PDLIM4 _ RIL
- Known as:
- PDLIM4 _ RIL
- Catalog number:
- Y213315
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PDLIM4 _ RIL
Related genes to: PDLIM4 _ RIL
- 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 _ RIL
Anti- PDLIM4 RIL Antibodyanti-RILanti-RILanti-RIL type: Primary antibodies host: MouseAntibodies: PDLIM4 _ RIL HOST: Goat Clonality: pAbBos taurus,Bovine,PDLIM4,PDZ and LIM domain protein 4Bovine PDZ and LIM domain 4 (PDLIM4) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine PDZ and LIM domain protein 4(PDLIM4) ELISA kitBovine PDZ and LIM domain protein 4(PDLIM4) ELISA kit SpeciesBovineChicken PDZ and LIM domain 4 (PDLIM4) ELISA kit, Species Chicken, Sample Type serum, plasmaChicken PDZ and LIM domain protein 4(PDLIM4) ELISA kitChicken PDZ and LIM domain protein 4(PDLIM4) ELISA kit SpeciesChickenChicken,Gallus gallus,LIM protein RIL,PDLIM4,PDZ and LIM domain protein 4,Reversion-induced LIM protein,RILELISA Kit FOR PDZ and LIM domain protein 4; organism: Mouse; gene name: Pdlim4ELISA Kit FOR PDZ and LIM domain protein 4; organism: Rat; gene name: Pdlim4 Related articles to: PDLIM4 _ RIL
- 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 - Understanding p53-independent regulatory mechanisms is crucial for predicting outcomes in lung adenocarcinoma (LUAD) and developing improved therapeutic strategies. - Source: PubMed
Publication date: 2026/01/17
Wang QingweiGuo LiangshengWang ShuaiGuan ChengdanPan JunhaoZhu ShaopingZheng LeiWu XuehuaGu YonghuiShu TaoLuo LianxiangLai TianwenGao Xiao - Breast cancer is composed of diverse cell populations, and this intratumoral heterogeneity profoundly affects clinical behavior. Here, we leveraged single cell RNA sequencing (scRNA-seq) of 68 breast cancer specimens to dissect tumor heterogeneity at high resolution. Unsupervised clustering identified all major cell types of the tumor microenvironment (TME)-including malignant epithelial cells, fibroblasts, T cells, macrophages, endothelial cells, and others-with striking variability in their proportions across molecular subtypes. For example, a BRCA1-mutant triple-negative breast cancer (TNBC) sample showed dense immune infiltration, whereas an estrogen receptor (ER)-positive tumor was mostly epithelial, consistent with known subtype differences in immunogenicity. We applied inference of copy number variations (inferCNV) to distinguish malignant epithelial cells, identifying ~90,000 tumor cells with significant copy-number aberrations enriched for cancer hallmark pathways. Re-clustering of these malignant cells revealed five discrete subpopulations. Notably, a KRT17-positive subcluster displayed the highest stemness score and a distinctive ETS-family transcription factor (ERG) regulon, suggesting a stem-like phenotype. Using The Cancer Genome Atlas (TCGA) cohort, we found that genes upregulated in this KRT17+ subpopulation, particularly NFKBIA, PDLIM4, and TCP1 stratified patient survival. An 8-gene risk signature derived from the KRT17 program segregated patients into high- and low-risk groups with markedly different outcomes. High-risk tumors were characterized by an immunosuppressive TME enriched in M2-like macrophages, whereas low-risk tumors more often harbored lymphocyte-predominant infiltrates. Focusing on TCP1, a chaperonin subunit upregulated in high-risk tumors, we demonstrate that TCP1 knockdown in breast cancer cell lines substantially impairs cell migration (~50% reduction in wound closure) and invasion ( < 0.01). These findings reveal functionally distinct malignant cell states within breast cancer and identify TCP1 as a promising therapeutic target to disrupt aggressive, stem-like tumor cell programs, ultimately guiding more personalized treatment strategies. - Source: PubMed
Publication date: 2025/12/09
Wu HoumanDu HaiyangSi GaoSong XuejieSi Fuchun