RELA (phospho-Ser276) Antibody
- Known as:
- RELA (phosphorilated-Ser276) Antibody
- Catalog number:
- abx000175
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- RELA (phospho-Ser276) Antibody
Related genes to: RELA (phospho-Ser276) 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-Ser276) Antibody
Related articles to: RELA (phospho-Ser276) Antibody
- - Source: PubMed
Publication date: 2026/04/23
Heymann Clément J FGouwy MiekeHermans RobinTwizere Jean-ClaudeAssone TatianeCasseb JorgeRacine IsaacCleynen IsabelleMurphy Edward LBruhn RobertaSchols DominiqueVanderlinden EvelienVan Weyenbergh Johan - Dimethyl fumarate (DMF), a cysteine targeting agent, is clinically used to treat multiple sclerosis and psoriasis. However, its precise molecular mechanism remains incompletely understood. Here, we investigated the effects of DMF on NLRP3 inflammasome activation. DMF suppresses NLRP3 inflammasome activity at both the priming and activation steps. Using chemoproteomics, we identified DMF targets in macrophages, including IRAK3/4 and RELA/B involved in the NLRP3 priming step, NEK7 involved in NLRP3 early activation, and GSDMD involved in NLRP3 late activation. To understand how DMF inhibits NLRP3 early activation, we showed that DMF modifies NEK7 Cys298 to disrupt NLRP3-NEK7 interaction and inflammasome activation. Interestingly, NEK7 Cys298 is critical for NLRP3 inflammasome activation. This study provides mechanistic insights into DMF's immunomodulatory effects and suggests that targeting NEK7 Cys298 can be a novel strategy for inflammatory diseases. Our work highlights the utility of DMF to identify functionally important cysteine residues in immune signaling pathways. - Source: PubMed
Publication date: 2026/04/21
Zhang YandongLindner HelenaSo BrianChen ZirongLi HaoyangXu JiashuWang JiaheXu JiePetre Alexandru MDistefano Mark DNúñez GabrielLin Hening - The concept of labor analgesia remains largely ambiguous to expectant women and pregnant individuals within the Indian healthcare system. The act of parturition is recognized as one of the most excruciating experiences in a woman's existence. Inadequately managed labor pain yields numerous detrimental ramifications for both the mother and the fetus. Insufficient levels of cognizance and prevailing attitudes toward labor analgesia among pregnant women constitute a significant impediment that adversely influences both maternal and fetal wellbeing. - Source: PubMed
Publication date: 2026/03/31
Srinivasan YuvasriPremSundar KalyaniPrabaAnuradha MSubramanian SGunaseelan DSaravanan ASelvi K Thamarai - High-density lipoprotein (HDL) functionality is emerging as a novel predictor of disease outcomes. The role of HDL functionality in patients with diabetes-related amputations is unexplored. We aimed to assess changes in HDL functionality in people with diabetes who had minor amputations and to determine the relationship between HDL functionality and wound closure (WC). - Source: PubMed
Publication date: 2026/04/21
Lotfollahi ZahraSolly Emma LTan Joanne T MNankivell Victoria ASandeman LaurenStretton LiamDorraki MohsenPena GuilhermeVerjans JohanSzpak ZygmuntDawson JosephMcMillan NeilPsaltis Peter JFitridge RobertBursill Christina A - Breast cancer remains the second leading cause of cancer-related mortality among women, with triple-negative breast cancer (TNBC) exhibiting a particularly poor five-year prognosis. Here, we demonstrated that, among genetic and pharmacological perturbations targeting DNA replication, suppression of DNA polymerase epsilon (POLE) induced a potent, TNBC-specific gene expression signature enriched in inflammatory cytokines that are transcriptional targets of NF-κB. TNBC cells exhibited markedly higher levels of DNA damage and canonical NF-κB activation compared to luminal breast cancer cells. Notably, NF-κB activation in this context depended on the canonical component RELA but not the non-canonical component RELB. Mechanistically, ATM, STING, and RIG-I each contributed to NF-κB activation following POLE suppression. POLE suppression in an in vivo murine TNBC model led to cancer cell-intrinsic elimination of tumor burden and increased immune cell infiltration. Together, these findings support a model in which replication stress from POLE inhibition triggers robust NF-κB-mediated inflammation and immune microenvironment remodeling in TNBC and can independently trigger tumor eradication. These results suggest a potential therapeutic avenue for targeting POLE in TNBC. - Source: PubMed
Publication date: 2026/04/21
Sher Elizabeth FFujihara Kenji MTao AnthonySastourne-Haletou PaulErenburg DianaSviderskiy Vladislav OMir HannanKarakousi TriantafylliaLoomis Cynthia ADeng JiehuiRuggles Kelly VWong Kwok-KinPossemato Richard