CONGENITAL ADRENAL HYPERPLASIA
\kənd͡ʒˈɛnɪtə͡l ɐdɹˈiːnə͡l hˌa͡ɪpəplˈe͡ɪzi͡ə], \kəndʒˈɛnɪtəl ɐdɹˈiːnəl hˌaɪpəplˈeɪziə], \k_ə_n_dʒ_ˈɛ_n_ɪ_t_əl ɐ_d_ɹ_ˈiː_n_əl h_ˌaɪ_p_ə_p_l_ˈeɪ_z_iə]\
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A group of syndromes caused by inherited defects in cortisol (HYDROCORTISONE) and, in some types, ALDOSTERONE biosynthesis. Each of the several types that occur, such as simple virilizing forms (adrenogenital syndrome), salt-wasting forms, and virilizing hypertension forms may be caused by a variety of defects. Defects in 21-hydroxylase (STEROID 21-MONOOXYGENASE) are most common. Other defects occur in the enzymes 11 beta-hydroxylase (STEROID 11 BETA-MONOOXYGENASE), 17 alpha-hydroxylase (STEROID 17 ALPHA-MONOOXYGENASE), or 3-beta-hydroxysteroid dehydrogenase (3-HYDROXYSTEROID DEHYDROGENASES).
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Proto Oncogene Proteins c erbB 2
- cell surface protein-tyrosine kinase that is found to be overexpressed in significant number adenocarcinomas. It has extensive homology can heterodimerize EGF EPIDERMAL GROWTH FACTOR), 3 receptor (RECEPTOR, 3) and the 4 receptor. Activation of erbB-2 receptor occurs during heterodimer formation with a ligand-bound erbB family members. EC 2.7.11.-.