Ask about this productRelated genes to: DHCR24 Blocking Peptide
- Gene:
- DHCR24 NIH gene
- Name:
- 24-dehydrocholesterol reductase
- Previous symbol:
- DCE
- Synonyms:
- KIAA0018, seladin-1
- Chromosome:
- 1p32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-27
- Date modifiied:
- 2019-04-23
Related products to: DHCR24 Blocking Peptide
Related articles to: DHCR24 Blocking Peptide
- Follicular development in the chicken ovary is a critical biological process that influences egg-laying performance and directly impacts poultry production efficiency. However, elucidating the dynamic regulatory networks involving key genes and transcription factors (TFs) during follicular development remains a major challenge. In this study, we performed a comprehensive transcriptomic analysis across six follicular stages - small white follicles, large white follicles, small yellow follicles, and three hierarchical follicles - in high and low egg-laying hens. We identified a set of essential genes and pathways closely associated with egg-laying performance, including steroid hormone biosynthesis (e.g., CYP19A1, HSD3B1) and steroid biosynthesis (e.g., CEL, DHCR24, FDFT1), which play central roles in lipid metabolism, amino acid biosynthesis, and signal transduction. Pearson correlation analysis further enabled the construction of stage-specific TF regulatory networks, highlighting pivotal TFs such as FOXO1 and HOXA10 in follicular development. Additionally, two key genes - FABP3 and ENSGALG00000054605 were identified as significantly associated with reproductive traits, showing negative correlations with egg-laying rate and age at first egg, respectively. Their differential expression trends between high and low egg-laying hens suggest potential roles in regulating laying performance and sexual maturity. Importantly, based on transcriptome predictions, we conducted functional validation of BMPR1B, a core receptor in the TGF-beta signaling pathway identified as a major regulatory hub during follicle hierarchy formation. In vitro experiments demonstrated that BMPR1B promotes granulosa-cell proliferation, confirming its essential role in follicle maturation. Collectively, this study provides new insights into the molecular regulation of chicken follicular development by integrating multi-stage transcriptomics with functional validation. The findings offer valuable molecular markers - including BMPR1B, FABP3, and ENSGALG00000054605 and potential targets for genetic improvement in poultry breeding, while also contributing to broader understanding of vertebrate reproductive biology. - Source: PubMed
Publication date: 2026/04/12
Bai YingLi HongtaiJi XiaoyuWang WeiShao TianjiaoChu QinYuan RuiWang YuxuanLiu Lei - Dysregulated lipid metabolism and chronic inflammation are hallmarks of aging, yet their interplay in age-related tissue disorders remains poorly defined. In the ocular surface, age-related meibomian gland dysfunction (ARMGD) is highly prevalent but mechanistically unclear, leading to significant visual impairment without targeted therapies. To identify key molecular drivers of ARMGD, we performed integrated multi-omics screening of aging mouse meibomian glands (MGs) and identified DHCR24, a key cholesterol metabolism enzyme, as a critical regulator of gland homeostasis. Single-cell sequencing identified age-associated downregulation of predominantly in meibocytes. Based on this finding, we generated a meibocyte-specific knockout (cKO) model, which exhibited typical ARMGD pathology including glandular atrophy, disrupted lipid homeostasis, and inflammatory activation. Further studies using SZ95 sebocytes demonstrated that DHCR24 deficiency induces mitochondrial dysfunction and cytosolic mitochondrial DNA (mtDNA) leakage, triggering cGAS/STING-dependent inflammatory senescence. Notably, AAV-mediated restoration of DHCR24 in mice reversed age-related gland pathology. Our findings establish DHCR24 as a dual-target regulator that maintains cholesterol metabolic homeostasis while suppressing mtDNA-driven inflammation via the cGAS-STING pathway, highlighting its therapeutic potential for ARMGD and related disorders characterized by lipid-inflammatory imbalance. - Source: PubMed
Publication date: 2026/03/28
Cai YuchenZhou TianyiSun JiamingCai XueyaoShi WenjunChen JunzhaoZouboulis Christos CSun HaoFu YaoChen Liangbo - To investigate the role and mechanism of DHCR24 in chemoresistance of ovarian cancer and to identify potential therapeutic targets for overcoming treatment resistance. - Source: PubMed
Publication date: 2026/03/17
Fu XinWang ZhaosongYang ZhiningXu YueDong QiupingCui YanfenWang Ke - - Source: PubMed
Publication date: 2026/04/15
Zhu HongLi ShunYang YiZhang ShiqingWang YinggeXiong Tianqing - Bladder cancer (BLCA) is a growing health burden with rising incidence and limited therapeutic options. To define the role of the Tripartite Motif (TRIM) family in BLCA, we integrated multi-cohort transcriptomic analyses with functional and mechanistic validation. TRIM28 was identified as the most consistently upregulated TRIM member in BLCA and correlated with poor prognosis. TRIM28 depletion suppressed, whereas its overexpression enhanced, BLCA cell proliferation. Mechanistically, TRIM28 directly bound to PPARG and acted as a SUMO E3 ligase to catalyze SUMOylation of PPARG at Lys94 within a noncanonical YKYD motif. This modification impaired PPARG recognition by the E3 ubiquitin ligase STUB1, reduced ubiquitin-proteasome degradation, and stabilized PPARG protein. Stabilized PPARG transcriptionally activated cholesterol biosynthetic genes, including DHCR7 and DHCR24, reprogramming cholesterol metabolism to promote BLCA progression. In summary, we identify a TRIM28-PPARG SUMO-ubiquitin crosstalk axis that drives metabolic remodeling and tumor growth in BLCA, highlighting TRIM28-mediated PPARG SUMOylation as a potential therapeutic target for metabolic intervention. - Source: PubMed
Publication date: 2026/04/13
Fan XuefengLi ZexuanGao QiongqiongHuang PeizhengLi ZheyuLu DongmeiWang LeiXiang PingHuang TaoShen DexinXiao Jun