Ask about this productRelated genes to: WDSOF1 antibody
- Gene:
- DCAF13 NIH gene
- Name:
- DDB1 and CUL4 associated factor 13
- Previous symbol:
- WDSOF1
- Synonyms:
- DKFZP564O0463, Gm83, HSPC064, Sof1
- Chromosome:
- 8q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-26
- Date modifiied:
- 2017-05-26
Related products to: WDSOF1 antibody
Related articles to: WDSOF1 antibody
- Colorectal cancer (CRC) remains one of the most common and lethal malignancies worldwide, with limited effective biomarkers for predicting prognosis and guiding immunotherapy response. The present study aimed to investigate the potential of DDB1- and CUL4-associated factor 13 (DCAF13) as a biomarker for CRC. Bioinformatics analyses were performed using public datasets from The Cancer Genome Atlas and Gene Expression Omnibus; ESTIMATE, CIBERSORT, immune checkpoint, TIDE score and Kaplan-Meier survival analyses were performed to assess the prognostic value and implications of DCAF13 expression in CRC. findings were validated through immunohistochemistry (IHC), cell-based assays and transcriptomic analysis. Increased DCAF13 expression levels were associated with reduced overall survival in patients with CRC based on the bioinformatics analysis, and this was validated using samples from patients using IHC. Immune profiling demonstrated an increased infiltration of M0 and M1 macrophages, activation of mast cells, neutrophils and CD4 memory T cells in the DCAF13-high expression group compared with the DCAF13-low expression group. DCAF13 expression was correlated with immune modulators and checkpoint genes. High DCAF13 expression was associated with lower TIDE scores. assays and transcriptomic analyses confirmed the pro-tumourigenic effects of DCAF13, which demonstrated roles in regulating cell proliferation, migration, clonogenicity, adhesion, metastasis, epithelial-to-mesenchymal transition and homologous recombination in CRC cells. The present study demonstrated that DCAF13 was upregulated in CRC and served a role in tumour progression, thus providing novel insights into the pro-tumourigenic functions of DCAF13 and its potential as a critical regulator in CRC. - Source: PubMed
Publication date: 2026/02/25
Zhang WenqiZhang RongrongJia MengxuanLan ShutingLiu FangyuanJin QinSu LiyaLiu Gang - Hematopoietic stem cells (HSCs) sustain lifelong blood production by balancing self-renewal and differentiation. The mechanisms regulating HSC homeostasis, particularly those involving ribosome biogenesis, remain incompletely understood. Here, we identify DCAF13 as a critical regulator of HSC maintenance by stabilizing RRS1, a key factor in ribosome biogenesis. Conditional deletion of Dcaf13 in murine hematopoietic cells results in severe pancytopenia, rapid mortality, and complete HSC depletion in both fetal and adult hematopoietic compartments. We show that DCAF13 deficiency disrupts ribosome assembly and protein synthesis, selectively affecting the translation of mRNAs from genes involved in myeloid differentiation, chromatin remodeling, and erythroid homeostasis. DCAF13 directly binds RRS1 and catalyzes its K27-linked polyubiquitination, a non-degradative post-translational modification that enhances RRS1 protein stability.While Dcaf13 deletion activates the p53 pathway, Trp53 ablation only partially restores HSC numbers and cell cycle progression, and does not prevent apoptosis and hematopoietic failure, indicating the involvement of both p53-dependent and p53-independent mechanisms. These findings establish a DCAF13-RRS1 axis essential for HSC function, in which DCAF13 acts as an essential regulator of ribosome biogenesis. This work provides molecular insights into the pathogenesis of hematopoietic disorders and ribosomopathies. - Source: PubMed
Publication date: 2026/03/06
Li MengkeWu YuxinZhou ShuaiTang PeipeiWei JiamingLiu LingWang ZhenyiShi DeyangYuan ShengnanZhang QingyuWang ShihuiZhang QingZhao HuanZhang RuiWang YingyingYang ShiweiChen XiangliShi XiaojingLiu GuangzhiZhang YuweiLi JinmingZhang Xu DongThorne Rick FWei DongpingZhu ZuminChen Song - [This corrects the article DOI: 10.1016/j.omtn.2017.12.010.]. - Source: PubMed
Publication date: 2025/12/30
Chen ZhiZhang WeiJiang KaibiaoChen BinWang KunLao LifengHou CanglongWang FeiZhang CaiguoShen Hongxing - Craniofacial morphogenesis requires precisely coordinated proliferation, migration, and differentiation of cranial neural crest (CNC) cells during development. Although DDB1- and CUL4-associated factor 13 (DCAF13) is known to play critical roles in early embryogenesis and tumorigenesis, its function in neural crest development remains unknown. Here, we identify a novel role for DCAF13 in craniofacial development. Conditional knockout of Dcaf13 in neural crest lineages resulted in severe craniofacial malformations characterized by impaired skeletal growth and differentiation. Mechanistically, DCAF13 deficiency in mesenchymal cells led to PTEN accumulation, a key negative regulator of PI3K/AKT signaling, thereby suppressing proliferation and differentiation of CNC-derived cells. Our findings establish DCAF13 as a crucial regulator of craniofacial morphogenesis through its control of the PTEN-PI3K/AKT signaling axis, which orchestrates neural crest cell proliferation and differentiation. - Source: PubMed
Liu LiXu XiaomingHuang PeijunWang WenhangLin YanhuiSong PandiCui XinranLv JunyaoWang FeixueYuman LinZhu ZiqingSun WenjingShen Jingling - This study aimed to identify a novel prognostic signature derived from an EGFR Tyrosine kinase inhibitors (TKI-resistant) macrophage subpopulation and to evaluate its clinical and therapeutic relevance in HCC. We utilized single-cell RNA sequencing data from HCC patients. An EGFR-TKI resistance score was calculated across all cell types. Macrophages, which exhibited the highest resistance score, were sub-clustered to identify the most resistant subpopulation. Marker genes from this sub-cluster were intersected with differentially expressed genes (DEGs) from the TCGA-LIHC cohort. A robust prognostic model was constructed. The model's performance was rigorously validated, and the signature was further characterized through multi-omics analysis and its correlation with immune checkpoint blockade (ICB) response and drug sensitivity. scRNA-seq analysis unequivocally identified macrophages as possessing the highest EGFR-TKI resistance score. We identified seven key prognostic genes: SLC41A3, DCAF13, PPM1G, NDC80, FAM83D, FUCA2, and UQCRH. A risk model built on these seven genes effectively stratified patients into high- and low-risk groups with significantly different overall survival (OS) in the TCGA cohort, a finding successfully validated in the independent GSE76427 cohort. A clinical nomogram integrating the risk score demonstrated excellent predictive accuracy, with AUC values for 1-, 3-, and 5-year OS of 0.816, 0.781, and 0.799, respectively. The low-risk group was associated with a favorable immune-infiltrated phenotype and was predicted to be more sensitive to immunotherapy. Conversely, the high-risk group exhibited distinct genomic features and was predicted to be more sensitive to specific targeted agents, including Navitoclax and Sorafenib. We identified and validated a novel 7-gene prognostic signature derived from a subpopulation of EGFR-TKI-resistant macrophages. This signature accurately predicts patient survival, offers insights into the molecular mechanisms of therapy resistance in HCC, and provides a promising tool for improved patient stratification and the development of personalized treatment strategies. - Source: PubMed
Li XiaominLi ZhilongZhai JinfangZou Binbin