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