CCT2 ELISA kit
- Known as:
- CCT2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CCT2-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CCT2 ELISA kit
Ask about this productRelated genes to: CCT2 ELISA kit
- Gene:
- CCT2 NIH gene
- Name:
- chaperonin containing TCP1 subunit 2
- Previous symbol:
- -
- Synonyms:
- Cctb
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-26
- Date modifiied:
- 2016-01-06
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- Mechanisms aimed at recovering from heat-induced damage are closely associated with the organism's ability to survive extreme temperature exposure. In such a scenario, we show that autophagy, as a cytoprotective mechanism, ensures recovery and viability after induced heat stress in . Our findings indicate that heat shock triggers the targeted degradation of ubiquitinated protein aggregates, mediated by the macroaggrephagy receptor Cue5. Moreover, heat stress induces the turnover of the aggrephagy receptor Cct2 and the polyglutamine repeats of the HTT (huntingtin) protein (polyQ-HTT). Notably, even though Cct2 and polyQ-HTT degradation is vacuole-dependent, it is mediated autonomously of canonical autophagy pathways. Collectively, this study demonstrates a novel role of autophagy in maintaining protein homeostasis after heat stress in yeast and provides insights into the potential medical applications of heat treatment.: Atg1: AuTophaGy related 1; Atg7: AuTophaGy related 7; Atg8: AuTophaGy related 8; Atg13: AuTophaGy related 13; Atg15: AuTophaGy related 15; Cct2: Chaperonin Containing TCP-1 2; CMA: chaperone-mediated autophagy; Cue5: Coupling of Ubiquitin conjugation to ER degradation 5; GFP: green fluorescent protein; HS: heat shock/stress; HTT: huntingtin; Pep4: carboxyPEPtidase Y-deficient 4; polyQ: polyglutamine; RFP: red fluorescent protein. - Source: PubMed
Publication date: 2026/09/03
Dialynaki DimitraHuang YuxiangKlionsky Daniel J - CCT2, a vital subunit of the chaperonin-containing TCP-1 (CCT) complex, has emerged as a critical regulator of protein homeostasis and cancer progression. In this study, we highlight the essential role of CCT2 in head and neck squamous cell carcinoma (HNSCC), where it is overexpressed and strongly associated with poor prognosis, advanced clinical stages, and aggressive tumor behavior. Mechanistically, CCT2 interacts with and stabilizes the oncogenic c-Myc protein to drive tumor cell proliferation, migration, and invasion. Furthermore, CCT2 contributes to cisplatin resistance by regulating c-Myc-dependent pathways and cell cycle-related proteins. Notably, apoptotic vesicles derived from drug-resistant tumor cells transfer CCT2 to neighboring cells, further enhancing chemoresistance. These findings position CCT2 as a key driver of HNSCC progression and c-Myc-mediated oncogenic pathways, presenting it as a promising therapeutic target for overcoming drug resistance and improving treatment outcomes in HNSCC patients. - Source: PubMed
Publication date: 2025/08/07
Lu LinShen YiLi XuerongZhao YiweiZhai XuefanCai MinBao BaichengLiao GuiqingSun Jianbo - Colorectal cancer (CRC) is a major global health burden. While immune checkpoint inhibitors have greatly advanced cancer therapy, their therapeutic effects are unsatisfactory in microsatellite-stable/proficient mismatch repair CRC. This study explored the molecular mechanisms underlying CRC immune evasion. - Source: PubMed
Publication date: 2026/08/12
Gu LiqiangLi ShaofeiTang YichaoJi Liechen - 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 - Advances in single-cell sequencing technologies greatly enhance our understanding of molecular and cellular features. However, effectively leveraging these data to uncover key biological factors remains a major challenge in integrative analyses across multiomic types and comparative studies across species, particularly livestock species such as pigs and cattle. To address this, we develop AlignCell, a deep learning model designed to learn robust biological features by integrating multisource omic data across platforms, omic types, and species, thereby facilitating the discovery of key factors, such as conserved and species-specific genes in cross-species comparative studies. Across various applications and benchmarking compared with existing tools, AlignCell performs well. Notably, using AlignCell to integrate female gonad data across four species (human, mouse, pig, and cattle), including the bovine single-cell data generated in this study, AlignCell reveals the unexplored species-conserved gene in primordial germ cells (PGCs). Additionally, it identifies unexplored species-specific genes and in pig and cattle PGCs, providing important insights for reproductive and developmental research. - Source: PubMed
Publication date: 2026/08/03
Du ZihuanZhang XiaoyuZhang QiangLi JingCao ZhijieGao GeLin TaoWang DongGao Shuai