ARNTL2 Antibody
- Known as:
- ARNTL2 Antibody
- Catalog number:
- 39937
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- ARNTL2 Antibody
Related genes to: ARNTL2 Antibody
- Gene:
- ARNTL2 NIH gene
- Name:
- aryl hydrocarbon receptor nuclear translocator like 2
- Previous symbol:
- -
- Synonyms:
- BMAL2, MOP9, CLIF, PASD9, bHLHe6
- Chromosome:
- 12p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2003-08-21
- Date modifiied:
- 2016-10-05
Related products to: ARNTL2 Antibody
Related articles to: ARNTL2 Antibody
- Circadian rhythms synchronize physiological processes with the light-dark cycle and regulate biological functions relevant to cancer, including cell-cycle control, metabolism, DNA repair, immunity, and tissue homeostasis. Growing evidence indicates that disruption of these temporal mechanisms contributes to tumor initiation, progression, metastasis, and treatment response. In colorectal cancer (CRC), circadian clock dysregulation has emerged as an important component of tumor biology. A systematic search identified 1338 records, of which 43 studies met the eligibility criteria (20 human, 19 experimental, and 4 chronotherapy studies). Across the included studies, statistically significant associations were consistently reported between dysregulation of clock genes such as , , , , , , and and alterations in proliferation, metabolism, epithelial plasticity, immune regulation, metastatic potential, and treatment responsiveness. Experimental evidence also supported interactions with Wnt signaling, ferroptosis, oxidative-stress adaptation, epithelial-mesenchymal remodeling, and a proposed clock-microbiota-immune axis. Overall, the available evidence indicates that circadian dysregulation represents a systems-level disturbance that gives rise to a multidimensional biological condition, here referred to as the Tumor Temporal State, integrating the metabolic, immune, invasive, and therapeutic dimensions of colorectal cancer biology. - Source: PubMed
Publication date: 2026/07/10
Tarasewicz MirosławZbroch EdytaMarkowski Adam R - The coexistence of skin diseases is common. Although molecular studies have made significant efforts to understand each disease entity, the shared molecular basis explaining their concurrence remains largely unknown. This study aims to identify common upregulated genes in skin diseases that may serve as potential biomarkers. - Source: PubMed
Alsabbagh Manahel Mahmood - Obsessive-compulsive disorder (OCD) and allergic diseases co-occur far more often than expected, yet genome-wide genetic correlations are typically modest or negative. The objective of this study was to test whether OCD and allergic diseases show convergence at the level of pre-specified biological pathways, especially synaptic pruning and circadian regulation, rather than at the level of broad genome-wide correlation. - Source: PubMed
Publication date: 2026/05/27
Cheung Ngo - This study investigated the prognostic value and molecular mechanisms of miR-517c-3p in lung cancer. miR-517c-3p in 112 lung cancer tissues was detected using qRT-PCR. Kaplan-Meier survival analysis and Cox regression were used to assess its prognostic significance. Functional experiments, including cell proliferation, migration, and invasion, were conducted in lung cancer cell lines (H1229, A549) after miR-517c-3p overexpression. Target gene prediction and validation were performed using bioinformatics tools and dual-luciferase reporter assays. The regulatory effects of miR-517c-3p on ARNTL2 were further explored through gene overexpression and rescue experiments. miR-517c-3p was significantly downregulated in lung cancer tissues (p < 0.001) and correlated with advanced TNM stage, lymph node metastasis, and larger tumor size. Patients with low miR-517c-3p expression exhibited poorer overall survival (p < 0.001), and Cox regression identified miR-517c-3p as an independent prognostic factor (HR = 0.110, 95% CI = 0.047-0.256). Functional assays demonstrated that miR-517c-3p overexpression inhibited lung cancer cell proliferation, migration, and invasion. Dual-luciferase reporter assays confirmed ARNTL2 as a direct target of miR-517c-3p, and ARNTL2 restoration reversed the suppressive effects of miR-517c-3p on tumor progression. miR-517c-3p is significantly downregulated in lung cancer and associated with poor patient prognosis. Furthermore, miR-517c-3p suppresses tumor progression by directly targeting ARNTL2. - Source: PubMed
Chen JiaRen QiuSun BowenSun YongJiang HongjieWang Junwen - Nonsmall cell lung cancer (NSCLC) is the predominant form of lung cancer. Ferroptosis is a novel therapeutic target against treatment resistance in NSCLC. However, its regulation by m6A RNA modification remains incompletely elucidated. m6A RNA modification mediates mRNA stability, translation, and splicing to target transcripts. Methyltransferase like 7B (METTL7B) has been implicated in tumor progression, but its role in NSCLC ferroptosis m6A modification has not been reported. We aimed to investigate the mechanism of METTL7B-mediated m6A modification in NSCLC cell ferroptosis. NSCLC cells (SK-MES-1/PC9/H1975/A549) and normal cells (BEAS-2B) were cultured. The expression of METTL7B, long non-coding RNA 02159 (LINC02159), and aryl hydrocarbon receptor nuclear translocator-like 2 (ARNTL2) was determined. After METTL7B knockdown, cell viability was measured by MTT assay; ferroptosis-related factors were analyzed. m6A quantification was performed. m6A enrichment on LINC02159 was analyzed. The interaction between LINC02159 and KAT2A was verified. KAT2A and H3K27ac enrichment on the ARNTL2 promoter was detected. The roles of LINC02159 and ARNTL2 were validated. METTL7B, LINC02159, and ARNTL2 were upregulated in NSCLC cells compared to BEAS-2B cells. METTL7B knockdown increased iron ions, reactive oxygen species, and malondialdehyde levels and decreased cell viability, superoxide dismutase, and glutathione levels. METTL7B potentially upregulated LINC02159 expression through m6A modification. LINC02159 may recruit KAT2A to enhance H3K27ac enrichment on the ARNTL2 promoter, thereby promoting ARNTL2 expression. Overexpression of LINC02159 or ARNTL2 partially reversed the pro-ferroptotic effects of METTL7B knockdown on NSCLC cells. In conclusion, METTL7B inhibits ferroptosis in NSCLC cells the LINC02159/KAT2A/ARNTL2 axis in an m6A-dependent manner. - Source: PubMed
Publication date: 2026/03/12
Tao RancenLiu ZuoZhang ZhenningZhang Zhenfa