HSD3B7

Last update 08 May 2025

Basic Info

Synonyms

3 beta-hydroxysteroid dehydrogenase type 7, 3 beta-hydroxysteroid dehydrogenase type VII, 3-beta-HSD VII

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Introduction

The 3-beta-HSD enzymatic system plays a crucial role in the biosynthesis of all classes of hormonal steroids. HSD VII is active against four 7-alpha-hydroxylated sterols. Does not metabolize several different C(19/21) steroids as substrates. Involved in bile acid synthesis (PubMed:11067870). Plays a key role in cell positioning and movement in lymphoid tissues by mediating degradation of 7-alpha,25-dihydroxycholesterol (7-alpha,25-OHC): 7-alpha,25-OHC acts as a ligand for the G protein-coupled receptor GPR183/EBI2, a chemotactic receptor for a number of lymphoid cells (By similarity).

100 Clinical Results associated with HSD3B7

100 Translational Medicine associated with HSD3B7

0 Patents (Medical) associated with HSD3B7

182

Literatures (Medical) associated with HSD3B7

01 Dec 2024·Journal of Biological Chemistry

Substrate specificity and kinetic mechanism of 3β-hydroxy-Δ5-C27-steroid oxidoreductase

Article

Author: Penning, Trevor M. ; Marmorstein, Ronen ; Vogt, Austin ; Penning, Trevor M ; Gardner, Sarah M. ; Gardner, Sarah M

Cholesterol is a key sterol whose homeostasis is primarily maintained through bile acid metabolism. Proper bile acid formation is vital for nutrient and fat-soluble vitamin absorption and emulsification of lipids. Synthesis of bile acids occurs through two main pathways, both of which rely on 3β-hydroxy-Δ⁵-C₂₇-steroid oxidoreductase (HSD3B7) to begin epimerization of the 3β hydroxyl of cholesterol into its active 3α conformation. In this sequence, HSD3B7 catalyzes the dehydrogenation of the 3β-hydroxy group followed by isomerization of the Δ⁵-cholestene-3-one. These reactions are some of the many steps that transform cholesterol for either storage or secretion. HSD3B7 has distinct activity from other 3β-HSD family members leaving significant gaps in our understanding of its mode of catalysis and substrate specificity. In addition, the role of HSD3B7 in health and disease positions it as a metabolic vulnerability that could be harnessed as a therapeutic target. To this end, we evaluated the mechanism of HSD3B7 catalysis and reveal that HSD3B7 displays activity toward diverse 7α-hydroxylated oxysterols. HSD3B7 retains its catalytic efficiency toward these substrates, suggesting that its substrate binding pocket can withstand changes in polarity upon alterations to this hydrocarbon tail. Experiments aimed at determining substrate order are consistent with HSD3B7 catalyzing a sequential ordered bi-bi reaction mechanism with the binding of NAD⁺ followed by 7α-hydroxycholesterol to form a central complex. HSD3B7 bifunctional activity is dependent on membrane localization through a putative membrane-associated helix giving insight into potential regulation of enzyme activity. We found strong binding of the NADH product thought to activate the isomerization reaction. Homology models of HSD3B7 reveal a potential substrate pocket that allows for oxysterol binding, and mutagenesis was utilized to support this model. Together, these studies offer an understanding of substrate specificity and kinetic mechanism of HSD3B7, which can be exploited for future drug development.

05 Nov 2024·Microbiology Spectrum

VSV infection and LPS treatment alter serum bile acid profiles, bile acid biosynthesis, and bile acid receptors in mice

Article

Author: Bai, Yangjuan ; Dai, Xinhua ; Xu, Lei ; An, Yunfei ; Luo, Yan ; He, Lin ; Li, Yamei ; Zeng, Dongmei ; Zhang, Hua ; Wang, Chao

ABSTRACT Pathogen infections remain a significant public health problem worldwide. Accumulating evidence regarding the crosstalk between bile acid (BA) metabolism and immune response reveals that BA metabolism regulates host immunity and microbial pathogenesis, making it an attractive target for disease prevention and infection control. However, the effect of infection on circulating BA profiles, the biosynthesis-related enzymes, and their receptors remains to be depicted. Here, we investigated the effect of viral (vesicular stomatitis virus, VSV) and bacterial (lipopolysaccharide, LPS) infections on BA metabolism and signaling. Infection models were successfully established by intraperitoneally injecting VSV and LPS, respectively. VSV and LPS injection significantly changed the circulating BA profiles, with highly increased levels of taurine-conjugated BAs and significant decreases in unconjugated BAs. Consistent with the decreased levels of circulating cholic acid (CA) and chenodeoxycholic acid (CDCA), the expression of BA biosynthesis-related rate-limiting enzymes ( Cyp7a1 , Cyp27a1 , Cyp8b1, and Hsd3b7 ) were significantly reduced. Furthermore, hepatic and pulmonary BA receptors (BARs) expression varied in different infection models. LPS treatment had an extensive impact on tested hepatic and pulmonary BARs, resulting in the upregulation of TGR5, S1PR2, and VDR, while VSV infection only promoted VDR expression. Our study provides insights into the involvement of BA metabolism in the pathophysiology of infection, which may provide potential clues for targeting BA metabolism and BAR signaling to boost innate immunity and control infection. IMPORTANCEThis study focuses on the crosstalk between bile acid (BA) metabolism and immune response in VSV infection and LPS treatment models and depicts the effect of infection on circulating BA profiles, the biosynthesis-related enzymes, and their receptors. These findings provide insights into the effect of infection on BA metabolism and signaling, adding a more comprehensive understanding to the relationship between infection, BA metabolism and immune responses.

01 Nov 2024·Experimental Dermatology

Construction of ceRNA Network and Disease Diagnosis Model for Keloid Based on Tumor Suppressor ERRFI1

Article

Author: Yao, Wanting ; Chen, Pengsheng ; Lin, Xingong ; Wang, Chaoyang ; Hua, Xiaxinqiu ; Huang, Yanyan ; Zhou, Xianying ; Liu, Huiyong ; Xie, Rongrong ; Su, Qingfu

ABSTRACTThe aim of this study is to identify the key biomarker of keloid (KD) with significant diagnostic value and to construct the related competing endogenous RNA (ceRNA) network and disease diagnostic model to provide new ideas for the early diagnosis and prevention of KD. Public databases were used to identify the key gene of KD. Enrichment analysis and immune cell infiltration (ICI) analysis revealed its functional and immune characteristics. Then, a ceRNA network was constructed to explore the potential pathways of it. Random forest (RF) analysis was applied to construct a predictive model for the disease diagnosis of KD. Finally, immunohistochemistry (IHC) and RT‐qPCR were used to verify the differential expression of key gene. ERRFI1 was identified as a key biomarker in KD and was lowly expressed in KD. The ceRNA network revealed that H0TAIRM1‐has‐miR‐148a‐3p‐ERRFI1 may be a potential pathway in KD. Finally, a 2‐gene diagnostic prediction model (ERRFI1, HSD3B7) was constructed and externally validated and the results suggested that the model had good diagnostic performance. ERRFI1 is a downregulated gene in KD and is expected to be a promising predictive marker and disease diagnostic gene. ICI may play a role in the progression of KD. The ceRNA network may provide new clues to the potential pathogenesis of KD. Finally, the new KD diagnostic model could be an effective tool for assessing the risk of KD development.

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HSD3B7

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