RELA antibody - middle region (ARP30371_P050)
- Known as:
- RELA (anti-) - middle region (ARP30371_P050)
- Catalog number:
- arp30371_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RELA antibody - middle region (ARP30371_P050)
Related genes to: RELA antibody - middle region (ARP30371_P050)
- 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 antibody - middle region (ARP30371_P050)
Related articles to: RELA antibody - middle region (ARP30371_P050)
- Acute lung injury (ALI) is a common critical respiratory illness. 3'-Hydroxypuerarin (3HP), a beneficial isoflavone from (Willd.) Ohwi, possesses significant pharmacological activities, but its effects on ALI remain limited. - Source: PubMed
Publication date: 2026/03/31
Hu HuiyuWang KongyanQiu YiXu ZaibinChen YanHu YingjieHuang JiawenLuo Zhuohui - Drug-induced dedifferentiation towards drug-tolerant persister states is a common mechanism cancer cells exploit to escape therapies, hindering durable responses. How early epigenomic and transcriptomic programs coordinate to initiate these reversible transitions remains largely unexplored. Here we employ high-temporal-resolution multi-omics profiling, information-theoretic approaches, and dynamic system modeling to probe these processes in BRAF-mutant melanoma models and patient specimens. We uncover a hysteretic transition trajectory in response to oncogene inhibition and subsequent release, driven by two tightly coupled transcriptional waves that orchestrate genome-scale chromatin reconfiguration. Modeling of these waves suggests NF-κB/RelA-driven chromatin remodeling as the underlying mechanism of cell-state dedifferentiation, which we validate experimentally. We identify RelA-target genes epigenetically modulated to drive this process and define a quantitative epigenome gauge of melanoma cell-state plasticity that supports targeting epigenetic machineries to potentiate oncogene inhibition. Across additional cancer models, oxidative stress-mediated NF-κB/RelA activation emerges as a common driver of transitions into drug-tolerant persister states, revealing a central role for NF-κB axis in coupling oxidative stress to cancer progression. - Source: PubMed
Publication date: 2026/04/15
Su YapengLiu ChunmeiLu XiangChuang Hui-YuLi GuidengShao ShiqunKong YanLee Jihoon WNg Rachel HWong StephanieRobert LidiaWarden CharlesLiu VictoriaChen JieWang ZhuoQin GuangrongTang YinCheng HanjunNg Alphonsus H CChen DanielPeng SongmingXue MinJohnson DazyXu YuWang JinhuiWu XiweiShmulevich IlyaShi QihuiLevine RaphaelRibas AntoniBaltimore DavidGuo JunHeath James RWei Wei - Breast cancer is the most common cancer diagnosed and the leading cause of death for women worldwide. Noni (Morinda citrifolia L.) contains an anthraquinone called damnacanthal (3-hydroxy-1-methoxy-anthraquinone-2-aldehyde), which is known to inhibit the growth of many types of cancer cells. The purpose of this study is to examine the anticancer effects of damnacanthal on cell proliferation, apoptosis, and cell cycle in breast cancer cells and its underlying signaling pathway, including nuclear factor kappa B (NF-ĸB), epidermal growth factor receptors (EGFR), and PI3K/AKT/PTEN. Damnacanthal reduced cell viability in both normal and triple-negative breast cancer cell lines, MCF-7 and MDA-MB-231, respectively. In MCF-7 cells, damnacanthal induced late apoptosis and increased cell cycle arrest in the G0/G1 and S phase, decreased RELA gene expression, and enhanced TNF-α gene expression. However, it had no effect on the protein expression of PI3K/AKT. Damnacanthal exerted anticancer activity on MCF-7 cell lines via blocking NF-ĸB (subunit p65) expression at mRNA levels in the PI3K/AKT-independent manner. These findings highlight the potential benefits of damnacanthal as a promising NF-ĸB inhibitor for cancer prevention or treatment against breast carcinoma. - Source: PubMed
Jongcharoen OnnicharReabroi SomrudeeSanvarinda PimtipTungmunnithum DuangjaiParichatikanond WarisaraPinthong Darawan - - Source: PubMed
Publication date: 2026/04/14
Jayaraman DhaaraniShanmugam Naresh PScott Julius XavierRangarajan VidhyalakshmiSampath SanthoshVij MukulBharathi NaveenMuthu AnurekhaKumar Praveen - To explore the regulatory aspects of mRNAs and miRNAs in suicide, we integrated transcriptomic data from GEO datasets. The analysis of mRNA expression in the prefrontal cortex of suicide victims with major depressive disorder revealed a differential profile with 27 downregulated mRNAs, including , , , , and , which are involved in proteostasis, transcriptional regulation, and apoptosis. Functional enrichment analysis using KEGG and Gene Ontology (GO) revealed significant associations with synaptic plasticity, neuronal survival, and signaling pathways, including MAPK, TGF-β, Wnt, p53, and neurotrophins. Subsequently, using the GSE34120 GEO dataset of miRNAs from the frontal cortex of suicide victims, 105 dysregulated miRNAs were identified. The networks revealed compact regulatory modules with hsa-miR-576-3p, hsa-miR-493, and hsa-miR-550, as well as highly connected central nodes such as hsa-miR-30b, hsa-miR-16a-5p, hsa-miR-181a-5p, and hsa-miR-184. The integration of both profiles allowed the elaboration of miRNA-mRNA regulatory networks in which , , , and interact with multiple dysregulated miRNAs. These findings support the notion that suicide involves complex post-transcriptional dysregulation, particularly related to astrocytic function and neurotrophic signaling, with potential diagnostic and therapeutic applications. - Source: PubMed
Publication date: 2026/03/30
Cortéz-Sánchez José LuisRivera-Escobar Hernán MauricioMuñoz Roa Esther NataliaZabala-Bello Carlos AndrésPérez-Sánchez GilbertoChin Chan José MiguelBautista-Ortiz MonserratLópez-Martínez Karla MaríaOsorio-Antonio FedericoGálvez-Romero José LuisCarrasco Carballo AlanSedeño-Monge VirginiaCastelán FranciscoBautista-Rodríguez Elizabeth