PDLIM4 Antibody (Center)
- Known as:
- PDLIM4 Antibody (Center)
- Catalog number:
- AP17994c-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- PDLIM4 Antibody (Center)
Related genes to: PDLIM4 Antibody (Center)
- Gene:
- PDLIM4 NIH gene
- Name:
- PDZ and LIM domain 4
- Previous symbol:
- -
- Synonyms:
- RIL
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-12
- Date modifiied:
- 2014-11-19
Related products to: PDLIM4 Antibody (Center)
Related articles to: PDLIM4 Antibody (Center)
- The prognosis for advanced colorectal cancer (CRC) remains poor, and 5-fluorouracil (5-FU)-based chemotherapy is the primary treatment option. Understanding the mechanisms that limit the effectiveness of this therapy is therefore clinically important. However, the molecular drivers of acquired chemotherapy resistance in advanced CRC are not fully understood. Here we show that expression of PDZ-LIM domain-containing protein 4 (PDLIM4) is significantly upregulated following neoadjuvant chemotherapy in patients with advanced CRC, and that its expression level is closely associated with patient prognosis. PDLIM4 promotes acquired resistance to 5-FU by enhancing the stemness, anti-apoptotic capacity, and drug efflux of colorectal cancer stem cells. Mechanistically, PDLIM4 facilitates the accumulation of sphingolipids, particularly sphingomyelin, and regulates the PI3K/Akt signaling pathway. These findings identify PDLIM4 as a potential biomarker and therapeutic target for overcoming chemoresistance in advanced colorectal cancer, opening new avenues for future treatment strategies. - Source: PubMed
Publication date: 2026/07/11
Song YingqiuXiong ZhiyongZhou DaguiRen Ya-HanLiu QianhuiLu XuWang JinyangZhu ZiyanTang YongshengLi HaoKang ManqiuLi LingYang XiaofengWang TiantianJia ChangchangFang Jiafeng - Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in reproductive-age women, characterized by limited therapeutic options that address its underlying mechanisms. This study aimed to identify novel druggable protein targets for PCOS using a multi-omics integrative approach. Proteome-wide association studies (PWAS)-Mendelian randomization (MR) and summary-based MR (SMR) analyses were performed on large-scale plasma proteomics data from deCODE and UK Biobank cohorts, integrated with PCOS genome-wide association study (GWAS) summary statistics to screen for causal associations. Validation and prioritization involved Bayesian colocalization, transcriptome-wide association studies (TWAS), methylome-wide association studies (MWAS), and Gene Expression Omnibus (GEO) differential expression analysis. Biological mechanisms, druggability, and potential side effects were evaluated through protein-protein interaction networks, Gene Ontology/Kyoto Encyclopedia of Genes and Genomes enrichment, single-cell expression profiling, drug prediction via DSigDB, molecular docking, and MR-phenome-wide association studies (PheWAS). Fifty-seven candidate proteins were nominally associated with PCOS risk. FSHB met the stringent high-colocalization criterion (PPH4 > 0.8), whereas THOP1, CAMKK1, PDLIM4, and ERBB4 met the broader colocalization criterion (PPH3 + PPH4 > 0.8). After robustness filtering, ERBB4 was retained as a secondary candidate, and THOP1, FSHB, CAMKK1, and PDLIM4 were prioritized as tier 1 targets, with pathway analyses implicating lysosomal and MAPK-related processes. Drug predictions identified compounds such as Triciribine and 1,3,5(10)-Estratriene-2,3-diol-17-one, demonstrating favorable docking affinities (e.g., - 9.7 kcal/mol for FSHB). MR-PheWAS indicated limited side effects for most targets, except for FSHB-associated reproductive risks. These findings offer robust evidence for prioritized therapeutic targets, facilitating advancements in precision medicine and drug development for PCOS. - Source: PubMed
Publication date: 2026/05/22
Xiao ZhiyongZhang XinZhang YuxinLiu JiajiaZheng XiaoyanLai RuiYang HanWu JieYang Jie - STAT transcription factors are activated by tyrosine phosphorylation after cytokine stimulation and are critical for the differentiation of T-helper (Th) cells into particular Th lineage subsets. How STAT-mediated Th cell differentiation is negatively regulated, however, is not fully understood. Here, we report that PDLIM4 binds to STAT3, 4, and 6 and suppresses gene activation mediated by these STATs. PDLIM4 acts as an adaptor that recruits PTP-BL, a protein tyrosine phosphatase, through its LIM domain, facilitating dephosphorylation of STAT proteins. PDLIM4-deficiency in CD4+ T cells resulted in augmented tyrosine phosphorylation of these STAT proteins and consequently enhanced Th1, Th2 and Th17 cell differentiation, suggesting that PDLIM4 regulates the differentiation of multiple lineages of Th cells by suppressing STAT signaling. We further found that a non-synonymous single-nucleotide polymorphism (nsSNP) in PDLIM4, which causes the substitution of a glycine residue with a cysteine in the LIM domain, is associated with susceptibility to rheumatoid arthritis and Graves' disease, both of which are known to be Th17 cell-driven autoimmune diseases. Notably, PDLIM4 containing this amino acid substitution in the LIM domain showed reduced binding to PTP-BL and was therefore partially impaired in its ability to dephosphorylate STAT3 and suppress STAT3 signaling. Our findings define an essential role of PDLIM4 in negatively regulating STAT-mediated T helper cell differentiation and preventing the onset of human autoimmune diseases. - Source: PubMed
Publication date: 2026/04/24
Jodo AyaNakahira MasakiyoKochi YutaSugimoto-Ishige AkikoKaisho TsuneyasuTanaka Takashi - Breast cancer (BC) incidence continues to rise, and recurrence and metastasis remain major contributors to mortality. The epithelial-mesenchymal transition (EMT), associated with the acquisition of invasive functions by epithelial cells, also promotes resistance to anticancer therapies. Here, an EMT-based prognostic model was developed to enhance BC outcome prediction. - Source: PubMed
Publication date: 2026/03/15
Wu ZizhengZheng JieMen ShuaiSui ShuangruiYan WeitaoLiu YinfengHan Meng - - Source: PubMed
Publication date: 2026/02/26
Zhu ChaoChen MengFan LinweiWang YuLiu MengweiKang GuiyuYin FangTang HongHe YunZhang SifanZeng LindaLiu WeiYu KuaiLe Aiping