预约演示

更新于：2025-05-07

DHCR24

更新于：2025-05-07

基本信息

别名

24-dehydrocholesterol reductase、3-beta-hydroxysterol Delta-24-reductase、DCE

+ [5]

简介

Catalyzes the reduction of the delta-24 double bond of sterol intermediates during cholesterol biosynthesis (PubMed:11519011, PubMed:21671375, PubMed:22178193, PubMed:25637936). In addition to its cholesterol-synthesizing activity, can protect cells from oxidative stress by reducing caspase 3 activity during apoptosis induced by oxidative stress (PubMed:11007892, PubMed:22010141). Also protects against amyloid-beta peptide-induced apoptosis (PubMed:11007892).

关联

项与 DHCR24 相关的药物

miR-370-3p

靶点

DHCR24

作用机制

DHCR24 inhibitors

在研机构

深圳市茵冠生物科技有限公司

原研机构

深圳市茵冠生物科技有限公司

在研适应症

宫颈癌

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

CN118973585

专利挖掘

靶点

DHCR24

作用机制

DHCR24 inhibitors

在研机构

Academisch Ziekenhuis Maastricht

原研机构

Academisch Ziekenhuis Maastricht

在研适应症

心血管疾病 [+4]

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 DHCR24 相关的临床结果

登录后查看更多信息

100 项与 DHCR24 相关的转化医学

登录后查看更多信息

0 项与 DHCR24 相关的专利（医药）

登录后查看更多信息

477

项与 DHCR24 相关的文献（医药）

2025-05-01·International Journal of Biological Macromolecules

3β-hydroxysteroid-Δ24 reductase integrates cholesterol metabolism and innate immune to promote PRRSV replication

Article

作者: Li, Yong ; Liu, Yijia ; Yan, Yuchao ; Cui, Daqing ; Jie, Qun ; Hua, Depin ; Li, Changyan ; Zhang, Junyang ; Huang, Jinhai

Cholesterol metabolism is a strategy used by PRRSV to inhibit host antiviral innate immunity. However, the key enzymes or the natural products and mechanisms involved have not been well elucidated. Here, we show that PRRSV infection upregulated DHCR24, the rate-limiting enzyme in the cholesterol synthesis pathway, to increase virus proliferation. We further elucidated that PRRSV Nsp4 interacts with the FAD domain of DHCR24, promoting its expression and increasing cellular cholesterol levels. In addition, U18666A treatment inhibited DHCR24 enzyme activity, significantly reduced cell cholesterol content and PRRSV replication, and exogenous cholesterol supplementation could rescued this effect. We also found that DHCR24 is a negative regulator of type I interferon (IFN-I) production upon viral infection. Mechanistically, DHCR24 interacts with TBK1 and disrupts the interaction of TBK1-IRF3, thereby inhibiting IRF3 phosphorylation and nuclear translocation. Taken together, these findings elucidate that DHCR24 is utilized by PRRSV to regulate host cholesterol content, inhibit the innate immune response, and promote virus proliferation.

2025-04-01·Insect Science

In vivo functional analysis of the cotton bollworm Helicoverpa armigera 24‐dehydrocholesterol reductase (HaDHCR24) in phytosterol metabolism

Article

作者: Ren, Jinchan ; Feng, Yuanze ; Fan, Yongliang ; Liu, Tong‐Xian ; Jing, Xiangfeng ; Yang, Zhen ; Lu, Shuning

AbstractInsects have to obtain sterols from food due to the inability to synthesize this essential nutrient de novo. For lepidopteran insects, they can convert a variety of phytosterols into cholesterol to meet their growth needs. The final step of the cholesterol biosynthesis is the metabolism of desmosterol catalyzed by 24‐dehydrocholesterol reductase (DHCR24). In this study, we identified a DHCR24 homolog in the cotton bollworm Helicoverpa armigera, designated as H. armigera 24‐dehydrocholesterol reductase (HaDHCR24)‐1. The quantitative expression analyses indicated that HaDHCR24‐1 was highly enriched in the midgut where dietary sterol uptake occurs. Compared to the control, the DHCR24‐1 mutant larvae generated by clustered regularly interspaced palindromic repeats (CRISPR) / CRISPR‐associated nuclease 9 technology accumulated more desmosterol in the gut, while the content of cholesterol was significantly reduced. A similar phenomenon was observed when the DHCR24 inhibitor, amiodarone, was applied to the insects. Moreover, DHCR24‐1 played an important role for the usage of β‐sitosterol, a major sterol in plants, in H. armigera, and loss of function of DHCR24‐1 resulted in higher mortality on β‐sitosterol. However, the DHCR24 homolog does not necessarily exist in the genomes of all insects. The loss of this gene occurred more frequently in the insects feeding on animals, which further support the role of DHCR24‐1 in using phytosterols. This gene may have important potential in developing new strategies to control herbivory pests in Lepidoptera and other insect orders.

2025-01-17·Stem Cells Translational Medicine

Human umbilical cord mesenchymal stem cells small extracellular vesicles-derived miR-370-3p inhibits cervical precancerous lesions by targeting DHCR24

Article

作者: Yang, Huan ; Ding, Lu ; Shi, Ming ; Zhang, Chi ; Li, Tian ; Gao, Tianshun ; Zhang, Changlin ; Deng, David Y B ; Sun, Yazhou ; Liu, Lixiang ; Li, Weizhao

AbstractBackgroundCervical cancer is often caused by persistent high-risk human papillomavirus (HPV) infection, causing precancerous lesions. Human umbilical cord mesenchymal stem cells-derived small extracellular vesicles (hucMSC-sEV) exhibit diverse effects on tumors. This study investigates hucMSC-sEV, the impact and mechanisms on HPV-positive cervical precancerous lesion cells to provide new treatment insights.Materials and MethodsWe previously obtained hucMSC and hucMSC-sEV. In vitro experiments evaluated hucMSC-sEV effects on the proliferation and migration of S12 cells (derived from cervical precancerous lesions). Bioinformatics identified key microRNA components, and their impact on S12 cell proliferation and migration was investigated. The target gene of the microRNA component was predicted and confirmed via bioinformatics and dual-luciferase reporter assays. Lentiviral systems overexpressed target gene in S12 cells to examine the effects on microRNA impacts. SH-42 inhibitor was used to investigate target gene treatment potential. Immunohistochemistry assessed target gene expression in cervical precancerous lesions tissue.ResultshucMSC-sEV significantly inhibited S12 cell proliferation and migration. Bioinformatics identified miR-370-3p as an effective cargo, which also suppressed S12 cell proliferation and migration. miR-370-3p was confirmed targeting DHCR24 (24-Dehydrocholesterol Reductase). DHCR24 overexpression reversed miR-370-3p’s inhibitory effects, while SH-42 counteracted DHCR24 overexpression’s promoting effects. Clinical specimen analysis supported these findings, demonstrating a positive correlation between DHCR24 protein expression and cervical precancerous lesions’ progression.ConclusionshucMSC-sEV inhibits S12 cell proliferation and migration, mediated by miR-370-3p targeting DHCR24 to regulate cellular cholesterol content. DHCR24 inhibition reduces the cholesterol level and cell functions, suggesting its potential as a therapeutic target in cervical precancerous lesions.