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Human Monoclonal SULT2A1 Primary Antibody für FACS, IF - ABIN2732966
Barrett, Fang, Gargano, Markovich, Kocarek, Runge-Morris: Regulation of murine hepatic hydroxysteroid sulfotransferase expression in hyposulfatemic mice and in a cell model of 3'-phosphoadenosine-5'-phosphosulfate deficiency. in Drug metabolism and disposition: the biological fate of chemicals 2013
Show all 2 Pubmed References
hyposulfatemia leads to hepatic phosphoadenosine-5'-phosphosulfate depletion, which causes loss of SULT2A1 activity and results in accumulation of nonsulfated bile acids and activated farnesoid X receptor (zeige xpr1 Antikörper) activation.
activation of PXR (zeige NR1I2 Antikörper) increases the activity and gene expression of the phase II conjugating enzyme dehydroepiandrosterone sulfotransferase (STD)
hydroxysteroid sulfotransferase has a protective role in lithocholic acid-induced liver toxicity
and Sult2a1 participate in an integrated pathway mediating elimination of sulfated (zeige SULF1 Antikörper) steroid and bile acid metabolites from the liver
decreased levels or activities of farnesoid X receptor (zeige xpr1 Antikörper), pregnane X receptor (zeige NR1I2 Antikörper), and constitutive androstane receptor (zeige NR1I3 Antikörper) during the acute-phase response could contribute to decreases in Sult2A1, resulting in decreased sulfation of DHEA
Increased Sult2A1 expression appears to be an adaptive response to ensure optimal metabolism of Sult2A1 substrates at old age.
Sult2A1 converts bile acids, steroids and a number of drugs to the corresponding sulfated (zeige SULF1 Antikörper) metabolites in the livers of 4-month- and 20-month-old mice.
nine human SULT2A1 allozymes plus the wild-type SULT2A1 were found to display differential sulfating activity toward DHEA and tibolone. Kinetic analysis revealed that different SULT2A1 allozymes exhibited differential substrate affinity and catalytic efficiency toward the two substrates tested.
Mass spectrometry analysis and structural modeling supported a reaction mechanism which involves the isomerization of Delta(4)-3-ketosteroids from the keto form to an enol form, prior to being subjected to sulfation. Results derived from this study suggested a potential role of SULT2A1 as a Delta(4)-3-ketosteroid sulfotransferase in steroid metabolism
Decreased SULT2A1 activity was found in the adrenal zona reticularis in Alzheimer's disease patients.
PSC is characterized by disease-specific impairment of SULT2A1 expression following PXR (zeige NR1I2 Antikörper) activation, a phenomenon which is not noted in PBC (zeige DLAT Antikörper), and may account for the impaired hepatoprotection in PSC.
The substrate, such as lithocholic acid (LCA), participated in regulating the structure and flexibility of sulfotransferase actively rather than merely being selected passively.
Our results show that SULT2A1 is important in the first trimester; particularly in the adrenals
results established human SULT2A1 as a novel LXRalpha (zeige NR1H3 Antikörper) target gene; the expression of LXRalpha (zeige NR1H3 Antikörper) is a potential predictor for the expression of SULT2A1 in human liver
It turns out the protective effect of DHEA was significantly decreased when Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signaling was activated, while inactivating Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signaling enhanced the effects of DHEA
The complete kinetic mechanism of human SULT2A1.
Fetal inflammatory response syndrome and funisitis are associated with an elevation of umbilical cord plasma concentrations of soluble sulfotransferase (ST)2.
This gene encodes a member of the sulfotransferase family. Sulfotransferases aid in the metabolism of drugs and endogenous compounds by converting these substances into more hydrophilic water-soluble sulfate conjugates that can be easily excreted. This protein catalyzes the sulfation of steroids and bile acids in the liver and adrenal glands, and may have a role in the inherited adrenal androgen excess in women with polycystic ovary syndrome.
sulfotransferase family, cytosolic, 2A, dehydroepiandrosterone-preferring, member 1
, sulfotransferase family, cytosolic, 2A, dehydroepiandrosterone (DHEA)-preferring, member 1
, alcohol sulfotransferase
, bile salt sulfotransferase 1
, hydroxysteroid sulfotransferase
, sulfotransferase 2A1
, sulfotransferase, DHEA preferring
, sulfotransferase, hydroxysteroid preferring 1
, bile salt sulfotransferase
, bile-salt sulfotransferase 2A1
, hydroxysteroid sulfotransferase a
, sulfotransferase family, cytosolic, 2A, dehydroepiandrosterone (DHEA) -preferring, member 1
, sulfotransferase hydroxysteroid gene 2
, sulfotransferase, hydroxysteroid preferring 2
, alcohol/hydroxysteroid sulfotransferase
, bile-salt sulfotranasferase 2A1