KIAA0101 Blocking Peptide
- Known as:
- KIAA0101 Blocking Peptide
- Catalog number:
- 33r-6606
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- KIAA0101 Blocking Peptide
Related genes to: KIAA0101 Blocking Peptide
- Gene:
- PCLAF NIH gene
- Name:
- PCNA clamp associated factor
- Previous symbol:
- KIAA0101
- Synonyms:
- NS5ATP9, OEATC-1, p15(PAF), PAF15
- Chromosome:
- 15q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-24
- Date modifiied:
- 2016-11-11
Related products to: KIAA0101 Blocking Peptide
Related articles to: KIAA0101 Blocking Peptide
- PCLAF (PCNA clamp-associated factor) is a protein involved in DNA replication and DNA repair. Aberrant PCLAF expression has been reported in multiple malignancies and is associated with tumor progression and poor clinical outcomes. However, the biological role of PCLAF in hepatocellular carcinoma (HCC) remains incompletely understood, particularly with respect to its relationship with the tumor immune microenvironment. Therefore, this study aimed to systematically investigate the clinical significance, biological functions, and therapeutic potential of PCLAF in HCC through integrated multi-omics analyses, experimental validation, and drug screening approaches. - Source: PubMed
Publication date: 2026/07/22
Shu FeihongChen YidanYang XiaorongGou GuoyouLi GuonianYu JieWang FangLiu YoujiaDu QianXu JingyuXie Rui - KIAA0101, also known as proliferating cell nuclear antigen (PCNA) clamp-associated factor (PCLAF), is a small PCNA-interacting protein linking DNA replication, DNA damage tolerance, cell-cycle progression, and genome maintenance. Aberrant KIAA0101 expression occurs across multiple human malignancies and is frequently associated with aggressive clinicopathological features, therapy resistance, and poor survival. Beyond its canonical role as a proliferation-associated PCNA cofactor, emerging evidence obtained from bulk transcriptomics, single-cell sequencing, and spatially resolved analyses suggests that KIAA0101-high tumor states mark proliferative, stem-like, immune-excluded, and treatment-resistant ecosystems. However, research in this field remains limited by descriptive correlations, small retrospective cohorts, isoform-blind assays, and incomplete mechanistic validation. In this review, we synthesize current evidence on the structural features, regulatory networks, cellular functions, disease-specific roles, immune-microenvironmental associations, and translational relevance of KIAA0101 in cancer. We emphasize that its immune-related effects are more plausibly mediated through indirect regulatory routes, including NF-κB- and Wnt/β-catenin-associated programs, rather than through the direct transcriptional control of immune checkpoint genes. We further discuss therapeutic strategies targeting the KIAA0101-PCNA interface, KIAA0101 degradation, RNA interference/CRISPR-based suppression, and rational combinations with DNA damage response inhibitors or approved targeted agents. Future work should prioritize isoform-resolved detection, non-PCNA interactome mapping, immune-competent functional models, and biomarker-driven validation to determine whether KIAA0101 can be advanced from a cancer-associated molecule to a clinically actionable biomarker or therapeutic vulnerability. - Source: PubMed
Publication date: 2026/07/01
Cao HeYang ShanshanSun WenjiaChen XiZhou Jianya - Prostate cancer (PCa), particularly in its advanced and castration-resistant forms, remains a major threat to men's health, with the tumor microenvironment (TME) playing a crucial role in its progression. Tumor-associated macrophages (TAMs), especially the M2 phenotype, are key components of the TME. Our previous work identified that M2 TAMs in PCa upregulate M-CSF secretion via the MS4A6A-MYC pathway. This study aims to identify the critical downstream effector within PCa cells that mediates the tumor-promoting effects of M-CSF. - Source: PubMed
Publication date: 2026/06/22
Ou YitianYe ChunweiJiang HaiyangZhu YongXia ChengxingYang Delin - Posterior cruciate ligament tibial avulsion fracture (PCLAF) is relatively rare. This fracture may be accompanied by soft tissue injuries, most commonly involving the medial collateral ligament (MCL). The present study aimed to determine the rate of MCL injury and its association with fracture characteristics in patients with PCLAF. - Source: PubMed
Publication date: 2026/05/19
Wang BinghaoYe TengXie XuetaoZhang BinbinWang YukaiSun LuhaoLuo CongfengZhu Yi - We integrated bulk, single-cell, and spatial transcriptomics to test whether intratumoral heterogeneity (ITH) aggravates CD8 T-cell exhaustion (TEX) in lung adenocarcinoma. In bulk cohorts, ITH and TEX were tightly coupled, with ITH-High tumors preferentially exhibiting deeper TEX phenotypes. This dually adverse (high ITH/high TEX) context was associated with increased antigenicity (higher TMB, predicted neoantigen and cancer/testis antigen scores) but reduced TCR diversity, lower global immune/stromal infiltration, more aggressive clinicogenomic features, and poorer survival. Joint ITH-TEX stratification further revealed an additive prognostic effect, with dual-low (low ITH/low TEX) best and dual-high (high ITH/high TEX) worst outcomes. Single-cell analyses implicated macrophages: ITH-High tumors exhibited coordinated upregulation of classical MHC-I antigen-presentation programs (processing/loading; HLA-A/B/C signaling), stronger macrophage→TEX communication, and enrichment of terminal TEX states. Spatially, in ITH-High tumors, TEX co-localized more closely with MHC-I macrophage niches than with macrophages overall, whereas in ITH-Low tumors this proximity was attenuated. B cells showed increased TEX communication but inconsistent MHC-I state spatial coupling, while dendritic cells showed high proximity without ITH-dependent communication increases and weakened colocalization when restricted to MHC-I. We also derived a six-gene decision-tree classifier (CDC45, CENPF, PCLAF, SCGB3A1, CDCA8, and NDC80) predicting ITH/TEX phenotypes. These data support a macrophage MHC-I axis linking ITH to terminal TEX and motivate combining checkpoint blockade with macrophage reprogramming or modulation of antigen-processing and presentation. - Source: PubMed
Publication date: 2026/04/25
Yin ShangzhenGao HaiyanLi QiangWang MengruiZhang PengGuo YurouNan PengyuKong WeihaoShen HongmeiWang LiqiangLu Jianping