DHX37
- Known as:
- DHX37
- Catalog number:
- ARP36514_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- DHX37
Related genes to: DHX37
- Gene:
- DHX37 NIH gene
- Name:
- DEAH-box helicase 37
- Previous symbol:
- DDX37
- Synonyms:
- KIAA1517, MGC4322, MGC2695, Dhr1
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-21
- Date modifiied:
- 2017-05-26
Related products to: DHX37
Related articles to: DHX37
- DEAH-box RNA helicase 37 (DHX37) is a highly conserved RNA helicase involved in ribosome biogenesis, RNA metabolism and immune regulation. Dysregulation of RNA helicases has been implicated in tumourigenesis; however, the clinical significance of DHX37 expression in tumours is still emerging and requires further study. This study investigated the expression of DHX37 in large breast and ovarian cancer patient cohorts using immunohistochemistry in 1512 breast and 420 ovarian cancer cases and complementary transcriptomic datasets. In breast cancer, low cytoplasmic DHX37 protein expression was significantly associated with adverse clinicopathological parameters including larger tumour size, higher grade, lymphovascular invasion and positive nodal status (all P < 0.001). Low DHX37 expression was associated with poor breast cancer-specific survival (P < 0.001), particularly among oestrogen receptor-positive patients. In ovarian cancer, low DHX37 expression was associated with lower FIGO stage, absence of residual disease and improved overall survival (P = 0.013). DHX37 shows contrasting prognostic associations in breast and ovarian cancer, suggesting context-dependent biological functions. Reduced DHX37 expression may promote tumour progression in ER-positive breast cancer, but is associated with favourable outcomes in ovarian cancer. These findings highlight DHX37 as a potential prognostic biomarker and underscore the need for functional studies to elucidate its mechanistic role in tumour biology and immune modulation. - Source: PubMed
Publication date: 2026/05/18
Ndeke DenysSam SandraPolchai NuanphanAlshammari KhalidGreener Megan RMarak Tangkam RJoyce JimmyHenman MaisieDeen SuhaGreen Andrew REllis Ian ORakha Emad AMartin Stewart GStorr Sarah J - The clinical phenotype and pathogenic mechanism of 46,XY disorders of sex development (DSD) are complex, and several pathogenic variants are identified by next-generation sequencing. However, these variants currently require additional interpretation and validation prior to their application in 46,XY DSD diagnosis and clinical guidance. - Source: PubMed
Publication date: 2026/04/29
Li CuiYang BinyuLi XuZhen ShuaiLiu XiaogangLi PingpingChen WeiWang XiaoyanXue Mei - - Source: PubMed
Publication date: 2026/04/27
Chen RuoxiDong ShiliangZhu XuanruChu XiaodongLiu Hongwei - The testicular microenvironment, with Sertoli cells as a key component, plays a pivotal role in spermatogenesis. DHX37, a member of the DEAH-box family of RNA helicases, has been identified as a pathogenic gene in 46, XY disorders of sex development (DSD), underscoring its potential significance in testicular development. Here, we focus on elucidating the role of Dhx37 in maintaining Sertoli-cell survival. RIP-seq and RNAi-RNA-seq reveal that Dhx37 safeguards nucleolar integrity and PI3K-AKT signaling, suppresses p53-driven apoptosis, and its loss triggers pro-apoptotic splicing. Cell-specific Dhx37 knockout mice (Dhx37) were subsequently generated to investigate the function of Dhx37 in testicular development. In the Dhx37 mice, we observed pronounced defects, including diminished testicular volume, lower testosterone levels, and marked vacuolization of the seminiferous tubules. Immunofluorescence staining revealed disruptions in both Sertoli and germ cell compartments, characterized by reduced cell proliferation and elevated apoptosis. The snRNA-seq disclosed marked changes in the expression of genes governing apoptosis and proliferation, findings that were further validated through qRT-PCR and Western blotting. In this study, we identified Dhx37 as a pivotal determinant of nucleolar architecture in murine testicular Sertoli cells. Preservation of the nucleolus safeguards supporting normal testicular morphogenesis. Graphical Abstract Schematic illustrating the proposed mechanisms by which Dhx37 deficiency affects testicular development and spermatogenesis. In normal testes (left), Sertoli cells maintain a well-organized nucleolus with intact nucleolar structures, including Granular Component (GC), Fibrillar Center (FC), Dense Fibrillar Component (DFC). In this context, MDM2 interacts with P53, preventing the accumulation of P53 and inhibiting apoptosis, thereby supporting normal testicular architecture and spermatogenesis. However, in Dhx37 mice (right), testicular volume is reduced, and seminiferous tubules undergo atrophy due to nucleolar stress in Sertoli cells. The disruption of nucleolar structure leads to the export of FBL from the nucleolus, where it binds to MDM2. This disruption is accompanied by downregulation of key factors in the PI3K pathway (Fgf2, Lpar2, PI3KR2, PI3KR5) and upregulation of the P53 pathway, culminating in apoptosis. As a result, Dhx37 deficiency impairs Sertoli cell function, leading to a failure in supporting testicular development and spermatogenesis. Created with BioGDP.com. - Source: PubMed
Publication date: 2026/01/14
Jiang YuqingChen JialiRen YanshuangPeng WenyuanShen WanjunZhang YingyuLiu JieFu LiujunLi LipingMa YujinJiang HongweiPeng Huifang - Variations in Sex Characteristics (VSC), also referred to as intersex traits or Differences of Sex Development (DSD), encompass diverse chromosomal, gonadal, and anatomical sex traits. The full spectrum of VSC remains under-recognized, partly due to diagnostic approaches that prioritize classic VSC/DSD conditions. We developed a 103-term Focused Genitourinary VSC Glossary (FGV Glossary) using Human Phenotype Ontology (HPO) terms and screened 8359 Online Mendelian Inheritance in Man (OMIM) entries for inclusion. Associated genes were evaluated for coverage in clinical DSD panels and assessed in ClinVar for pathogenic variants linked to VSC/DSD phenotypes. We identified 539 OMIM entries (~6.4%) with at least one FGV Glossary term. These entries were enriched for genitourinary, breast, and endocrine phenotypes. Of 56 high-confidence VSC/DSD genes identified, 23 (41%) were absent from a current representative DSD gene panel. A curated ClinVar review showed that 3 of these 23 genes (DHX37, SPRY4, TBX3) had pathogenic variants clearly associated with VSC/DSD traits. Genome-wide sequencing should be prioritized in VSC/DSD diagnostics, consistent with current best practices, to improve diagnostic yield and guide comprehensive, multidisciplinary clinical care. - Source: PubMed
Publication date: 2025/12/29
Ragno LeahPyle Tucker Louise C