair follicle keratinocytes and its levels are higher in the late anagen and catagen stages of the hair cycle [2]. These two stages are vital in the differentiation and proliferation of hair follicle keratinocytes, which regulate hair growth in the body. Much research has been done into the mechanism in which the VDR effects the hair follicle cycle with the overall mechanism still unknown. The mechanism was first believed that the binding of VDR to 1,25- dihydroxyvitamin D causing transactivation due to the fact that targeted expressions of wild-type VDR to the keratinocytes of VDR null mice rescued alopecia [2]. Although, this was disproven through investigations in vitamin D-deficient mice that had no detectable 1,25-dihydroxyvitamin D for the VDR to bind, yet the mice did not develop alopecia. This shows that the VDR transcriptional activation of DNA is not the main cause of the loss of hair follicles. Current research observes the ligand-independent actions of the VDR that have not been observed extensively as a mechanism [2]. Nuclear receptor co-repressor genes have been observed in studies to have an effect on the hair follicle cycle including the HR gene (Hairless). This corepressor has been shown to have interactions with the VDR in vivo and tests with the mutation of Hairless have caused alopecia in mice in vivo [2]. Thus, although the mechanism behind the interaction of Hairless and the VDR is still unknown it has been shown in studies that there is a relationship between the two and alopecia. | It has been shown that VDR has an effect on the hair folicle cycle through the elimination of the receptor. In null-VDR mice, it has been shown that with normal mineral ion levels that the mice result in alopecia, disease inducing hair loss [2]. VDR is expressed in the hair follicle keratinocytes and its levels are higher in the late anagen and catagen stages of the hair cycle [2]. These two stages are vital in the differentiation and proliferation of hair follicle keratinocytes, which regulate hair growth in the body. Much research has been done into the mechanism in which the VDR effects the hair follicle cycle with the overall mechanism still unknown. The mechanism was first believed that the binding of VDR to 1,25- dihydroxyvitamin D causing transactivation due to the fact that targeted expressions of wild-type VDR to the keratinocytes of VDR null mice rescued alopecia [2]. Although, this was disproven through investigations in vitamin D-deficient mice that had no detectable 1,25-dihydroxyvitamin D for the VDR to bind, yet the mice did not develop alopecia. This shows that the VDR transcriptional activation of DNA is not the main cause of the loss of hair follicles. Current research observes the ligand-independent actions of the VDR that have not been observed extensively as a mechanism [2]. Nuclear receptor co-repressor genes have been observed in studies to have an effect on the hair follicle cycle including the HR gene (Hairless). This corepressor has been shown to have interactions with the VDR in vivo and tests with the mutation of Hairless have caused alopecia in mice in vivo [2]. Thus, although the mechanism behind the interaction of Hairless and the VDR is still unknown it has been shown in studies that there is a relationship between the two and alopecia. | ||
==Quiz Question 1== | ==Quiz Question 1== | ||
Osteoporosis is a disease in which the bones become porous and fragile. The most common cause of the ailment is calcium deficiency. As the vitamin D receptor has association with calcium uptake, mutations in VDR could be detrimental.If an individual had a point mutation that would replace <scene name='48/483885/Point_mutation/1'>His305 and His397</scene> with serine amino groups, would that individual be more or less likely to develop osteoporosis? why? | |||
==See Also== | ==See Also== | ||
*[[3w0a]] | *[[3w0a]] | ||
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Additional Features - Patrick Murphy | Additional Features - Patrick Murphy | ||
Quiz Question 1 - | Quiz Question 1 - Roger Crocker | ||
==References== | ==References== | ||
<references/> | <references/> | ||