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
- 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 - Diffuse large B-cell lymphoma (DLBCL) is an aggressive malignancy with limited therapeutic options in the relapsed or refractory setting. Selinexor, a selective inhibitor of nuclear export targeting XPO1, has demonstrated clinical activity in DLBCL. However, the molecular mechanisms underlying its antitumor effects remain incompletely defined. - Source: PubMed
Publication date: 2026/03/19
Zhang WenqiShi LinLi YanHe CuiyingCui ShuixinLiu YuepingWang XiaoxiaoLiu LihongGao YuhuanDiao LanpingWu LiliYao YingzhenFeng YiWu XiaolinYin ShaoningLi WeijingSong BoningHuang Chen - Single-cell sequencing has revolutionized our understanding of cervical cancer (CC), revealing unprecedented cellular heterogeneity, tumor microenvironment (TME) dynamics, and molecular mechanisms underlying progression and therapy resistance. These technologies have identified distinct molecular subtypes (hypoxic, proliferative, and immunoreactive) and epithelial states (cytokeratin⁺, immune-interacting, and senescent), while uncovering HPV-driven oncogenic mechanisms, including viral integration hotspots (e.g., 8q24.21) and immune evasion strategies (e.g., SPP1⁺ TAMs and GALNT3-mediated immunosuppression). Metabolic reprogramming further stratifies tumors into spatially organized Warburg effect and OXPHOS-dominant niches, each associated with unique immune infiltration patterns. The TME exhibits a complex interplay between exhausted PD-1⁺LAG3⁺TIM3⁺ T cells, immunosuppressive stromal cells (MYH9⁺ CAFs, PODXL⁺ ECs), and rare but potent effector populations (FGFBP2⁺ NK cells, CXCL13⁺ TRMs). Despite these advances, clinical translation faces challenges, including resistance mechanisms (NFKB1 mutations, BCL10⁺ Treg suppression) and a lack of inhibitors for key targets (PCLAF⁺ TAEpis, MYH9⁺ CAFs). Promising therapeutic strategies include epigenetic modulation (SALL4), sialylation inhibition (GALNT3/12), and immune-stromal co-targeting (PD-1 + LAG3/TIM3, NRG1-ERBB3 blockade). Future efforts must prioritize functional validation of novel targets (DKK2, ELF3), spatial multi-omics to resolve CAF-immune-metabolic crosstalk, and biomarker-driven clinical trials integrating single-cell classifiers. By bridging single-cell insights with mechanistic and translational studies, the field can overcome stromal-mediated resistance and usher in an era of precision immunotherapy for CC. - Source: PubMed
Publication date: 2025/11/06
Pu CongliXing BiyuanWang ShujieLiu ZhaoZhao Yingchao - Head and neck squamous cell carcinoma (HNSCC) is a malignant tumor of the oral mucosal epithelium. The high incidence of recurrence and metastasis presents substantial challenges for treatment, underscoring the complex molecular landscape underlying the disease. The purpose of this work is to clarify how HNSCC tumor cells and cancer-associated fibroblasts (CAFs) interact. Spatial transcriptome sequencing and single-cell RNA sequencing had been employed to describe the biological characteristics of CAFs in HNSCC. The biological connection between CAFs and tumor cells was verified by molecular interaction experiments. In addition, the regulatory effect of CAFs on oxidative stress in tumor cells and the phenotypic conversion of neutrophils were explored through a coculture system, a knockdown/overexpression method, flow cytometry, and animal experiments. Finally, potential small-molecule inhibitors were screened by molecular dynamics simulation and validated through in vitro and in vivo assays. Growth differentiation factor 15 (GDF15) promoted tumor cell growth and invasion by enhancing PCNA clamp associated factor (PCLAF) transcription through interferon regulatory factor 5 modulation. Its interaction with the receptor GDNF family receptor alpha like (GFRAL) triggered chronic inflammatory signaling via the phosphatidylinositol-3 kinase/protein kinase b/signal transducer and activator of transcription 3 pathway, which led to oxidative stress imbalance and contributed to tumor progression and the development of drug resistance. Moreover, GDF15 activated the extracellular signal-regulated kinase 1/2 pathway through tumor necrosis factor-α, thereby facilitating neutrophil infiltration and promoting lung metastasis in HNSCC. Notably, risperidone (SM-2) emerged as a potential inhibitory regulator capable of disrupting the cascade effects mediated by the GDF15-GFRAL axis, underscoring its therapeutic relevance. This study identifies the GDF15-GFRAL signaling axis as a critical regulator of oxidative stress and immune evasion in HNSCC and demonstrates that the novel small-molecule SM-2 effectively targets this pathway, highlighting its potential as a promising therapeutic strategy. - Source: PubMed
Publication date: 2025/09/30
Zhao ZhijieCai HuabaoZhao ZhenzhenWang XiaojingNie WenyangZhao FuChen YishengDing YanyuLuo ZhiwenLin ZhihengDing Yantao