Ask about this productRelated genes to: WRNIP1 Blocking Peptide
- Gene:
- WRNIP1 NIH gene
- Name:
- WRN helicase interacting protein 1
- Previous symbol:
- -
- Synonyms:
- WHIP, FLJ22526, bA420G6.2
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-13
- Date modifiied:
- 2019-04-11
Related products to: WRNIP1 Blocking Peptide
Related articles to: WRNIP1 Blocking Peptide
- Immunogenic cell death (ICD) plays a critical role in the host’s antitumor immune response, and its dysregulation is linked to poor prognosis in colorectal cancer (CRC). Identifying ICD-related genes and developing prognostic models can enhance the prediction of patient outcomes and facilitate personalized treatments. Utilizing data from CRC patients in the Cancer Genome Atlas, we employed weighted gene co-expression network analysis, LASSO regression analysis, and multivariate Cox regression screening to identify immunogenic cell death-related prognostic genes (IPGs) in CRC patients. An IPGs scoring system was constructed, allowing for the stratification of patients into high-risk and low-risk groups based on the best cutoff ICD-RiskScore, with the Gene Expression Omnibus dataset serving as a validation cohort. We then examined the correlations between the high-risk and low-risk groups concerning clinicopathological features, immune infiltration, immunotherapy responses, and tumor mutational burden. Additionally, we analyzed the cellular landscape and cell-cell interactions in colorectal cancer at a single-cell resolution. A prognostic model comprising 12 immune-related prognostic genes (IPGs)—CAV2, NOXA1, TGFB2, WRNIP1, CCL22, ICAM2, APOBEC3F, COTL1, CTSD, IDO1, NFATC1, and RUNX3—was established, demonstrating a high area under the curve value in survival analysis, which indicates robust predictive performance. In comparison to the low-risk group, the high-risk group exhibited lower survival rates, higher mutation rates of genes, and was associated with more advanced tumor stages. Single-sample gene set enrichment analysis revealed that the low-risk group possessed a stronger immune surveillance function. Additionally, single-cell analysis uncovered a lower abundance of immune cells and an increased proportion of epithelial cells within tumor samples. The frequency of interactions among epithelial cells, endothelial cells, and fibroblasts was found to be elevated in tumor samples. Subsequently, validation of the prognostic genes revealed that COTL1 expression was significantly elevated in CRC tissues compared to adjacent normal tissues ( < 0.05). This study presents a prognostic model for colorectal cancer that integrates 12 immune-related genes. The model holds potential clinical value in predicting patient prognosis and guiding personalized treatment strategies. These findings also provide insights into the molecular mechanisms of immune cell dynamics in colorectal cancer and highlight potential therapeutic targets. - Source: PubMed
Publication date: 2026/01/21
Dong XianwenYang WenjuanGong ChunxiangWang ChangrongWan QijunYang Ti - Werner helicase-interacting protein 1 (WRNIP1) binds to Polδ and promotes its activity in vitro; however, the functional relationship between WRNIP1 and Polδ in the DNA damage tolerance process remains unclear. In this study, we performed genetic analyses of WRNIP1 and Polδ in the chicken DT40 cell line by generating WRNIP1/POLD3 (POLD3 is the p66 subunit of Polδ) conditional knockout cells using the auxin degron system, where the WRNIP1and POLD3 genes are knocked out, and degradation-inducible WRNIP1 is expressed. Upon auxin treatment, the ultraviolet (UV) sensitivity of WRNIP1/POLD3 cells was suppressed and compared to that of the POLD3 cells or WRNIP1/POLD3 cells without auxin. Additionally, a decrease in cyclobutane pyrimidine dimers was seen in WRNIP1/POLD3 cells following WRNIP1 depletion at 24 h after UV irradiation. The mutation induction rate after UV irradiation did not change in auxin-treated WRNIP1/POLD3 cells compared to that of single mutant cells or WRNIP1/POLD3 cells cultured without auxin. UV-induced sister chromatid exchange (SCE), a process mediated by homologous recombination, was higher in POLD3cells than in wild-type cells, whereas SCE in WRNIP1/POLD3 cells was moderately increased by depletion of WRNIP1. We have identified a genetic interaction between WRNIP1 and POLD3. We will discuss the potential molecular mechanisms underlying this interaction. - Source: PubMed
Publication date: 2025/11/24
Yoshimura AkariAbe TakuyaHirota KoujiSeki Masayuki - Ageing is a general, intrinsic, and progressively deleterious process that affects all cells, tissues, and organs albeit at different extent and rate in each individual. The complexity and universality of its phenotypic manifestations suggest a multifactorial origin. The autosomal recessive disorder Werner syndrome likely represents a segmental progeroid disorder since patients show several, but not all phenotypes of premature ageing. - Source: PubMed
Publication date: 2025/09/19
Poot Martin - Y-family DNA polymerases (Pols) are intrinsically highly error-prone; yet they conduct predominantly error-free translesion synthesis (TLS) in normal human cells. In response to DNA damage, Y-family Pols assemble and function together with WRN, WRNIP1, and Rev1 in TLS. Among these proteins, WRN possesses a 3'→5' exonuclease activity and an ATPase/3'→5' DNA helicase activity, and WRNIP1 has a DNA-dependent ATPase activity. In a previous study, we identified a role of WRN 3'→5' exonuclease activity in the high in vivo fidelity of TLS by Y-family Pols. Here we provide evidence for a crucial role of WRN and WRNIP1 ATPase activities in raising the fidelity of TLS by these Pols. Defects in WRN and WRNIP1 ATPase activities cause a diversity of nucleotide (nt) misincorporations opposite DNA lesions by Y-family Pols, implicating an unprecedented role of these activities in restraining nt misincorporations, which they could accomplish by tightening the active site of the TLS Pol. Altogether, the combined actions of WRN and WRNIP1 ATPases in preventing nt misincorporations and of WRN exonuclease in removing misinserted nts confer such an enormous rise in the fidelity of Y-family Pols that they perform error-free TLS - essential for genome stability and cellular homeostasis. - Source: PubMed
Publication date: 2025/09/03
Yoon Jung HoonSellamuthu KarthiPrakash LouisePrakash Satya - DNA metabolism genes play pivotal roles in the regulation of cellular processes that contribute to cancer progression, immune modulation, and therapeutic response in prostate cancer (PC). Understanding the mechanisms by which these genes influence the tumor microenvironment and immune evasion is crucial for identifying prognostic biomarkers and developing targeted therapies. We performed an integrative analysis using transcriptomic data from the TCGA cohort and external validation datasets. Differentially expressed genes (DEGs) were identified using the edgeR algorithm with an FDR < 0.01 and a minimum fold change of 1.5. Gene enrichment analysis was conducted through GO and KEGG pathways to explore the biological significance of DNA metabolism genes in PC. In addition, clustering analyses, machine learning models, and single-cell RNA sequencing (scRNA-seq) were employed to investigate the immune characteristics, prognostic value, and therapeutic relevance of these genes. A total of 536 DEGs were identified across six subtypes of prostate cancer, with key DNA metabolism genes such as POLD2, RAD9A, REV3L, MSH6, and WRNIP1 highlighted as critical players. Gene enrichment analyses revealed that these DEGs were significantly associated with pathways involved in DNA repair, cellular aging, and telomere maintenance. Clustering analysis identified two distinct subgroups (C1 and C2) based on DNA metabolism gene expression, with C1 exhibiting a more aggressive phenotype, higher immune infiltration, and poorer prognosis. Machine learning models, particularly the CoxBoost algorithm, identified 21 key genes contributing to an effective prognostic model. Furthermore, scRNA-seq analysis confirmed the upregulation of DNA metabolism genes in PC cells compared to normal cells. Our findings highlight the importance of DNA metabolism genes in the progression and immune dynamics of PC. These genes not only serve as potential biomarkers for prognosis but also offer promising targets for personalized therapies. The integration of multi-omics data and advanced computational models provides new insights into the molecular underpinnings of PC and holds potential for improving treatment strategies. - Source: PubMed
Publication date: 2025/07/18
Abroudi Ali ShakeriDjamali MelikaAzizi Hossein