I finished a 10 page genetics research paper on the molecular basis of Androgen Insensitivity Syndrome or what leads to testicular feminization. I even found the molecular basis of the mutation in the androgen receptor gene!! Sorry I know many of you won't have a clue as to what I'm talking about, but it's a big deal to me. This is what leads to intersexed conditions or "hermaphroditic" people and birth defects of the genitals. YAAAAY!!! I'm proud of me, are you?
2007-04-19
03:37:09
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20 answers
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I_color_outside_the_lines
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Society & Culture
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➔ Lesbian, Gay, Bisexual, and Transgender
Rollthedice....no sorry, no such luck for a CURE, but what I've found in my research is that there is possibly a molecular basis that leads to intersexed conditions, and well, it's kind of hard to explain, but see, in males, androgens like testosterone are made in the testes. This testosterone gets kinda "sucked up" if you will, by something called the androgen receptor, or AR gene. If that AR gene is "broken" then you can't use testosterone or at least not in the quantitities you should be. If an AR gene doesn't work, then it also can't produce mullerian duct hormone which makes male reproductive organs, and what you end up getting is someone that looks totally female on the outside but still has the male, XY chromosome.
Anyway, there's a mututation in the AR gene that causes this. The AR gene has 3 main domains. The DNA-binding domain, the ligand-activated domain, and the transactivation domain. In the transactivation domain (I think) is where the amino acids are formed
2007-04-19
04:09:58 ·
update #1
and sometimes a repeat of CAG or gluatamine is made here. They've found that an "average" length of this CAG is around 22 base pairs. People with shortened CAG can lead to certain neurological defects, and lengthened CAG can lead to increased androgen action and can lead to an early incidence of prostate cancer and breast cancer in women too.
2007-04-19
04:11:32 ·
update #2