Endocrine Lab

Androgen Receptor Signaling & DSD Simulator

CLINICAL PRESETS:
2D Molecular Kinetics & Receptor Activation
Testo (T)
DHT
AR Receptor
Active Complex
AR Affinity (Kd)
0%
Active Complexes
0
Transcription Output
0.0%
DHT Ratio
0.0%
Testosterone Level 600 ng/dL
5α-Reductase Activity 100%
AR Binding Affinity (Kd) 0%
AR Receptor Density 100%
Embryonic Tissue Morphogenesis (6–12 Gestational Weeks) 46,XY Genotype
Gestational Timeline Scrubber Week 8
INTERNAL DUCTS EXTERNAL GENITALIA Testis Wolffian Duct (Regressed) Müllerian Duct (Regressed) Female Phenotype MIS present → Müllerian regression. Low AR binding → Wolffian regression & Female external genitalia.

CAIS (Complete Androgen Insensitivity)

Despite a 46,XY genotype and functional testes producing testosterone & MIS (Müllerian Inhibiting Substance), complete AR non-responsiveness (Kd = 0%) prevents Wolffian duct survival and external virilization. Müllerian ducts regress normally due to MIS, resulting in female external genitalia, unvirilized phenotype, and absent internal uterus/ovaries.

CANONICAL COMPUTED RESULT:
Preset: CAIS
Karyotype: 46,XY
AR Kd: 0%
Transcription: 0.0%
Wolffian: Regressed
External: Female

Androgen Receptor Signaling & Morphogenesis

Read the explanation

In 46,XY development, testicular testosterone diffuses across the cell membrane where 5-alpha reductase converts a fraction into potent dihydrotestosterone. When androgen receptor affinity is zero, as in Complete Androgen Insensitivity Syndrome, no active complexes form and transcriptional output drops to zero percent. Adjusting AR binding affinity to one hundred percent restores receptor dimer formation, driving nuclear translocation and stimulating high transcriptional output. Consequently, embryonic tissue diverges: functional AR retains the Wolffian ducts and virilizes external genitalia, whereas receptor insensitivity causes duct regression and female external morphology.

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