The expressed SRY protein has a characteristic highmobility group (HMG), DNA-binding domain.
It was genetically mapped by the study of patients with Klinefelter and Turner syndromes.
It is synonymous with the H-Y antigen.
It is synonymous with Sry in humans.
It is a zinc finger gene on the Y chromosome known as ZFY.
It functions normally in patients with hernia uteri inguinale.
It is secreted by the fetal testis at 10 weeks of gestation, after testosterone production has begun.
It acts systemically to produce müllerian regression.
It is secreted by the fetal Leydig cells.
It is secreted at 7 to 8 weeks of gestation, representing the initial endocrine function of the fetal testis.
Mutations in WT1 can result in either Denys-Drash or Frasier syndrome.
Loss of WT1 function has not been associated with genitourinary anomalies.
Duplication of WT1 has been associated with dosagesensitive sex reversal.
The gene was originally isolated in cloning experiments and localized to the X chromosome.
Mutations in WT1 are associated with adrenocortical carcinoma.
It is produced primarily by the adrenal gland.
It acts locally to virilize the urogenital sinus and genital tubercle.
It results in regression of the müllerian ducts.
It acts locally to virilize the internal wolffian duct structures.
It enters target tissue by active diffusion.
It produces virilization of the urogenital sinus.
It is converted by 5α-reductase to testosterone in target tissues.
It acts locally to produce regression of müllerian structures.
It produces virilization of wolffian duct structures.
It is secreted in large quantities by the fetal testis.
They are characteristically fertile.
They undergo replacement of Leydig cells with hyaline.
They are at increased risk for development of adenocarcinoma of the breast.
They bear little resemblance to XX males.
They have at least one X and two Y chromosomes.
is located in the round ligament.
in the presence of a Y chromosome results in increased risk for development of seminoma.
can descend to the scrotum.
in the presence of a Y chromosome results in risk for development of gonadoblastoma.
has a reduced number of oocytes.
They lack the somatic defects associated with Turner syndrome.
They derive similar benefit from synthetic growth hormone as do patients with Turner syndrome.
They frequently have chromosomal anomalies.
They have gonadal histology different from that of patients with Turner syndrome.
They are at lesser risk for gonadal tumors than are patients with Turner syndrome.
Progressive renal failure
Nephropathy with early-onset proteinuria
They have normal testosterone and elevated estradiol levels.
They have castrate testosterone and normal gonadotropin levels.
They have normal follicle-stimulating hormone but decreased luteinizing hormone levels.
They have castrate testosterone and elevated gonadotropin levels.
They have normal testosterone but decreased DHT levels.
It is impossible to cleave surgically.
It cannot descend from the retroperitoneum.
It can be unilateral or bilateral.
It has testicular and ovarian elements randomly distributed.
It is found in the minority of patients.
the impossibility of precisely dividing an ovotestis surgically.
that malignant degeneration of gonads does not occur.
the potential for fertility.
the unresponsiveness of the external genitalia to testosterone.
the familial pattern of inheritance of the disorder.
It is transmitted in an autosomal dominant pattern.
It occurs with a predictable phenotype.
It occurs with simple virilization in 75% of cases and salt wasting in 25% of cases.
It occurs as a result of gene inactivation in the majority of cases.
It accounts for 99% of CAH cases.
acts by suppressing maternal corticotropin.
is initiated after a diagnosis of CAH is confirmed.
is demonstrated to be effective.
is appropriate therapy in seven of eight at-risk fetuses.
is of no risk to the fetus.
They are transmitted in an autosomal dominant pattern.
They may be associated with fertility.
They appear clinically with a predictable phenotype.
They are associated with persistent müllerian structures.
They may involve impaired glucocorticoid and mineralocorticoid synthesis.
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