NFKB1 (phospho-Ser337) Antibody
- Known as:
- NFKB1 (phosphorilated-Ser337) Antibody
- Catalog number:
- abx000177
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- NFKB1 (phospho-Ser337) Antibody
Related genes to: NFKB1 (phospho-Ser337) Antibody
- Gene:
- NFKB1 NIH gene
- Name:
- nuclear factor kappa B subunit 1
- Previous symbol:
- -
- Synonyms:
- KBF1, p105, NFKB-p50, p50, NF-kappaB, NFkappaB, NF-kB1
- Chromosome:
- 4q24
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-14
- Date modifiied:
- 2019-04-23
Related products to: NFKB1 (phospho-Ser337) Antibody
Related articles to: NFKB1 (phospho-Ser337) Antibody
- Immune dysregulation (ID), defined as aberrant immune activation or suppression, may result in autoimmune or inflammatory disorders, lymphoproliferative malignancies, and allergic diseases. Apoptosis, nuclear factor-κB (NFκB), and phosphoinositide 3-kinase (PI3K) pathways are major pathways involved in ID. - Source: PubMed
Publication date: 2026/07/04
Bildik Hacer NeslihanYaz IsmailEsenboga SalihaCagdas Deniz - Cognitive decline is a hallmark of neurodegenerative diseases. The complex pathophysiology of these diseases has limited the efficacy of current therapies. The co-administration of epidermal growth factor (EGF) and growth hormone-releasing peptide 6 (GHRP6) emerges as a promising neuroprotective candidate. The present study evaluated the therapeutic potential of this combination in two preclinical models of cognitive impairment: (i) age-related decline and (ii) impairment induced by intracerebroventricular administration of streptozotocin (STZ). In both experiments, C57BL/6 mice were used and distributed into three experimental groups, each comprising 14-15 animals per group. Cognitive and motor function was assessed through gait pattern, Y-maze and novel object recognition tests. Differential gene expression was analyzed using qPCR. Both models reproduced hallmark features of cognitive decline, including deficits in working and spatial memory and changes in the expression of genes associated with oxidative stress, neuroinflammation and synaptic plasticity. In aged animals, EGF + GHRP6 treatment increased step length (p = 0.04). In the forced alternation Y-maze test, aged-EGF + GHRP6 animals made more visits to the novel arm than to the familiar arm 1 (p = 0.001) or to the familiar arm 2 (p = 0.04). Cognitive benefits were also observed in the STZ-induced model. STZ-EGF + GHRP6 group exhibited an alternation percentage higher than the STZ-vehicle group (p = 0.03). Moreover, EGF + GHRP6 treatment significantly increased the expression of genes associated with antioxidant defense (Hmox1), synaptic plasticity (Creb1), and oligodendrocyte differentiation (Olig1) while concurrently reducing the expression of Nfkb1. These findings highlight the therapeutic potential of EGF + GHRP6 co-administration as a neuroprotective strategy to mitigate neurodegeneration and preserve cognitive function. - Source: PubMed
Publication date: 2026/07/04
Risco-Acevedo DanielaSubirós-Martínez NelvysCamacho-Rodríguez HanletRamírez-Sánchez JeneyRodríguez-Virulich YaimaEtchegoyen-Amoros Ana YansiHernández-Estrada WendyWong-Guerra MaylinMontano-Peguero YanayEstrada-Olivares ThaliaFuentes-Morales DashaPalenzuela-Gardón DanielPérez-Saad HéctorNúñez-Figueredo YanierWen LiGuillén-Nieto Gerardo EGarcía-Del-Barco-Herrera Diana - Chronic migraine (CM) represents a highly prevalent neuroinflammatory disorder with limited therapeutic options. Xiongzhi Qufeng Zhitong Granules (XZQF), a clinically used traditional Chinese medicine, displays promising anti-migraine potential with favorable safety profiles; however, its systematic efficacy and underlying mechanisms remain poorly defined. - Source: PubMed
Publication date: 2026/07/03
Huang LianzhanZhou JieruHan YiyueMou XiaotongZheng YixinLiu ChangjiangOu YanghanDing XuanshengHan Bing - Exertional heat stroke (EHS) is a life‑threatening condition characterized by hyperthermia, systemic inflammation and central nervous system injury, particularly in desert dry‑heat environments. Excessive activation of inflammatory signaling pathways, notably the Toll‑like receptor (TLR)4/myeloid differentiation factor 88 (MyD88)/NF‑κB axis, critically contributes to brain damage and neuroendocrine dysfunction in EHS. Curcumin exhibits anti‑inflammatory and neuroprotective effects; however, poor bioavailability limits its clinical application. Notably, nanocrystal formulations may improve the therapeutic efficacy of curcumin. In the present study, network pharmacology and molecular docking were employed to identify the potential therapeutic targets of curcumin in EHS. A rat model of desert dry‑heat‑induced EHS was established and nanocurcumin was administered intravenously following heat exposure. Histopathological examination, ELISA analyses of neuroendocrine hormones and inflammatory cytokines, serum biochemical assays and western blotting were subsequently performed. These evaluations assessed brain injury, hypothalamic‑pituitary‑adrenal and hypothalamic‑pituitary‑thyroid axes functions, systemic inflammation, peripheral organ injury indicators and activation of the TLR4/MyD88/NF‑κB signaling pathway. Network analysis revealed 138 overlapping target genes between curcumin and EHS, identifying AKT1, TNF, EGFR, BCL2, STAT3, SRC and NFKB1 as key hub genes. Kyoto Encyclopedia of Genes and Genomes pathway analysis highlighted enrichment of the 'Toll‑like receptor signaling pathway' and 'NF‑κB signaling pathway'. Molecular docking indicated favorable binding affinities of curcumin to essential inflammatory proteins, including TLR4, MyD88 and NFKB1. In vivo experiments demonstrated that nanocurcumin reduced neuronal injury in the cerebral cortex and hypothalamus of rats. Furthermore, nanocurcumin significantly decreased serum concentrations of corticotropin‑releasing hormone, corticosterone, thyrotropin‑releasing hormone and thyroid‑stimulating hormone, and restored adrenocorticotropic hormone, total triiodothyronine and free triiodothyronine levels. Nanocurcumin also lowered serum TNF‑α, IL‑6 and IL‑1β levels, and improved biochemical markers of liver, kidney and tissue injury (alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen, creatine kinase and lactate dehydrogenase). Within the 4‑h observation period, medium and high doses of nanocurcumin did not worsen biochemical markers compared with those in the EHS or saline groups. Additionally, nanocurcumin administration dose‑dependently inhibited TLR4, MyD88 and NF‑κB protein expression in brain tissues. In conclusion, nanocurcumin may alleviate brain injury, neuroendocrine dysfunction and systemic inflammation associated with desert dry‑heat‑induced EHS, and may improve biochemical indicators of peripheral organ damage; these effects likely involve suppression of the TLR4/MyD88/NF‑κB signaling pathway. These findings support the use of nanocurcumin as a promising adjunctive therapy for managing EHS. - Source: PubMed
Publication date: 2026/07/03
Su LisongQu JinquanLi JiajiaShi WenhuiSong LaiyangLiang FeixingLiu Jiangwei - Bronchial asthma (BA), a common chronic airway inflammatory disease, significantly impairs lung function and quality of life due to pathological features such as airway remodeling, inflammatory imbalance, and oxidative damage. This study aimed to investigate the clinical efficacy of Zhichuanling Oral Liquid (ZCL) in children with BA and elucidate its mechanism of action through network pharmacology, animal experiments, and cellular studies. Methods: Sixty children with BA were randomly divided into a control group (conventional treatment) and an observation group (+ ZCL). Clinical efficacy, lung function, and serum markers (IL-6, SAA, IgE) were evaluated. Network pharmacology identified potential targets and pathways. An OVA-induced BA mouse model and cultured airway smooth muscle cells (ASMCs) were used to validate the mechanism. Results: Results showed ZCL significantly improved lung function (FVC, FEV1, PEF), reduced symptom scores, and decreased IL-6, SAA, IgE levels compared to control. Symptom relief times were shorter, and overall effective rate was higher (86.67% vs 60.00%). Network pharmacology revealed core targets (NFKB1, SIRT1, HIF1A, MMP9) and component QCT, involving IL-17 pathway. In mice, ZCL reduced behavioral scores, IL-17, IL-4, MDA, and increased SOD, GSH-Px, alleviating airway inflammation. Medium-dose ZCL was most effective. In ASMCs, ZCL upregulated SIRT1, reduced NF-κB, IL-17, and oxidative stress, enhanced by SIRT1 overexpression. Conclusions: ZCL effectively treats childhood BA, as demonstrated by improvements in lung function and symptoms. Its mechanism is likely mediated by QCT regulating the SIRT1/NF-κB/IL-17 pathway to reduce airway inflammation and oxidative damage. - Source: PubMed
Publication date: 2026/07/01
Wang JiaoLi JiaxinWang XianheZhang LihaiLiu QiuyanYang Duo