ANKRD37
- Known as:
- ANKRD37
- Catalog number:
- 001640A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANKRD37
Related genes to: ANKRD37
- Gene:
- ANKRD37 NIH gene
- Name:
- ankyrin repeat domain 37
- Previous symbol:
- -
- Synonyms:
- Lrp2bp
- Chromosome:
- 4q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-22
- Date modifiied:
- 2016-01-14
Related products to: ANKRD37
Related articles to: ANKRD37
- BACKGROUND: Prostate cancer (PCa) is a heterogeneous disease characterised by a highly complex cellular ecosystem within its tumour microenvironment (TME). However, the crosstalk patterns between tumour and immune cells remain poorly understood. METHODS: Single cell RNA sequencing, spatial transcriptomics and bulk RNA-seq data were integrated to explore key Tregs cells modules and genes involved in PCa processes in the tumour microenvironment. RESULTS: We found that the oxidative phosphorylation and apoptosis signaling pathways of Tregs cells in PCa patients is significantly activated. Tregs cells and Tumour cells may interact through PPIA-BSG ligand-receptor pairs to form an immunosuppressive microenvironment. Using high-dimensional weighted gene co-expression network analysis, we identified 6 key functional modules in Tregs from PCa. The spatial localization of these modules in tumor tissues was further validated using spatial transcriptomics data. Subsequent differential modules analysis revealed that the M2 module exhibited the most significant changes. A Cox proportional hazards model was then constructed based on this module, leading to the identification of 8 key prognostic genes, including ANKRD37, CHORDC1, DOK2, HSPA6, RGCC, SERPINH1, STIP1, and UBB. These genes hold promise as potential molecular markers for the diagnosis and prognostic evaluation of PCa. CONCLUSION: These findings reveal potential ligand-receptor interactions in the tumour microenvironment of PCa patients and key Tregs cell module genes involved in the formation of an immunosuppressive microenvironment. Targeting these cells and genes will help advance the treatment of PCa. - Source: PubMed
Publication date: 2026/02/23
Mei ZongweiChen ChenZhou JilongJiang Qing - Vibrational spectroscopy offers a rapid, cost-effective approach for studying biological systems. This study employs Fourier Transform Infrared (FTIR) spectroscopy, combined with Soft Independent Modeling of Class Analogy (SIMCA), to evaluate treatment outcomes for iron deficiency anemia (IDA). The model was built using spectra from healthy and anemic cells, then validated with cells treated with commonly used iron supplements. In calibration, 9 of 10 control and all IDA samples were correctly classified; 14 of 15 validation samples were identified as healthy. The model was applied to cells treated with protein-iron complexes. All samples treated with a 60:1 protein-iron ratio matched the healthy group, while 3 of 4 treated with a 10:1 ratio matched the IDA group. These results were further supported by iron-regulated gene expression of transferrin receptor (TFR) and (Ankyrin Repeat Domain 37) ANKRD37. FTIR coupled with chemometrics enables rapid assessment of functional effects and shows potential for screening functional ingredients in anemia-targeted food products. - Source: PubMed
Publication date: 2026/01/27
Dalyan EdaÇavdaroğlu ÇağrıÖzen BanuGüleç Şükrü - To investigate the biological behavior, differentiation ability, and differential gene expression of lymph node mesenchymal stem cells (MSCs) in patients with diffuse large B-cell lymphoma (DLBCL) and reactive lymphoid hyperplasia (RLH), providing a theoretical basis for clinical chemotherapy resistance. - Source: PubMed
Ma Yu-ShuoLiu Zhi-HeSun YangZhang Yu-HangWang Wen-QiuWang Li-ShengZhao Xia - Depression in patients with prostate cancer (PC) has become a significant public health issue. Given the high treatment failure rate and short life expectancy of patients with castration-resistant prostate cancer (CRPC), their risk of developing major depressive disorder (MDD) is significantly increased. However, the exact mechanisms of comorbidity between CRPC and MDD are not yet clear, and there is a lack of standardized intervention strategies to address this clinical issue. This study used bioinformatics methods combined with Mendelian randomization (MR) analysis to explore the molecular mechanisms of CRPC/MDD comorbidity and predict potential therapeutic drugs for this comorbidity. Three hub genes of the comorbidity (AUTS2, AOC1, ANKRD37) were identified, which have excellent diagnostic value in both diseases. AOC1 and ANKRD37 showed prognostic significance in CRPC, and the risk association of AUTS2 with MDD was also validated through MR analysis. The study also found that immune, inflammatory, androgen response pathways are key mechanisms of comorbidity, but the role of apoptosis should not be overlooked. The study further suggested that the JAK/STAT inhibitor WP1066 may be a potential drug for treating CRPC/MDD comorbidity, and this was validated through molecular docking. These findings not only provide a new perspective on the relationship between CRPC and MDD but also offer important clues for the development of treatment strategies. - Source: PubMed
Publication date: 2025/10/23
Xu LeiZhang MingqiangShi MenghuaLin XuyaoQin GuozhengFu WeiHuang Bin - The gastrointestinal epithelium relies on activation of the hypoxia-inducible factor (HIF) to promote cell survival and maintain bioenergetic homeostasis during hypoxia. While many pathogens can activate HIF, the effects of enteric protozoa on HIF activation in gastrointestinal epithelial cells remain unclear. Giardia duodenalis, a prevalent protozoan enteropathogen, causes intestinal barrier dysfunction characterized by epithelial malabsorption, mucus depletion, altered mucin glycosylation, and microbiota dysbiosis. Findings from the present study reveal an epithelial hypoxic signature upon Giardia infection. Human intestinal epithelial cells were exposed to vehicle or Giardia duodenalis isolate GS/M under normoxic (21% O) or hypoxic (1% O) conditions. In normoxia, infected cells displayed a time-dependent increase in HIF-1α protein expression, the oxygen-dependent subunit of HIF-1. In normoxia, Giardia infection upregulated HIF-1 target genes involved in cellular stress (i.e., VEGFA, ANKRD37, GADD45A) and glycolysis (i.e., HK2, LDHA). This was accompanied by changes in the abundance of glycolytic intermediates (i.e., glucose-6-phosphate, pyruvate, lactate). Although infection in hypoxia failed to augment the hypoxia-induced HIF-1α stabilization, HIF-1 target genes were still upregulated, albeit to a lesser degree. These findings indicate that Giardia induces a transient epithelial hypoxic response in normoxic conditions, revealing a hitherto unrecognized epithelial rescue response to this intestinal parasite. - Source: PubMed
Publication date: 2025/08/07
DeMichele EmilySosnowski OliviaFlood DarraghTaylor Cormac TLewis Ian AAllain ThibaultBuret Andre G