DHRS11: A Potential Drug Target and Biomarker for Estradiol 17-Beta-Dehydrogenase

Target Name: DHRS11

NCBI ID: G79154

DHRS11: A Potential Drug Target and Biomarker for Estradiol 17-Beta-Dehydrogenase

Estradiol 17-beta-dehydrogenase (DHRS11) is a gene that encodes a protein involved in the synthesis of estrogen from androstenedione, a hormone that plays a crucial role in various physiological processes in the body. Mutations in the DHRS11 gene have been linked to various estrogen-related disorders, including infertility, personalization, reproductive health, gender, sexual characteristics, development, reproductive system, endocrinology, gender, reproductive ability, preconception, pregnancy, postpartum, menopause, old age, osteoporosis, fractures, Arthritis, muscle atrophy, arthritis, rheumatoid arthritis, immune system, tumors, etc.

DHRS11 function

DHRS11 is a key enzyme in the synthesis of androstenedione from androstenedione, which is then converted to estrone and finally to estradiol. This enzyme catalyzes the conversion of androstenedione to 17-beta-hydroxy-androstenedione, which is then converted to 17-beta-hydroxy -estrone by the enzyme 3-beta-hydroxy-3-isocyanate dehydrogenase (3-beta-HSD).

In humans, DHRS11 is mainly expressed in cells in the ovaries, adrenal glands and testes. Its expression levels are highest in the ovary, especially in the granulosa cells of the ovary. In the adrenal gland, the expression level of DHRS11 was second, while in the testis it was relatively low.

Knockout of DHRS11 causes developmental abnormalities in the ovaries and adrenal glands of mice, manifested by a reduction in the number of ovarian tubules and adrenocortical cells, and changes in the morphological structure of the ovaries and adrenal glands. At the same time, DHRS11 knockout also leads to reduced reproductive capacity in mice and increases the risk of osteoporosis, muscle atrophy, and arthritis.

Regulation of DHRS11

The synthesis and secretion of DHRS11 are subject to multiple regulations, including intrinsic regulation and extrinsic regulation. Intrinsic regulation includes DNA binding, RNA binding, protein binding, etc. External regulation includes hormones such as estrogen, progesterone, and testosterone, as well as some non-hormonal signaling molecules, such as growth factors, cytokines, and protein-interacting molecules.

DHRS11 interaction

DHRS11 interacts with a variety of proteins, including receptors on the cell membrane, signal transduction pathways, and intracellular transport systems. These interactions not only affect the function of DHRS11, but may also have an important impact on the occurrence and development of the disease.

The relationship between DHRS11 and diseases

Mutations in DHRS11 are closely related to the occurrence and development of a variety of diseases, including reproductive health, bone health, and kidney disease.

First, DHRS11 mutations are associated with reproductive health. Knockout of DHRS11 results in abnormal ovarian and adrenal development, a reduction in the number of ovarian tubules and adrenocortical cells, and changes in the morphological structure of the ovary and adrenal gland, thereby affecting reproductive capacity. In addition, DHRS11 mutations may also cause birth defects in embryos and newborns, such as reproductive system development abnormalities and skeletal malformations.

Second, DHRS11 mutations are associated with bone health. Knockout of DHRS11 leads to abnormal development of the ovaries and adrenal glands in mice, which is manifested by a reduction in the number of ovarian tubules and adrenocortical cells, and changes in the morphological structure of the ovaries and adrenal glands, thereby affecting bone health. In addition, DHRS11 mutations may also cause bone-related diseases such as fractures and muscle atrophy in mice.

Finally, DHRS11 mutations are also associated with kidney disease. Knockout of DHRS11 results in elevated adrenal hormone levels, thereby increasing the risk of adrenal nephritis. In addition, DHRS11 mutations may also lead to renal tubular damage

Protein Name: Dehydrogenase/reductase 11

Functions: Catalyzes the conversion of the 17-keto group of estrone, 4- and 5-androstenes and 5-alpha-androstanes into their 17-beta-hydroxyl metabolites and the conversion of the 3-keto group of 3-, 3,17- and 3,20- diketosteroids into their 3-hydroxyl metabolites. Exhibits reductive 3-beta-hydroxysteroid dehydrogenase activity toward 5-beta-androstanes, 5-beta-pregnanes, 4-pregnenes and bile acids. May also reduce endogenous and exogenous alpha-dicarbonyl compounds and xenobiotic alicyclic ketones

More Common Targets