CAPG Recombinant Protein
- Known as:
- CAPG Recombinant Protein
- Catalog number:
- XW-RP3029
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CAPG Recombinant Protein
Related genes to: CAPG Recombinant Protein
- Gene:
- CAPG NIH gene
- Name:
- capping actin protein, gelsolin like
- Previous symbol:
- AFCP
- Synonyms:
- MCP
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-14
- Date modifiied:
- 2016-01-18
Related products to: CAPG Recombinant Protein
Related articles to: CAPG Recombinant Protein
- The PD-1/PD-L1 blockade is a cornerstone of breast cancer immunotherapy, yet predictive biomarkers for immunotherapy outcomes remain scarce, restricting its clinical benefit. Glycosylated PD-L1 (gPD-L1) regulates tumor progression, immune suppression, and immune-checkpoint blockade (ICB) response, but it remains undetectable by conventional immunohistochemistry (IHC) due to glycan-mediated epitope shielding. This "detection blind spot" largely undermines current ICB biomarker prediction. To address this unmet clinical need, we developed an ultrasensitive CAP-g bioplatform with a novel CF/DPEDOT:PSS/Au nanoflexible scaffold. It integrates a dual-recognition-driven proximity cascade amplification for accurate gPD-L1 on small extracellular vesicle (gPD-L1-sEV) detection. We constructed this three-dimensional (3D) CF/DPEDOT:PSS/Au nanonetwork scaffold electrode, where π-π stacking synergistically minimizes charge-transfer resistance to improve electron transfer efficiency and maximizes the effective reaction area. Co-anchoring of a PD-L1 aptamer and a glycan probe further triggers hybridization chain reaction (HCR) for signal amplification, and this integrated design outperforms conventional electrochemical or immunological detection strategies. The CAP-g platform achieves an ultralow limit of detection (LOD) of 52 particles/mL, which is 1-2 orders of magnitude lower than existing gPD-L1-sEV or PD-L1-sEV detection methods, and a broad linear dynamic range of 10-10 particles/mL. Clinical validation in breast cancer patients and healthy controls showed robust discrimination between the two groups ( < 0.0001), with high specificity and reproducibility. This work overcomes the technical bottleneck of glycosylation interference in gPD-L1 detection, establishes a new liquid-biopsy paradigm for gPD-L1-sEV detection, and provides a reliable tool for predicting ICB efficacy in breast cancer, thus laying a critical foundation for personalized immunotherapy. - Source: PubMed
Publication date: 2026/05/01
Qiu XiaopeiYang FeiGuo XinlinXu PeijunWang XiaoxingLv LinxiXie JieYu ZhenghengLi PingyunXiao HuiWang TianWang YongzhongGu WeiZhang HongLuo Yang - The actin-binding protein CAPG (Capping Actin Protein, Gelsolin Like) is implicated in oncogenesis, but its role in pancreatic ductal adenocarcinoma (PDAC) remains unclear. This study combined bioinformatic analysis of TCGA/GEO datasets, immunohistochemistry on clinical samples, and functional in vitro assays to define CAPG's significance in PDAC. We found CAPG significantly overexpressed in PDAC tissues (n = 179 tumor vs. 171 normal, p < 0.05), with levels correlating with advanced tumor stage (T3 vs. T1) and predicting poorer overall (p = 0.0085) and disease-free (p = 0.015) survival. In vitro, siRNA-mediated CAPG knockdown in PANC-1 and AsPC-1 cells markedly inhibited proliferation (CCK-8 assay) and migration (wound healing assay), and significantly sensitized cells to gemcitabine-induced apoptosis. Mechanistically, CAPG knockdown was associated with reduced ERK1/2 phosphorylation and Cyclin D1 expression, and ERK1/2 inhibition phenocopied the anti-proliferative and chemosensitizing effects. Our results establish CAPG as a negative prognostic biomarker in PDAC, demonstrate its critical role in driving proliferation and migration-potentially via modulating ERK pathway activity-and highlight its promise as a therapeutic target whose inhibition can enhance chemotherapy efficacy. - Source: PubMed
Publication date: 2026/03/31
Qin ZhongyuLi KaixiaLi XuanjieWang HaoruiZhang Yiqiang - Hepatocellular carcinoma (HCC) is characterized by its insidious onset and rapid progression. Investigating diagnostic and therapeutic strategies targeting programmed cell death (PCD) represents a promising research direction. - Source: PubMed
Publication date: 2026/03/06
Lei LixingLiu NianTang LinglingLiu QianqianPan KeHuang Xiaohua - Hepatocellular carcinoma (HCC) is characterized by substantial heterogeneity and immune tolerance, and its therapeutic efficacy is profoundly influenced by the immune microenvironment. Ferroptosis, an iron-dependent form of regulated cell death, is closely linked to tumor immune regulation. We conducted an integrative multi-omics analysis to systematically delineate the composition and function of the ferroptosis-immunity network in HCC. Using TCGA data, we identified ferroptosis-related prognostic genes. By integrating these with immune features via weighted gene co-expression network analysis (WGCNA), we defined 55 ferroptosis-immune microenvironment-related genes (FIMRGs). Single-cell transcriptomic analysis showed that, among immune cell types, macrophages exhibited the highest ferroptosis-immunity activity. Spatial transcriptomics revealed that macrophages with high ferroptosis signaling (FehighMac) preferentially infiltrated tumor nests. These macrophages engaged in robust interactions with T cells via ligand-receptor axes such as ICAM1-ITGAX/ITGB2, TNF-TNFR, and LGALS9-CD45, potentially promoting T-cell exhaustion and shaping an immunosuppressive microenvironment. We identified CAPG-positive macrophages (CAPG + Mac) as the key driver of this process. Characterized by suppressed ferroptosis, enhanced glutathione metabolism, and upregulated immune checkpoints, CAPG + Mac appear to foster an immune-tolerant microenvironment. A prognostic model constructed from CAPG + Mac signature genes effectively stratified HCC patients into high- and low-risk groups and demonstrated stable predictive performance in external validation. This study reveals that CAPG + Mac putatively modulate ferroptosis signaling to influence immune homeostasis, highlighting them as a key target for HCC progression and immunotherapy responsiveness. - Source: PubMed
Publication date: 2026/02/22
Yin XishengLi YantongZheng ShiPan ChunhuiTian ZihanZhong Xiaolin - Explore the causes and mechanisms of bladder cancer-induced Cardiovascular diseases (CVD) death. - Source: PubMed
Publication date: 2026/02/17
Shen JunwenZhao ZhuchengLi ZhaojunWang Rongjiang