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
- The Wnt/β-catenin pathway plays a critical role in colorectal cancer (CRC) development. The significance of Wnt/β-catenin in maintaining the stability of adult tissues and challenges in identifying suitable molecular targets have limited the application of targeting the Wnt/β-catenin pathway. As one of the Cullin RING Ligase 4 adapters, DNA damage-binding protein 1 (DDB1) - and CUL4 correlation factor 13 (DCAF13) appears strongly expressed in different tumors. Our findings confirm enhanced expression of DCAF13 in tissues of CRC origin and related cell. In colon cancer cells, DCAF13 regulated adenomatous polyposis coli membrane recruitment 2 (AMER2) through ubiquitination, DCAF13 deletion increased AMER2 expression, which inhibited Wnt/β-catenin activity, suppressing cell proliferation. This effect was further validated in mice with gut-specific DCAF13 knockout. The ubiquitin-proteasome system is a potential target for drug development and cancer treatment. Beta-propeller proteins, such as CRL4 adapter DCAFs, are easily targeted by drugs. DCAF-proteolysis-targeting chimeras (PROTACs) can overcome drug resistance and selectively target tumor drivers by leveraging the unique substrate specificity of the DCAF subunits. DCAF13 emerges as a promising target for CRC, acting via the DCAF13-AMER2-Wnt /β-catenin axis. - Source: PubMed
Publication date: 2026/07/13
Hua Yu-XinGao JieSun Qing-QingWang Xiao-MinWang Jing-YuZhou YuanZhang LongZhang Xian-ChaoXu Chun-WeiBao BingTao Su-PingXu YingPan Wei-WeiCheng Shu-QunLiu Sheng-Bing - Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with poor prognosis. DDB1 and CUL4 associated factor 13 (DCAF13) has been implicated in tumor progression, but its clinical relevance and biological function in PDAC remain unclear. - Source: PubMed
Publication date: 2026/06/26
Fan XiaofangZhao HengpingWu BinLv YichenChen WeiChen QiHu LingyuYu ShenjieWang JialeHe YahuiYu Jiaqi - 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