Ask about this productRelated genes to: ZNF131 antibody
- Gene:
- ZNF131 NIH gene
- Name:
- zinc finger protein 131
- Previous symbol:
- -
- Synonyms:
- ZBTB35, pHZ-10
- Chromosome:
- 5p12
- Locus Type:
- gene with protein product
- Date approved:
- 1993-02-11
- Date modifiied:
- 2014-11-18
Related products to: ZNF131 antibody
Related articles to: ZNF131 antibody
- Exploring targeted therapies for esophageal squamous cell carcinoma (ESCC) remains challenging. Although investigating the roles and therapeutic applications of liquid-liquid phase separation (LLPS) is increasingly of interest, its relationship with ESCC remains unclear. After improving the assay for transposase-accessible chromatin using sequencing (ATAC-seq) protocol for limited-amount clinical samples, we unravel transcription factor AP-2 beta (TFAP2β) as a key downregulated transcription factor (TF) through combined chromatin accessibility and gene expression analyses with cancerous and paracancerous tissues from early-stage ESCC patients. TFAP2β undergoes condensation in the nucleus to bind the zinc finger protein 131 (ZNF131) promoter, thereby inhibiting ZNF131 expression and ESCC progression. The other two crucial downregulated TFs uncovered are incorporated into TFAP2β condensates to bind their corresponding target, suggesting that LLPS may be a hallmark of ESCC transcription. In addition, we obtained compound A6 that mediates intrinsically disordered region conformational changes to enhance TFAP2β condensation and specific ESCC suppression in cells, mice, and patient-derived organoids. Thus, we indicate an LLPS-mediated transcriptional mechanism and a potential therapeutic approach for ESCC. - Source: PubMed
Publication date: 2025/12/16
Deng ZhaominPu LuDeng KaiLiu WenchengZhang JifaZhang LiangMeng QianZhou WanwanJin HaoranXu DongqinQi ShaochongWu ZhihanMa YongxinLiu XingYao XuebiaoKe BowenKerr David JYang LiYang JinlinJiang Hao - PBK/TOPK is a mitotic kinase implicated in haematological and non-haematological cancers. Here we show that the key haemopoietic regulators Ikaros and Aiolos require PBK-mediated phosphorylation to dissociate from chromosomes in mitosis. Eviction of Ikaros is rapidly reversed by addition of the PBK-inhibitor OTS514, revealing dynamic regulation by kinase and phosphatase activities. To identify more PBK targets, we analysed loss of mitotic phosphorylation events in Pbk preB cells and performed proteomic comparisons on isolated mitotic chromosomes. Among a large pool of C2H2-zinc finger targets, PBK is essential for evicting the CCCTC-binding protein CTCF and zinc finger proteins encoded by Ikzf1, Ikzf3, Znf131 and Zbtb11. PBK-deficient cells were able to divide but showed altered chromatin accessibility and nucleosome positioning consistent with CTCF retention. Our studies reveal that PBK controls the dissociation of selected factors from condensing mitotic chromosomes and contributes to their compaction. - Source: PubMed
Publication date: 2025/09/23
Dimond AndrewGim Do HyeonIng-Simmons ElizabethWhilding ChadKramer Holger BDjeghloul DouniaMontoya AlexPatel BhavikCheriyamkunnel SherryBrown Karen EShliaha Pavel VVaquerizas Juan MMerkenschlager MatthiasFisher Amanda G - Circular RNAs (circRNAs) play critical roles in the occurrence of gastric cancer (GC). However, the roles of proteins encoded by circRNAs in GC remain largely unknown. This study aimed to investigate the role of ZNF131-354aa in GC. circZNF131 overexpression plasmids and short hairpin RNAs were used to overexpress and silence circZNF131 expression levels, respectively. Mass spectrometry, co-immunoprecipitation, and Western blotting were used to identify the circZNF131-encoded protein, named ZNF131-354aa. Chromatin immunoprecipitation assay was used to examine the DNA-binding activity of ZNF131-354aa. A subcutaneous tumor model was established in nude mice to examine the effects of ZNF131-354aa on GC growth. Overexpression of circZNF131 was found to inhibit the proliferation, migration and invasion of GC cells, while knockdown of circZNF131 had the opposite effect. Furthermore, immunoprecipitation and mass spectrometry verified that circZNF131 encoded a 40.5 kDa protein, ZNF131-354aa. ZNF131-354aa was shown to inhibit GC progression. ZNF131-354aa was found to be degraded by tripartite motif-containing 28 (TRIM28)-mediated ubiquitination. Moreover, ZNF131-354aa was found to promote E-cadherin and phosphatase and tensin homolog (PTEN) expression by interacting with the intron of the C-terminal binding protein 2 (CTBP2) gene and repressing its expression. In conclusion, ZNF131-354aa acts as a tumor suppressor in GC by inhibiting CTBP2 transcription. - Source: PubMed
Publication date: 2025/05/15
Wu XinxinLi ZheCao ChunliGe JiaxinShen XiaobanSun WeiliangGuo JunmingGuo Jie - Modern sedentary lifestyles are prevalent among individuals with osteoarthritis. However, direct evidence linking such behaviours as causative factors of osteoarthritis remain limited due to the presence of confounding variables. - Source: PubMed
Ho JustinMak Christopher Chi HangLau Lawrence Chun ManTo KendrickKhan Wasim - Both bulk RNA-sequencing and GEO database upon chemotherapy to non-small cell lung cancer (NSCLC) cells reveal that ZNF131 (Zinc Finger Protein 131) maybe a crucial transcriptional factor involved. However, it is a recently discovered protein with largely unexplored expression patterns and biological functions. Bioinformatics analyses and immunohistochemistry staining were assessed to detect both mRNA and protein levels of ZNF131 in NSCLC specimens and cell lines. Next, colony formation assay, MTT assay, EdU assay, transwell assay, flow cytometric analysis, sphere formation assay, western blotting analysis, mouse xenograft model analysis, immunofluorescence assay, and reverse transcriptase-polymerase chain reaction were performed to investigate the effect of ZNF131 interaction on proliferation, invasion, stemness, chemotherapy sensitivity. RNA-sequencing assay, RNA-microarray, and ChIP-sequencing assay were used to identify candidate downstream target genes. Further, liquid chromatography-tandem mass spectrometry analysis, GST pull-down assay, and immunoprecipitation assays were performed to evaluate the interactions between ZNF131, BACH1, and CUL3. ZNF131 was elevated in NSCLC specimens and cell lines, which significantly correlates with advanced TNM stage and poor prognosis in NSCLC patients. ZNF131 overexpression promotes NSCLC cell proliferation, invasion, and stemness both and . ZNF131 appears to target the RAD51 gene within a well-defined region (-668bp to -403bp) of the RAD51 promoter. ZNF131 contributes to RAD51-dependent homologous recombination (HR), primarily through its Zinc Finger and BTB domains. ZNF131-BACH1 interaction, mediated by their respective BTB domains, enhances the stability of both proteins, effectively preventing their ubiquitin-mediated degradation by CUL3. The ZNF131-BACH1 partnership significantly amplifies RAD51-dependent HR, resulting in expedited resistance to both radiotherapy and chemotherapy in NSCLC patients. Desoxyrhaponticin was shown to halt NSCLC progression and orchestrate a synergistic effect together with chemotherapy at least partially by targeting ZNF131. Our findings indicate that ZNF131 exhibits heightened expression in NSCLC, driving essential processes such as proliferation, invasion, and stemness by transcriptionally activating RAD51. The ZNF131-BACH1 interaction serves as a crucial enhancer, further boosting RAD51 transcription and ultimately accelerating therapy resistance in NSCLC. - Source: PubMed
Publication date: 2024/10/28
Fan MingweiLiu QuanboMa XiaowenJiang YufengWang YilongJia ShutingNie YingtongDeng RuoyiZhou PengchongZhang ShuyuJiang SiyuGuan MengyaoHou YuekangMiao YuanZhang YongZhang Xiupeng