Ask about this productRelated 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
- Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, characterized by poor survival rates and limited therapeutic options. Oncogenic KRAS mutations are frequent in pancreatic cancer patients and are key drivers of tumorigenesis. Recent studies have underscored the essential role of extracellular signal-regulated kinase (ERK) in sustaining KRAS-mutant tumors and mediating resistance to KRAS-ERK-targeted therapies. However, the specific prognostic value of KRAS-ERK-associated genes in KRAS-mutant pancreatic cancer remains largely undefined. In this study, we performed a comprehensive analysis of molecular stratification based on KRAS-ERK-associated genes and established a five-gene KRAS-ERK prognosis signature (KEPS) comprising ARNTL2, ZWILCH, KIAA0513, KIAA0913, and C4orf43. The KEPS model effectively stratified patients into high- and low-risk groups, with significantly poorer prognosis observed in the high-risk group. External validation using independent KRAS-mutant pancreatic cancer cohorts validated the prognostic performance of KEPS. Further analyses revealed that the high-risk group was enriched in tumor progression-related pathways and exhibited elevated expression of immune checkpoint molecules, including PD-L1, PD-L2, and CD276. Among the KEPS signature genes, ARNTL2 was prioritized for further functional characterization. In two anti-PD-L1-treated cohorts, ARNTL2 correlated with immune checkpoint expression and therapeutic response, suggesting potential relevance to immune checkpoint blockade. Functional assays confirmed that ARNTL2 depletion suppressed malignant phenotypes of KRAS-mutant PDAC cells in vitro and impaired tumor growth in vivo. In conclusion, this work establishes KEPS as a novel molecular tool for risk stratification in KRAS-mutant pancreatic cancer and highlights that ARNTL2 may represent a potential personalized therapeutic target. - Source: PubMed
Publication date: 2026/09/10
Lin WeihaoXu ChunguiLiu ChaoqunZhou Rui - Despite the prevalence of the KRAS G12D mutation in approximately 40% of pancreatic ductal adenocarcinoma (PDAC) cases and its association with the poorest prognosis among KRAS variants, the downstream transcriptional effectors driving its aggressive metastatic phenotype remain poorly defined. Through integrated bioinformatics and experimental validation, we identified ARNTL2 as a factor associated with KRAS G12D-mutant PDAC. ARNTL2 directly bound to the SERPINE1 promoter to activate its expression, establishing an ARNTL2-SERPINE1 axis that orchestrated epithelial-mesenchymal transition and drove metastasis and . Rescue experiments confirmed SERPINE1 as the indispensable downstream mediator. Clinical validation demonstrated that ARNTL2 and SERPINE1 protein levels correlated positively and stratified patients into distinct prognostic subgroups. Furthermore, this axis altered sensitivity to selective KRAS G12D inhibition . These findings identify an experimentally supported ARNTL2-SERPINE1 transcriptional axis in KRAS G12D-mutant PDAC that warrants further validation in genotype-faithful and clinically relevant models. - Source: PubMed
Publication date: 2026/09/08
Shi XiaohanYin XiaoyiGao SuizhiWu XinqianWang HuanWang BeileiXu XiongfeiZheng KailianJing WeiLi GangGuo ShiweiJin Gang - Immunotherapy resistance in lung adenocarcinoma (LUAD) remains a critical clinical challenge, and the mechanisms underlying resistance-associated intratumoral heterogeneity are poorly characterized. - Source: PubMed
Publication date: 2026/08/15
Qiu ZhengangZhao HuiLyu QiongLi ZhigangXi QiujiangYe BingqingLong QianshanLai ZhengxinCao XiangZhong WenjuanZhang YuLiu Rongrong - 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