Ar chat sex
If the affected child is a genetic female, she, too, will be a carrier. A genetic female with mutations in both AR genes could theoretically result from the union of a fertile man with AIS and a female carrier of the gene, or from de novo mutation.However, given the scarcity of fertile AIS men and low incidence of AR mutation, the chances of this occurrence are small.The AR translocates to the nucleus where dimerization, DNA binding, and the recruitment of coactivators occur.Target genes are transcribed (m RNA) and translated into proteins.A genetic male conceived by a man with AIS would not receive his father's X chromosome, thus would neither inherit nor carry the gene for the syndrome.A genetic female conceived in such a way would receive her father's X chromosome, thus would become a carrier.
Individuals with partial AIS, unlike those with the complete or mild forms, present at birth with ambiguous genitalia, and the decision to raise the child as male or female is often not obvious.
The Quigley scale can be used in conjunction with the traditional three classes of AIS to provide additional information regarding the degree of genital masculinization, and is particularly useful when the diagnosis is PAIS.
Location and structure of the human androgen receptor: Top, the AR gene is located on the proximal long arm of the X chromosome.
Thus the AR activates these genes to mediate the effects of androgens in the human body, including the development and maintenance of the male sexual phenotype and generalized anabolic effects. AIS is divided into three categories that are differentiated by the degree of genital masculinization: complete androgen insensitivity syndrome (CAIS) is indicated when the external genitalia are that of a normal female; mild androgen insensitivity syndrome (MAIS) is indicated when the external genitalia are that of a normal male, and partial androgen insensitivity syndrome (PAIS) is indicated when the external genitalia are partially, but not fully, masculinized.
Management of AIS is currently limited to symptomatic management; no method is currently available to correct the malfunctioning androgen receptor proteins produced by AR gene mutations.
Women (chromosomal XX) who are heterozygous for the AR gene have normal primary and secondary sexual characteristics; this female carrier will pass the affected AR gene to any child she has with 50% likelihood.