RELA (phospho-Ser536) Antibody
- Known as:
- RELA (phosphorilated-Ser536) Antibody
- Catalog number:
- abx000176
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- RELA (phospho-Ser536) Antibody
Related genes to: RELA (phospho-Ser536) 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-Ser536) Antibody
Related articles to: RELA (phospho-Ser536) Antibody
- The role of human umbilical cord mesenchymal stem cell-derived extracellular vesicles (hUCMSC-EVs) in liver regeneration is promising, yet their clinical translation is hampered by insufficient production. Current strategies targeting their secretion are inefficient and lack a clear mechanistic understanding. We isolated and characterized hUCMSC-EVs pretreated with the H89 and other mTORC1 inhibitors. Our findings revealed that H89 effectively enhances the secretion of hUCMSC-EVs across diverse cell types, demonstrating universal efficacy. Importantly, H89 upregulates GABARAPL1 expression, a key negative regulator of the PKA/mTORC1 pathway, to inhibit mTORC1 activity and promote the formation of amphisomes and SNARE-mediated hUCMSC-EVs release. Furthermore, EVs derived from H89-pretreated hUCMSCs (H-EVs) exhibited altered cargo composition, significantly increased proliferative activity, and potentiated liver regeneration via the RELA/miR-29a axis, which regulates the homeostasis of hepatic stellate cells. Our results highlight that H89 enhances hUCMSC-EV secretion through mTORC1 inhibition, with the resulting benefits for liver regeneration mediated by the RELA/miR-29a network. These findings demonstrate the great promise of H89 in EV-based liver regeneration, offering a promising platform for clinical translation. - Source: PubMed
Fu YuMa YiZhang JiajunLiang LiweiLi TingGuo ZeyiLi ZhongzheFeng LeiWang YiHe GuolinLi ShaoLi YangXu XiaopingLiao HuiGao Yi - Liver fibrosis is a progressive pathological process triggered by chronic liver disorders, which may progress to hepatocellular carcinoma (HCC) if left untreated. Currently, there are no specific therapeutic agents for liver fibrosis, highlighting an urgent need for novel pharmacological strategies. Tomatidine (TD), a major steroidal glycoal-kaloid abundant in immature tomato fruits, leaves, and stems, exhibits diverse biological activities including anti-inflammation, anti-tumor effects, and autophagy regulation. However, its role in liver fibrosis and the underlying molecular mechanisms remain incompletely understood. In this study, we combined network pharmacology, molecular docking, and experimental validation to investigate the potential effects of TD against liver fibrosis and its associated mechanism of action. In vitro experiments using the human hepatic stellate cell (HSC) line LX-2 demonstrated that TD inhibited HSC proliferation in a dose- and time-dependent manner, and downregulated the expression of fibrosis-related markers α-smooth muscle actin (α-SMA) and collagen type I α1 chain (COL1A1) at the gene, protein, and cellular levels. Network pharmacology analysis identified 18 common targets between TD and liver fibrosis, with core targets including MAPK3, RELA, and MAPK1 involved in intracellular signal transduction and stress-activated MAPK cascade. Although no autophagy-related targets were identified in the current database among these common targets, pharmacological evidence and experimental validation confirmed that TD promoted autophagy in LX-2 cells, as indicated by reduced P62 expression, increased LC3-II/LC3-I ratio and Beclin-1 levels, and enhanced autophagic flux. Further mechanism exploration revealed that TD exerted its autophagy-promoting effect by regulating the ERK/MAPK-mTOR-ULK1 signaling pathway: TD suppressed the phosphorylation of ERK and mTOR, while activating ULK1 phosphorylation. Molecular docking verified stable binding affinity between TD and key proteins in this pathway (ERK, MAPK, mTOR, ULK1) as well as autophagy-related proteins (P62, Beclin-1, LC3) and fibrosis-related protein COL1A1, with specific amino acid residues mediating hydrogen bond formation. Collectively, our findings demonstrate that TD modulates fibrosis-related markers in hepatic stellate cells by promoting autophagy in HSCs via the ERK/MAPK-mTOR-ULK1 pathway. This study enriches the biological function research of TD and provides a novel potential candidate and theoretical basis for the development of anti-liver fibrosis therapeutics. - Source: PubMed
Publication date: 2026/05/08
Fan YutingZhang YuxinLi WeitongDu YinSong YangWang JinhuiTang BinDeng FengmeiCheng Li - Malaria represents a major global health challenge. Excessive activation of inflammatory response is critical for the pathogenesis of severe malaria. The NF-κB signaling pathway regulates inflammatory responses; saturated anacardic acid (SAA) inhibits NF-κB activation. The aim of this study was to evaluate whether SAA modulated inflammatory mediators in BV-2 microglia and THP-1 monocytes, whose overproduction contributes to the development of severe malaria. Survival rate was assessed in cerebral malaria-susceptible CBA mice infected with Plasmodium berghei ANKA and treated or not with SAA. THP-1 monocytes and BV-2 microglia were incubated with or without SAA and with or without co-incubation with P. falciparum or P. berghei ANKA, respectively. After 24 h, terminal molecules of the NF-κB pathway RelA and RelB, TNF-α, IL-6, IL-8, MCP-1, ROS, NO, COX-2 and 5-LOX were assessed by flow cytometry. SAA increased survival in P. berghei-Infected CBA mice. BV-2 microglia exhibited higher RelB expression than THP-1 monocytes. Co-incubation with Plasmodium and SAA decreased RelB but increased RelA expression in BV-2 microglia, whereas RelA expression increased in THP-1 monocytes. Co-incubation with SAA and Plasmodium decreased TNF-α, IL-8, MCP-1, ROS, NO, and COX-2 expression but increased IL-6 production, all of which are associated with inflammatory responses involved in severe malaria. To our knowledge, this study is the first to demonstrate that SAA modulates the key components of severe malaria immunopathogenesis, particularly TNF-α production, ROS and NO generation in BV-2 microglia and THP-1 monocytes. These findings indicate that SAA may represent a promising adjunct therapy to prevent progression to severe malaria. - Source: PubMed
Publication date: 2026/05/06
Gontijo Andreia Cristina Gonçalves CascaesCorazza DaniloAlbuquerque Lucas Fraga FriaçaCiarlini Ana Carolina Laraiade Oliveira Andressa SouzaMonteiro Natália Ciprianode Oliveira Mariangela SouzaCouto Shirley Claudino PereiraRomeiro Luiz Antonio SoaresBorges Tatiana Karla Dos SantosMuniz-Junqueira Maria Imaculada - Periodontitis (PD) is a prevalent chronic inflammatory disorder in adults, and moderate-to-severe PD (Stage II-III/IV) may accelerate brain aging and neurodegenerative changes via the peripheral-central immune-neural axis, although the molecular connections and mechanisms of interaction have yet to be fully elucidated. This study sought to identify senescence-associated molecules potentially shared by PD and Alzheimer's disease (AD) using integrated transcriptomic analysis, machine learning, and RNA interference assays, and to further assess the role of TMEM140 in linking PD to brain aging. - Source: PubMed
Publication date: 2026/04/22
Zhao HaoRanWang HongTaoLi WangXingSu RuiLi JingLiu YanWang Lei - Diabetic bone defects repair is severely hindered by impaired angiogenesis and delayed osteogenesis. Conventional tissue-engineered scaffolds often fail to achieve effective vascularization due to the compromised angiogenic capacity of host endothelial cells in the hyperglycemic microenvironment. Here, we developed a prevascularized scaffold by encapsulating stem cells from human exfoliated deciduous teeth (SHED), which shared developmental origin to craniofacial bone, within a reduced graphene oxide (rGO)-integrated hydrogel. rGO significantly accelerated SHED-mediated formation of vascular networks in vitro. The scaffold's therapeutic efficacy was confirmed in a clinically relevant diabetic beagle dog mandibular defect model, which showed increased vascular density and accelerated bone regeneration. Mechanistic validation revealed that rGO activates the FAK-Src/RELA pathway to upregulate P4HA1, subsequently enhancing collagen I synthesis and driving extracellular matrix (ECM) remodeling to create a pro-angiogenic niche. This study demonstrates that engineering the ECM with rGO is a novel strategy to accelerate prevascularization and bone repair in diabetic conditions. - Source: PubMed
Publication date: 2026/05/07
Zhang CanKang YiyuanLai ShulinWang ChunyiHe GuixinJian KehuiYin SuhanTan XinerZhou XinruLiu WenjingZhao FujianLiu JiaShao Longquan