Human SULT1B1 / ST1B2 Protein
- Known as:
- Human SULT1B1 / ST1B2 Protein
- Catalog number:
- SU1-H5148
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human SULT1B1 / ST1B2 Protein
Related genes to: Human SULT1B1 / ST1B2 Protein
- Gene:
- SULT1B1 NIH gene
- Name:
- sulfotransferase family 1B member 1
- Previous symbol:
- -
- Synonyms:
- ST1B2
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-10
- Date modifiied:
- 2015-11-06
Related products to: Human SULT1B1 / ST1B2 Protein
Related articles to: Human SULT1B1 / ST1B2 Protein
- Metabolic syndrome (MetS) is a cluster of risk factors increasing the likelihood of cardiovascular and metabolic diseases. This study investigated the relative mRNA expression of key hepatic and intestinal phase II drug-metabolising enzymes, specifically UDP-glycosyltransferases (UGTs) and sulfotransferases (SULTs), in four non-obese rat models of MetS characterised by different dominant traits: the hereditary hypertriglyceridaemic (HHTg) rat, spontaneously hypertensive rat (SHR), SHR-expressing transgenic human C-reactive protein (SHR-CRP) rat, and bilaterally ovariectomised female Wistar (W-OVX) rat, compared to Wistar controls. Gene expression was quantified by RT-PCR with data normalised using the ΔΔCt method. Measurements showed significant model-specific differences, especially in the liver. HHTg rats exhibited significant hepatic suppression of (-90%) and undetectable transcripts, alongside compensatory upregulation of (196%) and (277%). The SHR model showed significant hepatic upregulation of (330%), (266%), and (328%). Chronic inflammation in SHR-CRP rats caused a significant decrease in hepatic , whereas a significant induction occurred in the intestine. Oestrogen deprivation (W-OVX) led to significant downregulation of hepatic and . These findings highlight that the alterations in phase II metabolism strongly depend on the pathophysiological context, potentially affecting drug disposition in preclinical models. - Source: PubMed
Publication date: 2026/05/27
Soukop JanPoruba MartinRácová ZuzanaZapletalová IvetaMalínská HanaHüttl MartinaMarková IrenaVečeřa Rostislav - Metabolic dysfunction-associated steatotic liver disease (MASLD) disrupts core hepatic physiological functions, with super-enhancers (SEs) playing a pivotal role in orchestrating the expression of genes associated with disease pathogenesis. This study aimed to elucidate the regulatory mechanisms of SEs in MASLD pathogenesis. - Source: PubMed
Publication date: 2026/04/10
Lu XuejinYan YuxuanLv JingPei XingyueZhao MingtaoZhuang XinruiZheng FeiTang YunshuZhu Yaling - Protective cerebral responses against stresses are fundamental quests of medical science. Here, we report that upregulation of histone sulfation is a protective cerebral response against ischemic injury. Ischemia upregulates the SLC26A1-PAPSS1-SULT1B1 axis, which mediates the transportation of sulfate into cells, conversion of sulfate into PAPS, and catalysis of histone sulfation (H3Y99sulf) using PAPS, respectively. Upregulated H3Y99sulf promotes metabolic genes transcription and glycolysis, sustaining cell survival in ischemic stress. In the mouse model of transient middle cerebral artery occlusion, both PAPSS1 overexpression and sulfate supplementation can boost the neuroprotective H3Y99sulf mechanism, reduce brain injury, and improve neurological functions; disruption of H3Y99sulf exacerbates ischemia-induced brain injury and counteracts the neuroprotective effect of sulfate. Ischemia patients with higher serum sulfate levels are prone to have smaller infarcts, alleviated severity assessments, and better clinical outcomes. This study unearths an undocumented protective cerebral response against ischemia that might be targeted for ischemic stroke treatment. - Source: PubMed
Jiang LiXie JunchangWang JianfengYi YiliZhou RunxinGuo DingyuanWang YuZeng XiaoShi MingxuanDing JianingWu JiadiZhao JunFeng SiyuWang NanShen QianYin YupingLi MingchangWang Yugang - Head and neck squamous cell carcinoma (HNSCC) has a poor prognosis and a high fatality rate. To predict the prognosis of HNSCC, this study developed a prognostic model based on nitrogen metabolism (NM)-related genes. - Source: PubMed
Publication date: 2026/01/09
Shen YimingSun WenfangDai Chunfu - Sulfotransferases (SULTs) can transfer sulfonate group from a donor molecule, typically 3'-phosphoadenosine-5'-phosphosulfate (PAPS), to a variety of acceptor molecules including hormones, drugs, and xenobiotics, thus play key roles in animal xenobiotic metabolisms and hormone regulations. Here, the first protein crystal structure of a chicken SULT1B1 BtSULT1B1 was obtained and its catalytic mechanism and substrate binding mode was elucidated by analyzing its structures in complex with substrates and donors like PAP, PAPS, pNP, pNPS and 2-Bromophenol. Notably, the gating loop of the substrate-binding pocket of BtSULT1B1 exhibits an enlarged cavity compared to homologous SULT structures from Human and Mouse, facilitating the acceptance of bulky substrates/products. Through conservative amino acid analysis and site-directed mutagenesis, a variant with 3.6-fold enhanced activity, A44S was obtained, and its mechanism was further illustrated by molecular dynamics simulations. The findings of the chicken SULT1B1 in this study expand the knowledge of substrate binding of sulfotransferases, and offer a rational approach for engineering enzymes with improved activities for specific applications, provide molecular basis for the design of in vitro sulfation platform and drug development. - Source: PubMed
Publication date: 2026/01/15
Yan MingzhuZhang QianliYang ShuyaoYin LiangWang JiayingLiu WeidongGao JianLi Jinshan