E2F2 antibody - middle region (ARP31611_P050)
- Known as:
- E2F2 (anti-) - middle region (ARP31611_P050)
- Catalog number:
- arp31611_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- E2F2 antibody - middle region (ARP31611_P050)
Related genes to: E2F2 antibody - middle region (ARP31611_P050)
- Gene:
- E2F2 NIH gene
- Name:
- E2F transcription factor 2
- Previous symbol:
- -
- Synonyms:
- E2F-2
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-08-31
- Date modifiied:
- 2016-10-05
Related products to: E2F2 antibody - middle region (ARP31611_P050)
Related articles to: E2F2 antibody - middle region (ARP31611_P050)
- Cordycepin, a natural nucleoside analogue, exhibits anti-inflammatory and antitumor activity in multiple malignancies. However, the molecular basis of its action in pancreatic cancer and its potential role in chemosensitization remain incompletely defined. In this study, the effects of cordycepin on malignant phenotypes of pancreatic cancer cells were investigated in vitro. Network pharmacology was applied to identify candidate targets and construct a disease-drug-target-pathway network. Reverse virtual screening and molecular docking were used to predict key binding proteins, while RNA sequencing identified downstream pathways regulated by cordycepin. Target engagement was validated using cellular thermal shift assays, molecular docking, and molecular dynamics simulations. The underlying mechanistic pathways were further confirmed by functional experiments, and the therapeutic efficacy of cordycepin in combination with gemcitabine was evaluated. Our results demonstrated that cordycepin reduced the growth of pancreatic cancer cells and induced G2/M phase arrest and apoptosis. Network pharmacology identified 56 hub targets enriched in oncogenic pathways, including PI3K/AKT pathway. Reverse virtual screening revealed 111 candidate binding proteins, and intersection with hub targets highlighted five key effectors: CDK2, GSK3B, IL2, NOS3, and PARP1. Transcriptomic profiling showed marked disruption of cell cycle pathways, and CDK2 was validated as a direct molecular target of cordycepin. Cordycepin suppressed TNNI2 transcription by inhibiting the CDK2/E2F2 axis. Furthermore, cordycepin acted synergistically with gemcitabine to enhance antitumor responses and promote apoptosis in pancreatic cancer models. Collectively,cordycepin exerts antitumor activity in pancreatic cancer by targeting the CDK2/E2F2 axis to suppress malignant progression and by concurrently sensitizing cells to gemcitabine, thus holding promise as a therapeutic agent. - Source: PubMed
Publication date: 2026/07/29
He RuDu YanJiang WenkaiZhou Wence - Porcine β-defensin 2 (pBD2) is an antimicrobial peptide with both antibacterial and immunomodulatory activities and plays an important role against pathogens. Our previous results suggested that pBD2 might exert its protective effects against E. coli by regulating cell apoptosis and proliferation through the Akt signaling pathway. However, the specific roles and underlying mechanisms of pBD2 in regulating these cellular processes remain unclear. In this study, porcine intestinal epithelial cells (IPEC-J2) were treated with pBD2 in the presence of Enterotoxigenic E. coli (ETEC) K88 challenge. pBD2 inhibited ETEC-induced apoptosis, decreased the levels of cleaved caspase-3 and caspase-9, and restored mitochondrial membrane potential, suggesting that pBD2 inhibited ETEC-induced apoptosis via the intrinsic apoptotic pathway. Moreover, pBD2 restored cell proliferation and attenuated ETEC-induced cell cycle arrest in the G0/G1 phase, and upregulated the expression of proliferation-related genes including CDC25A, CDC6, E2F2 and PCNA. In addition, the results further revealed that pBD2 attenuated cell apoptosis and restored cell proliferation in ETEC K88-infected IPEC-J2 cells by inhibiting the Akt signaling pathway. Our results provide further evidence for the protective effects of pBD2 on intestinal epithelial cells and extend its known biological roles. This study elucidates an anti-apoptotic and pro-proliferative mechanism of pBD2 against ETEC infection and provides insights into its potential application. - Source: PubMed
Publication date: 2026/07/07
Zhu GuixinGu MingkeZhao QingboDu ZhilongWang KejunLi Chunli - DYRK1A (dual-specificity tyrosine phosphorylation-regulated kinase 1A) is a dosage-sensitive regulator of central nervous system development. Dysregulation contributes to major neurodevelopmental disorders, including Down Syndrome (DS), Autism Spectrum Disorder (ASD), and Intellectual Developmental Disorder (IDD). This review critically examines how DYRK1A dosage shapes neurodevelopment, neurotransmitter regulation, and disease phenotypes. - Source: PubMed
Publication date: 2026/07/02
Paul SampritiDubey SonalTiwari Prashant - AML is an aggressive blood cancer associated with poor clinical outcomes. Chemotherapy remains the standard of treatment, but unfortunately relapse is very common, highlighting the need for alternative therapies. T cell dysfunction and exhaustion are prominent in AML and may represent a barrier to effective immunotherapy yet remains poorly studied in AML. DNA methylation is a major driver of T cell exhaustion and inhibition of methylation can block exhaustion and restore T cell function in chronic viral infections and other cancers but is understudied in AML. Here, we investigated the impact of azacytidine (Aza), an FDA-approved hypomethylating agent, on T cell exhaustion in AML. Using a spontaneous AML mouse model and samples from patients with AML, we found that Aza treatment modulates T cell function. Aza-treatment of AML-bearing mice decreased tumor burden and reshaped CD8+ T cell states, with increases in frequencies of memory subsets and decreases in regulatory T cells (Tregs). Functionally, Aza treatment overcame the impaired proliferation displayed by both CD4 and CD8+ T cells in our model. DNA methylation sequencing of T cells after Aza treatment revealed hypomethylation and increased expression of stem-like precursor gene and , a regulator of cell cycle progression and proliferation. Similar changes in phenotypes were observed in cultures of AML patient samples treated with Aza. Collectively, we show that Aza remodels epigenetic and functional states in AML and has the potential to reverse T cell exhaustion, with enhanced memory and proliferation capacity. Our work generates a mechanistic framework that provides rationale of combining hypomethylating agents with T cell-based immunotherapies in this lethal disease. - Source: PubMed
Publication date: 2026/06/17
Pandita RavinaKosaka YokoMulkey Jessica SLayman Cora EDavis Brett ACarbone LuciaLind Evan F - Glycolipid metabolism and microRNAs (miRNAs) play important roles in hepatitis C virus (HCV)-induced type 2 diabetes mellitus (T2DM). Our study aimed to explore the mechanism of action of miR-378b in liver glycolipid metabolism disorders caused by HCV infection. - Source: PubMed
Publication date: 2026/06/12
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