RELA (phospho-Ser529) Antibody
- Known as:
- RELA (phosphorilated-Ser529) Antibody
- Catalog number:
- abx000267
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- RELA (phospho-Ser529) Antibody
Ask about this productRelated genes to: RELA (phospho-Ser529) Antibody
- Gene:
- RELA NIH gene
- Name:
- RELA proto-oncogene, NF-kB subunit
- Previous symbol:
- NFKB3
- Synonyms:
- p65
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2016-10-05
Related products to: RELA (phospho-Ser529) Antibody
Related articles to: RELA (phospho-Ser529) Antibody
- Bacterial quorum sensing (QS) governs metabolically costly cooperative behaviors such as biofilm formation and virulence. How bacteria prevent unwanted QS under nutrient limitation is unknown. Using pv. , a pathogen of rice, as a model, we identify the stringent response alarmone ppGpp as a metabolic checkpoint that directly inhibits diffusible signal factor (DSF)-mediated QS. The loss of the alarmone synthetase RelA increased DSF production, unwound QS-responsive genes, and enhanced social behaviors at stationary phase. Structural, biochemical, and genetic studies showed that ppGpp directly inhibits phosphodiesterase activity of the QS response regulator RpfG, elevating the cyclic di-GMP levels. Increase in cyclic di-GMP reduces the DNA binding by the QS transcriptional regulator Clp, disrupting a positive auto-regulatory loop required for DSF synthesis and social behavior. This may be a conserved mechanism used by bacteria to limit social behaviors with saving of energy when resources are low or under stringent condition. - Source: PubMed
Publication date: 2026/07/13
Gondu ParimalaVerma Raj KumarBhattacharjee ChayanMohanty Amaresh KuChatterjee Subhadeep - This study aimed to investigate the antiinfi ammatory effects and potential molecular mechanisms of star anise-cinnamon compound essential oil (SCEO) against multidrug-resistant Salmonella Thompson (MDR S. Thompson) infection in mice. - Source: PubMed
Publication date: 2026/07/13
Xu ZihengZhang JieLin RongdianLuan ZuxiangShao KaiChen YanhuaLiang JieHuang ChuangrongZhang DapeiTao JunyuTang HaiboHuang WeizhongHuang LongjianLi HaiChen Dingqiang - The effects of scandium on skeletal muscle cells remain poorly understood. This study aims to determine whether scandium chloride (ScCl) affects C2C12 myoblast proliferation, and the cellular responses were assessed using CCK-8, flow cytometry, RNA-seq, and bioinformatic analyses after treatment with 0.01 mM and 1 mM ScCl. We verified that 1 mM ScCl significantly promoted cell proliferation by inducing the G1/S phase transition, while the low concentration had no significant effect. However, GO enrichment analysis failed to capture proliferation-related terms among the top 20 ranked terms. To address this, we grouped genes based on their expression patterns and combined transcription factor activity inference with Hallmark pathway enrichment. This strategy identified distinct functional modules responsive to scandium, involving mitosis, myogenesis, and metabolism, with key regulators including Foxo1, Rela, and myogenic transcription factors. Collectively, our findings suggest that scandium may exert regulatory effects on myoblast proliferation and modulate genes involved in differentiation and metabolism by coordinating multiple functional modules. - Source: PubMed
Publication date: 2026/07/16
Zhao JingyuAn YingnanShi JiankaiMa LibingHe XiaoyingLiu YingLiu Chuncheng - : Two novel copper(II) coordination complexes, PH-Cu [(1,10-phenanthroline)(malonato)copper(II)] and PC-Cu [(1,10-phenanthroline)(cyclobutane-1,1-dicarboxylato)copper(II)], were synthesized and evaluated as potential anticancer agents, aiming to characterize structural properties, explore antiproliferative activity and generate mechanistic hypotheses through experimental and computational approaches. : Complexes were characterized by EPR, FTIR-ATR, and ESI-MS, with preliminary SC-XRD data for PH-Cu. Antiproliferative activity was evaluated against six human cancer cell lines using the MTT assay (24 h). Subcellular effects were assessed by fluorescence microscopy and RT-qPCR. Computational studies included DFT geometry optimization, target prediction, molecular docking, and ADMET profiling. : Based on spectroscopic and spectrometric data and comparison with analogous Cu(II) complexes, a distorted square-pyramidal coordination geometry was proposed; this assignment was not confirmed by SC-XRD. Both complexes exhibited potent antiproliferative activity, with PH-Cu showing the highest potency in HeLa cells (IC = 4.22 µM). Under the same conditions, cisplatin showed substantially lower activity (HepG2: 191.1 µM; Caco-2: 129.6 µM; NCI-H69: >333.3 µM; HeLa: 21.9 µM). Fluorescence microscopy at 18 h revealed pyknosis, karyorrhexis, and microtubule disorganization, consistent with regulated cell death. RT-qPCR of PH-Cu indicated intrinsic apoptotic pathway engagement (BAX +3.20-fold; BCL2 to 0.39-fold of control). DFT-optimized bond lengths were consistent with crystallographic data for analogous complexes. Molecular docking suggested PRKCG, RELA (p65), Caspase-3, and α/β-tubulin as interaction candidates, while ADMET profiling predicted favorable intestinal absorption (>92.8%) and low BBB permeability. : These results suggest that the [Cu(phen)] unit constitutes the primary pharmacophore, with the dicarboxylate co-ligand as a modulator of the antiproliferative profile, suggesting promising anticancer pharmacological potential. - Source: PubMed
Publication date: 2026/07/20
García-Díaz Jesús MagdielBacilio-Beltrán Héctor AlejandroGaribaldi-Ríos Asbiel FelipeGallegos-Arreola Martha PatriciaRangel-Salas Irma IdaliaDelgado-Saucedo Jorge IvánCastro-García PaolaMartínez-Velázquez MoisésPuebla-Pérez Ana María - Atherosclerotic plaque instability is driven by complex interactions among inflammatory, structural, and cellular remodeling programs. While bulk RNA sequencing provides insight into tissue-level transcriptional states and single-cell RNA sequencing (scRNA-seq) defines cellular heterogeneity, integration across these transcriptomic layers remains limited. We aimed to identify coordinated transcriptional programs associated with stable and unstable plaque phenotypes and map these programs to specific cellular compartments and regulatory networks. - Source: PubMed
Publication date: 2026/07/02
Lee EunseukSutihar AnshuTousif MeirajuddinAng Song PengTran DanielIglesias Jose