Редактирование: SULT2B1

Sulfotransferase 2B1 (EC 2.8.2.2) (Alcohol sulfotransferase) (Hydroxysteroid sulfotransferase 2) (Sulfotransferase family 2B member 1) (Sulfotransferase family cytosolic 2B member 1) (ST2B1) [HSST2]

==Publications==

{{medline-entry
|title=Perimenopausal regulation of steroidogenesis in the nonhuman primate.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/21683476
|abstract=Human aging is characterized by a marked decrease in circulating levels of dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEAS), hormonal changes associated with cognitive decline. Despite beneficial effects of DHEA supplementation in rodents, studies in elderly humans have generally failed to show cognitive improvement after treatment. In the present study we evaluate the effects of age and estradiol supplementation on expression of genes involved in the de novo synthesis of DHEA and its conversion to estradiol in the rhesus macaque hippocampus. Using reverse transcription polymerase chain reaction (RT-PCR) we demonstrate the expression of genes associated with this synthesis in several areas of the rhesus brain. Furthermore, real-time PCR reveals an age-related attenuation of hippocampal expression level of the genes [[CYP17A1]], [[STS]], and 3BHSD1/2. Additionally, short-term administration of estradiol is associated with decreased expression of [[CYP17A1]], [[STS]], [[SULT2B1]], and AROMATASE, consistent with a downregulation not only of estrogen synthesis from circulating DHEA, but also of de novo DHEA synthesis within the hippocampus. These findings suggest a decline in neurosteroidogenesis may account for the inefficacy of DHEA supplementation in elderly humans, and that central steroidogenesis may be a function of circulating hormones and menopausal status.
|mesh-terms=* Aging
* Animals
* Biomarkers
* Dehydroepiandrosterone
* Estradiol
* Female
* Hippocampus
* Hydrocortisone
* Macaca mulatta
* Male
* Perimenopause
* Primates

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3196783
}}
{{medline-entry
|title=LXR signaling couples sterol metabolism to proliferation in the acquired immune response.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/18614014
|abstract=Cholesterol is essential for membrane synthesis; however, the mechanisms that link cellular lipid metabolism to proliferation are incompletely understood. We demonstrate here that cellular cholesterol levels in dividing T cells are maintained in part through reciprocal regulation of the LXR and SREBP transcriptional programs. T cell activation triggers induction of the oxysterol-metabolizing enzyme [[SULT2B1]], consequent suppression of the LXR pathway for cholesterol transport, and promotion of the SREBP pathway for cholesterol synthesis. Ligation of LXR during T cell activation inhibits mitogen-driven expansion, whereas loss of LXRbeta confers a proliferative advantage. Inactivation of the sterol transporter [[ABCG1]] uncouples LXR signaling from proliferation, directly linking sterol homeostasis to the antiproliferative action of LXR. Mice lacking LXRbeta exhibit lymphoid hyperplasia and enhanced responses to antigenic challenge, indicating that proper regulation of LXR-dependent sterol metabolism is important for immune responses. These results implicate LXR signaling in a metabolic checkpoint that modulates cell proliferation and immunity.
|mesh-terms=* Aging
* Animals
* Cell Proliferation
* DNA-Binding Proteins
* Humans
* Liver X Receptors
* Lymphocyte Activation
* Mice
* Mice, Inbred C57BL
* Orphan Nuclear Receptors
* Receptors, Cytoplasmic and Nuclear
* Signal Transduction
* Sterol Regulatory Element Binding Protein 2
* Sterols
* T-Lymphocytes

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626438
}}