Ask about this productRelated genes to: CCT5 Blocking Peptide
- Gene:
- CCT5 NIH gene
- Name:
- chaperonin containing TCP1 subunit 5
- Previous symbol:
- -
- Synonyms:
- KIAA0098
- Chromosome:
- 5p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-29
- Date modifiied:
- 2019-04-23
Related products to: CCT5 Blocking Peptide
Related articles to: CCT5 Blocking Peptide
- This Mendelian randomization study aimed to systematically investigate the causal associations of 2,821 plasma protein ratios with UC susceptibility and validate potential biomarkers through multi-omics approaches. - Source: PubMed
Publication date: 2026/08/10
Kang KuoWei LinfengLi XuanxuanWang ShalongHuang ChanghaoWu Zhiwei - Heart failure with preserved ejection fraction (HFpEF) is an increasingly common form of heart failure (HF) that is best understood as a systemic, multiorgan syndrome rather than a disease of left-ventricular filling alone. This review has three specific aims: first, to synthesize genetic and molecular pathways that are most relevant to non-ischemic HFpEF; second, to distinguish HFpEF-enriched mechanisms from evidence extrapolated from ischemic cardiomyopathy or HFrEF; and third, to consider translational implications for populations with high consanguinity, including the Kingdom of Saudi Arabia. The available evidence indicates that chronic inflammatory signaling involving CCL2, CCL5, TLR3, PTGS2/COX-2, IL-6/JAK/STAT3, NF-kB, and NLRP3 acts upstream of endothelial dysfunction, nitric-oxide/cGMP/PKG impairment, mitochondrial reactive oxygen species generation, and fibroblast activation. Extracellular-matrix regulators including ASPN, COL1A1, and MMP2 then amplify collagen deposition and myocardial stiffness, whereas mitochondrial genes and proteins such as ATP5C1 contribute to impaired oxidative phosphorylation, reduced ATP reserve, defective fatty-acid oxidation, and blunted mitophagy. Protein-quality-control pathways involving HSP90AA1, CCT2/CCT5, PSMA3, and stress-responsive STAT3 further link metabolic stress to proteotoxic injury. Epigenetic mechanisms, including DNA methylation and microRNAs such as miR-155, miR-1297, and miR-4649-3p, add a regulatory layer that may improve risk stratification but remains insufficiently validated for routine clinical use. In high-consanguinity settings, recessive cardiomyopathy variants can cluster in families and contribute to earlier NIHF presentations; however, population-level HFpEF-specific variant frequencies remain limited, and findings from HFrEF or dilated cardiomyopathy should be interpreted as candidate pathway evidence rather than definitive HFpEF markers. Translationally, SGLT2 inhibitors, mineralocorticoid-receptor antagonism, biomarker panels, and structured genetic evaluation provide the most clinically actionable bridge from molecular mechanisms to precision HFpEF care. - Source: PubMed
Publication date: 2026/07/11
Abou Al-Saud Sara - Inferring gene regulatory networks (GRNs) from single-cell RNA sequencing (scRNA-seq) data is fundamentally challenged by severe data sparsity, where pervasive dropout events obscure true regulatory signals and compromise the reliability of downstream inference. Existing supervised methods, while leveraging prior network structures, remain highly susceptible to this noise due to their end-to-end learning paradigm. To address this bottleneck, we propose SGMHA, a novel two-stage framework that decouples representation learning from link prediction. Specifically, SGMHA first employs a self-supervised graph masked autoencoder (GraphMAE) to learn robust gene representations by reconstructing randomly masked expression values, thereby mitigating sparsity-induced distortions. Subsequently, an MHA (multi-head attention)-based fine-tuning module integrates these pre-trained representations with raw expression data to accurately infer directed regulatory links. Extensive benchmarking across seven scRNA-seq datasets demonstrates that SGMHA consistently outperforms eight state-of-the-art methods in both area under the receiver operating characteristic curve (AUROC) and area under the precision-recall curve (AUPRC). Applying SGMHA to breast cancer metastasis revealed context-specific GRNs and identified 26 high-confidence candidate drivers. Among these, six (NDUFAF4, ENY2, CCT5, PGK1, DCTPP1, and H2AFZ) were validated as prognostic biomarkers, with their mechanistic roles in metastatic adaptation detailed through multi-omics integration. Collectively, SGMHA provides an accurate, scalable, and biologically interpretable tool for GRN inference, holding strong promise for biomarker discovery in complex diseases. - Source: PubMed
Publication date: 2026/06/09
Zhang XujianLi WenhaoPan YuliangWang XupengGuan JihongCao Zhiwei - While Chaperonin Containing TCP1 Subunit 5 (CCT5) is recognized for its involvement in the oncogenesis and advancement of diverse malignancies, its functional significance within the context of colon adenocarcinoma (COAD) has yet to be elucidated. - Source: PubMed
Publication date: 2026/04/28
Wang BoLiu XinruiLi JianmeiDong HuiFan XingxiuWang RuijunGuo JianpingLi Yifeng - Colorectal cancer (CRC) is a leading cause of cancer-related mortality, and early tumorigenesis is closely associated with mitotic dysregulation and chromosomal instability. To define molecular mechanisms supporting mitotic fidelity during CRC initiation, we combined multi-omics profiling, genetically engineered mouse models, and functional assays to examine the role of the chaperonin subunit CCT5. Transcriptomic and proteomic analyses revealed elevated CCT5 expression in stage I CRC and precancerous lesions, indicating diagnostic relevance. The genetic depletion of CCT5 suppressed epithelial proliferation, reduced dysplastic transformation, and limited tumor initiation . In CRC cells, CCT5 silencing impaired proliferation and induced G2/M arrest. Mechanistically, CCT5 interacts with CDC20 and facilitates turnover of the MCC-CDC20-APC/C complex, enabling metaphase-to-anaphase progression. These findings position CCT5 as a regulator of early CRC development with implications for early detection and therapeutic intervention. - Source: PubMed
Publication date: 2026/03/04
Ji MeijunZhuang WenhanGuo YuminXu PengfeiZhou XiaoluLong YanGeng XiaogeJing JiyongZhou XuelongPan WenshengZhang Chenjing