OTF2 Blocking Peptide
- Known as:
- OTF2 Blocking Peptide
- Catalog number:
- 33r-10812
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- OTF2 Blocking Peptide
Related genes to: OTF2 Blocking Peptide
- Gene:
- POU2F2 NIH gene
- Name:
- POU class 2 homeobox 2
- Previous symbol:
- OTF2
- Synonyms:
- OCT2
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-08
- Date modifiied:
- 2017-07-07
Related products to: OTF2 Blocking Peptide
Related articles to: OTF2 Blocking Peptide
- Preeclampsia (PE) is a major pregnancy complication that poses risks to both the mother and the fetus. Oxidative stress (OS) plays a crucial role in its pathogenesis. This study aims to explore the diagnostic value of oxidative stress-related genes for PE. - Source: PubMed
Ye WenhuaYin Haiyan - The overall survival rate of acute myeloid leukemia (AML) remains less than 30%. Metabolic reprogramming of leukemia cells, such as the Warburg effect, enables them to adapt to the microenvironment and thereby develop. Elucidating the landscape of lactate regulation in AML helps clarify the pathogenesis from the perspective of metabolic reprogramming and identify possibilities for optimizing current treatment modalities. - Source: PubMed
Publication date: 2026/03/23
Guo ZhiboZhang WenleiGao ZengliangLi QiGuo DanYue LijuanLiu YutongNi XiaotingFan ShengjinHai Xin - HER2-low breast cancer is a biologically heterogeneous subgroup in which hormone receptor (HR) expression critically shapes prognosis and treatment, but the underlying regulatory mechanisms remain unclear. MicroRNAs (miRNAs) are key post-transcriptional regulators of gene expression and may contribute to HR heterogeneity. This study aimed to identify deregulated miRNAs and associated gene networks distinguishing HER2-low/HR-positive from HER2-low/HR-negative tumors, elucidating the molecular mechanisms underlying this divergence. Differential expression analyses of miRNAs and genes were performed using Wilcoxon tests and DESeq2 (|logFC| > 1; FDR-adjusted -value < 0.05). Survival analyses were conducted using Cox proportional hazards models to evaluate the individual miRNAs and miRNA signature. Functional enrichment analyses, including GO, KEGG and Reactome pathways, were performed. Correlation analysis and the miRNA target prediction were integrated to identify regulatory interactions. Comparisons between HER2-low/HR-positive and HER2-low/HR-negative tumors identified 165 significantly deregulated miRNAs and 170 strongly deregulated genes. Intersection analysis highlighted miR-9-5p, miR-532-5p and miR-576-5p as specifically associated with HR-negative status. Survival analyses showed non-significant trends for the overall survival and progression-free interval. Functional enrichment analysis revealed hormone-related pathways in HR-positive tumors and immune, inflammatory and proliferative pathways in HR-negative tumors. Integrative correlation and target prediction analyses identified two miRNA-mRNA regulatory axes, miR-576-5p/TGFBI and miR-9-5p/POU2F2. Our study demonstrated that HER2-low breast cancer exhibits distinct miRNA and gene expression profiles, which highlight different transcriptomic profiles according to HR status for the first time. Specific miRNA-gene networks may drive transcriptional heterogeneity, serving as potential biomarkers for stratification and as therapeutic targets. These findings provide insight into the molecular basis of HER2-low tumor diversity and support future development of HR-directed therapeutic strategies. - Source: PubMed
Publication date: 2026/03/03
Carvalho EduardaBrandão AndreiaSchmitt FernandoVale Nuno - Uncovering the mechanisms that generate the immense diversity of neuronal cell types remains a fundamental goal of developmental biology. Different "cardinal classes" of spinal neurons that share a common molecular identity are produced from spatially segregated progenitor domains. Within many classes, a stereotyped sequence of neuronal subtypes of related function is generated over time, raising the question of the mechanisms that control this process. Here, we show that the successive expression of mouse transcription factors Onecut2, Pou2f2, and Pou3f1 correlates with the emergence of sequentially generated subpopulations within several cardinal classes. We demonstrate that loss of Pou2f2 impairs the development of two early-born motor neuron columns and respecifies anterolateral system projection neurons into a later-born subset. Similarly, we show that Pou3f1 expression is required for the normal development of later-born subsets of motor neurons and anterolateral system projection neurons. Together, our observations provide functional evidence that horologic diversification of spinal circuits is driven by a conserved sequence of transcription factors. - Source: PubMed
Publication date: 2026/03/18
Segarra Laia CaudetSangster KevinSagner JuliaKania ArturSagner Andreas - The biological basis of the afternoon nap, a widespread yet poorly understood phenomenon, has remained elusive. Here we identify NPAS2, among core circadian regulators, as a sex-independent determinant of the nap behavior in mice. Specifically, medial prefrontal cortex (mPFC)-expressed NPAS2 orchestrates nap regulation through circadian modulation of local dopaminergic activity. We demonstrate that tyrosine hydroxylase-positive (TH) neurons in mPFC exhibit time-of-day dependent wake-promoting activity, showing minimal excitation precisely during nap hours. Mechanistically, NPAS2 achieves this circadian suppression through a POU2F2-TH regulatory pathway: 1) transcriptional activation of the transcription repressor POU2F2, and 2) consequent downregulation of TH expression (a rate-limiting enzyme for dopamine synthesis) and dopamine production in mPFC TH neurons. These findings establish an endogenous circadian mechanism where mPFC NPAS2 periodically inhibits wake-promoting dopaminergic activity to drive nap behavior, providing fundamental insights into the neural and molecular regulation of nap biology. - Source: PubMed
Publication date: 2026/03/16
Guo LianxiaCen HaobinHuang YuweiLi ZanjinZeng KengranWu ZicongWeng JiaxianGuo XiaocaoHe DiLiu XinyuYang ZhehanXu HaimanHao TingyingWei BinbinDiao XingxingWu Baojian