Per2 (Phospho-Ser662) Polyclonal Antibody
- Known as:
- Per2 (Phospho-Ser662) Polyclonal Antibody
- Catalog number:
- 12332
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- Per2 (Phospho-Ser662) Polyclonal Antibody
Related genes to: Per2 (Phospho-Ser662) Polyclonal Antibody
- Gene:
- PER2 NIH gene
- Name:
- period circadian regulator 2
- Previous symbol:
- -
- Synonyms:
- KIAA0347
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-11
- Date modifiied:
- 2017-10-02
Related products to: Per2 (Phospho-Ser662) Polyclonal Antibody
Related articles to: Per2 (Phospho-Ser662) Polyclonal Antibody
- T-2 toxin induces severe cytotoxicity and immunosenescence, but the underlying mechanisms, particularly the role of circadian rhythm disruption, still lack a clear understanding. This study explores the function of the circadian PER2 and the Hippo/MST1 signaling in T-2 toxin-induced immunosenescence using RAW 264.7 macrophages model. We found that T-2 toxin (14nM, 0-24h) disrupted the oscillatory rhythm of PER2, attenuating its amplitude and altering its peak-trough pattern. This disruption was mediated by T-2 toxin-induced and sustained activation of HIF-1α, as HIF-1α inhibition significantly suppressed PER2 expression. Functionally, pharmacological inhibition of PER2 with KL044 alleviated T-2 toxin-induced senescence, as evidenced by reduced SA-β-gal activity, downregulation of SASP factors (IL-6, IL-8, CCL-2), and attenuation of G1 phase cell cycle arrest. Mechanistically, we identified that PER2 acts as a positive regulator of the Hippo/MST1 signaling. T-2 toxin activated Hippo signaling, increasing MST1 and phospho-YAP levels while reducing total YAP. PER2 inhibition blunted this activation. Crucially, direct inhibition of the Hippo kinase MST1 mirrored the protective effects of PER2 inhibition, significantly reducing cellular senescence, SASP expression, and apoptosis. Our findings demonstrate that T-2 toxin promotes immunosenescence by hijacking the circadian PER2 via a HIF-1α-dependent mechanism. The upregulated PER2, in turn, activates the Hippo/MST1 signaling, driving senescence. This study unveils the PER2/Hippo axis as a novel signaling cascade critical for T-2 toxin-induced immunosenescence. - Source: PubMed
Publication date: 2026/05/14
Li JunyaoHuang XueqinWei WeiWang XuYou LiNepovimova EugenieWu QinghuaKuca Kamil - Seed aging is a critical biological process that leads to progressive loss of seed vigor, thereby constraining germplasm conservation and agricultural productivity. To elucidate the molecular mechanisms underlying this process in grass species, we performed transcriptomic analyses to characterize regulatory networks underlying seed aging in , a dominant forage species on the Qinghai-Tibet Plateau. Seeds were subjected to artificial accelerated aging (45 °C, 80% relative humidity, 1-6 days), followed by physiological evaluation and RNA sequencing. Seed vigor and germination percentage declined markedly with aging, accompanied by extensive transcriptional reprogramming. Integrative analyses identified pyruvate metabolism, MAPK signaling, and peroxisome function as key processes associated with vigor loss during late-stage aging. WGCNA further revealed that genes encoding heat shock proteins and glutathione metabolism-related enzymes were co-localized within the same module, suggesting a possible synergistic role in preserving seed viability during aging. In addition, WRKY24, ARF9, and ARF19 were identified as candidate hub transcription factors. WRKY24 may contribute to aging by modulating antioxidant defense-related genes (e.g., and ), while ARF9 and ARF19 may regulate ROS homeostasis through predicted downstream targets, including , , , , and . Together, these findings support a hypothetical regulatory model in which WRKY and ARF transcription factors coordinate redox homeostasis and hormone signaling to regulate seed longevity in . This study provides a systems-level framework for understanding seed aging in perennial grasses and identifies potential genetic targets for improving seed storability, with implications for germplasm conservation and alpine grassland sustainability. - Source: PubMed
Publication date: 2026/04/27
Sun MingWang LiSun XinchaoYan JiajunGou WenlongLiu JingWu ChanjuanHe YilinYue GuoLi DongbinWang RongxiaLei XiongBai Shiqie - Dexamethasone (DEX) is used in clinical practice as a life-saving therapy in threatened preterm birth; however, such treatment also represents a powerful signal that can reprogram fetal physiology, including the circadian system. The effect of DEX on the fetal circadian clock in the suprachiasmatic nuclei (SCN) has been demonstrated, but the underlying mechanism has been unaddressed. The aim of this study was to provide insight into the DEX-induced transcriptional effects in the fetal SCN of mPer2 mice. We used triple-labeled immunofluorescence to localize glucocorticoid receptors (GR) in the fetal SCN, cultured ex vivo fetal SCN explants to monitor PER2-driven bioluminescence (PER2::LUC) rhythms, and RNA-seq and RT qPCR analyses to identify genes differentially expressed after DEX and vehicle treatments. We demonstrate that GRs are homogenously expressed in all cells (neuronal and glial nuclei and glial processes) of the fetal SCN. Monitoring PER2::LUC in fetal SCN explants confirmed that most cells respond to DEX with increased amplitude and mesor of the rhythms. The RNA-seq and RT-qPCR data revealed that DEX increases expression of GR-sensitive clock gene Per1 and changes the expression of other genes that may affect the clock (e.g., Hif3a, Klf9, Zbtb16, Mt1-3). The effects were more significant when the treatment timing matched the temporal window of highest sensitivity of the SCN clock to DEX. Our findings advance the largely unexplored field of chrono-ontogenesis and define the effects of DEX on the fetal brain transcriptional landscape, with specific implications for the circadian clock. - Source: PubMed
Publication date: 2026/05/09
Sládek MartinCadenato PedroSemenovykh KaterynaHoudek PavelSumová Alena - While lung-protective ventilation strategies are standard care, effective adjunctive pharmacotherapies for ventilator-induced lung injury (VILI) remain lacking. Disruption of circadian (diurnal) rhythms is implicated in various lung pathologies, and the exploration of circadian regulation in VILI has emerged as a clinically relevant research direction for optimizing mechanical ventilation strategies. We hypothesized that the pulmonary Bmal1/Per2 axis confers protection against VILI by activating the Nrf2 antioxidant pathway. - Source: PubMed
Publication date: 2026/05/05
Li De-ChaoWu Ming-HuiRuan Hong-Yan - This study examines the impact of a light-cycle shift regimen on corneal and conjunctival tissues in menopausal rats and evaluates the protective role of combined hormone therapy. - Source: PubMed
Publication date: 2026/05/02
Acer SemraArgun MehmetÖzmen ÖzlemAçıkgöz CaferYavuz Mustafa