NQO1 mAb (A180)
- Known as:
- NQO1 mAb (A180)
- Catalog number:
- ASAOSA-700F
- Product Quantity:
- 200 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- NQO1 mAb (A180)
Related genes to: NQO1 mAb (A180)
- Gene:
- ABLIM2 NIH gene
- Name:
- actin binding LIM protein family member 2
- Previous symbol:
- -
- Synonyms:
- KIAA1808
- Chromosome:
- 4p16.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-19
- Date modifiied:
- 2019-03-21
- Gene:
- LRRIQ1 NIH gene
- Name:
- leucine rich repeats and IQ motif containing 1
- Previous symbol:
- -
- Synonyms:
- FLJ12303, KIAA1801
- Chromosome:
- 12q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-01
- Date modifiied:
- 2016-10-05
- Gene:
- MAP3K21 NIH gene
- Name:
- mitogen-activated protein kinase kinase kinase 21
- Previous symbol:
- -
- Synonyms:
- KIAA1804, MLK4
- Chromosome:
- 1q42.2
- Locus Type:
- gene with protein product
- Date approved:
- 2016-10-19
- Date modifiied:
- 2016-11-15
- Gene:
- NQO1 NIH gene
- Name:
- NAD(P)H quinone dehydrogenase 1
- Previous symbol:
- NMOR1, DIA4
- Synonyms:
- DHQU, QR1, DTD
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2017-07-12
- Gene:
- ZNF333 NIH gene
- Name:
- zinc finger protein 333
- Previous symbol:
- -
- Synonyms:
- KIAA1806
- Chromosome:
- 19p13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-07
- Date modifiied:
- 2015-02-26
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- Cellular senescence is closely associated with various age-related diseases. Sodium butyrate (NaB), a short-chain fatty acid and histone deacetylase (HDAC) inhibitor, exhibits potential anti-aging properties; however, its precise mechanisms remain unclear. This study aimed to investigate the protective effects of NaB against D-galactose (D-gal)-induced senescence in WI-38 human fibroblasts and elucidate the underlying mechanisms. WI-38 cells were co-treated with D-gal and NaB simultaneously to investigate whether NaB could mitigate D-gal-induced senescent changes. Senescence phenotypes were assessed by SA-β-Gal staining, ROS detection, and ELISA. Western blotting and chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) were performed to evaluate signaling pathways and histone acetylation, while siRNA knockdown validated Nrf2 function. NaB dose-dependently reduced SA-β-Gal-positive cells, ROS levels, and MDA content, while restoring SOD and GSH-Px activities and suppressing IL-6 and IL-1β secretion. Mechanistically, NaB promoted Nrf2 nuclear translocation by downregulating Keap1, thereby upregulating HO-1 and NQO1 expression. NaB also inhibited p53 phosphorylation and reduced p21 and p16 expression at both the mRNA and protein levels, as confirmed by RT-qPCR and Western blotting. Furthermore, NaB suppressed HDAC activity and restored H3K9ac and H3K27ac levels. Nrf2 knockdown reversed NaB's protective effects. ChIP-qPCR revealed that NaB restored H3K9ac enrichment at p21 and p16 promoters. These results indicate that NaB may attenuate D-gal-induced cellular senescence through coordinated modulation of the Nrf2/ARE pathway, p53/p21/p16 signaling, and HDAC-mediated epigenetic regulation. These findings provide preliminary evidence supporting NaB as a candidate modulator of aging-associated cellular processes, warranting further validation . - Source: PubMed
Publication date: 2026/06/01
Song Kangping - Spinal muscular atrophy (SMA) is caused by loss of SMN protein and is increasingly recognized as a multisystem disorder involving molecular pathology beyond motor neurons. Recently, we identified dysregulated NRF2-KEAP1 signaling in SMA mice. Since NRF2 coordinates transcriptional programs that maintain cellular redox homeostasis and adaptive stress responses, we investigated whether NRF2 signaling is similarly altered in fibroblasts derived from individuals with SMA type I and whether it can be pharmacologically engaged. Compared with control fibroblasts, SMA fibroblasts displayed reduced basal expression of NRF2 target proteins, including NQO1 and xCT (SLC7A11), along with decreased levels of PGC1α. Omaveloxolone (OMAV), a pharmacological NRF2 activator approved for the treatment of Friedreich's ataxia, increased cell viability and upregulated NRF2 target proteins in both control and SMA fibroblasts. Notably, OMAV produced a modest increase in SMN protein abundance and PGC1α levels selectively in SMA cells. Together, these findings support diminished NRF2 pathway activity as a feature of SMA fibroblasts and demonstrate that OMAV activates NRF2 signaling in this human SMA cellular model, consistent with enhanced cytoprotective signaling. These results support further investigation of NRF2 activation, including OMAV, as a potential adjunctive strategy in SMA. - Source: PubMed
Vrettou SofiaZetzsche SebastianWirth Brunhilde - The senescence of lung epithelial cells impairs self-repair and exacerbates lung damage in idiopathic pulmonary fibrosis. The potential of natural phytochemicals to reverse premature senescence warrants investigation. Information regarding the independent multifaceted effect of quercetin and artemisinin on epithelial senescence has not been delineated yet. The present investigation aimed to comprehend their attributes on HO-induced hallmark of premature senescence via controlling the vicious circle of oxidative-inflammatory stress, impaired cell proliferation, apoptosis, DNA damage, and inflammatory senescence cascades. An in vitro model of HO-exposed BEAS-2B cells was used to explore senescence using microscopy, qRT-PCR, immunoblotting, flow cytometry, and NMR· HO (100 µM) treatment induced cellular senescence-associated features without significant cytotoxicity, as evidenced by enhanced SA-β-galactosidase activity, irreversible irregular enlargement, shrinking, and flattened cell appearance, which was reversed by quercetin and artemisinin at varying degree. Results revealed that quercetin and artemisinin restored disrupted mitochondrial function in senescent cells, as evidenced by reduced MMP, GLS, ARRDC4, TXNIP, creatine, and increased NRF-2, HO-1, NQO-1, Sirt-1/5, and glycine levels. Furthermore, quercetin and artemisinin promoted proliferative ability, DNA repair, S-phase cell cycle transition, apoptosis, and suppressed SASP, as evidenced by enhanced Ki67 expression, annexin-V-positive cells, and diminished expression of interleukins, COX-2, MMPs, and the Atm/p53/p16/p21/Bcl-2 axis. Subsequently, activation of NOD-1, Stat-1, NF-κB, ERK1/2, p38, and JNK was decisively thwarted by quercetin and artemisinin. Intriguingly, Lamin B1 restoration and ROS inhibition were only noticed in quercetin, indicating both are effective in halting senescence through an alternative pathway. Overall, the present investigation emphasizes that quercetin and artemisinin exhibit both senolytic and senomorphic properties and could be valuable senotherapeutics for stress-induced premature senescence. - Source: PubMed
Publication date: 2026/06/08
Karadagatla SumanPadhy Hara PrasadSharma Anamika - Traumatic brain injury (TBI) induces oxidative stress, contributing to secondary neuronal damage. This study aimed to elucidate the role of the stress-responsive kinase HIPK2 in regulating endogenous antioxidant defenses in neural tissue following TBI. - Source: PubMed
Zhu QiangbinWang FanZhang BojunPan ZhigangKang XiaodongHu Weipeng - Swertiamarin (STM), one of the main bioactive compounds of Swertia plants, exerts its potential anti-CLI effects. The objective of this study was to prepare liver-targeting solid lipid nanoparticles (SLNs) with STM, using a galactosylated lipid, N-hexadecyl lactobionamide (N-HLBA), and evaluate its cholestatic effect on alpha-naphthylisothiocyanate (ANIT)-induced CLI. STM-loaded galactosylated SLN (STM@GalSLN) was prepared using the melt-emulsification-ultrasound method. The influence of STM@GalSLN on liver damage, oxidative stress, hepatocyte apoptosis, and Sirtuin 1 (SIRT1)/NF-E2 p45-related Factor 2 (Nrf2) pathway in ANIT-injured mice was evaluated. Also the cell survival, intracellular ROS, apoptotic rate, expression of SIRT1/Nrf2 pathway ralated proteins in ANIT-induced human liver HepG2 cells were measured. The mean diameter and zeta potential of STM@GalSLN was 167.30 nm and - 13.10 mV respectively. STM@GalSLN (100 mg/kg) alleviated ANIT-induced CLI in vivo, as evidenced by improved histopathology, decreased levels of liver biochemical indicators and cholestatic markers. Also STM@GalSLN (50 µM) notably increased cell survival, reduced ROS overproduction and apoptotic rate in ANIT-injured hepatocytes. Furthermore, STM@GalSLN significantly upregulated the protein expression levels of hepatic SIRT1, pNrf2, HO-1, and NQO1 during CLI. The protective effect of STM@GalSLN in vitro was blocked using EX-527 (10 mM), a selective SIRT1 inhibitor. Taken together, STM@GalSLN alleviated experimental CLI by enhancing the SIRT1/Nrf2 pathway. - Source: PubMed
Publication date: 2026/06/13
Wu JiWu TaoGuan XinleiZhu XiaoqiangLei LiangWu TaoZhang Qinarui