SQSTM1 Antibody (N-term S24)
- Known as:
- SQSTM1 Antibody (N-terminus S24)
- Catalog number:
- AP19120a-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SQSTM1 Antibody (N-term S24)
Related genes to: SQSTM1 Antibody (N-term S24)
- Gene:
- CHMP3 NIH gene
- Name:
- charged multivesicular body protein 3
- Previous symbol:
- VPS24
- Synonyms:
- NEDF, CGI-149
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-11
- Date modifiied:
- 2014-11-19
- Gene:
- HSPA4 NIH gene
- Name:
- heat shock protein family A (Hsp70) member 4
- Previous symbol:
- -
- Synonyms:
- HS24/P52, HSPH2
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-26
- Date modifiied:
- 2015-11-19
- Gene:
- KLRK1 NIH gene
- Name:
- killer cell lectin like receptor K1
- Previous symbol:
- D12S2489E
- Synonyms:
- NKG2D, KLR, NKG2-D, CD314
- Chromosome:
- 12p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-12
- Date modifiied:
- 2016-10-05
- Gene:
- MRPS24 NIH gene
- Name:
- mitochondrial ribosomal protein S24
- Previous symbol:
- -
- Synonyms:
- MRP-S24, HSPC335
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-26
- Date modifiied:
- 2016-10-05
- Gene:
- RNA5SP24 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 24
- Previous symbol:
- RN5S24
- Synonyms:
- -
- Chromosome:
- 13q12.11
- Locus Type:
- pseudogene
- Date approved:
- 2011-08-08
- Date modifiied:
- 2012-08-07
Related products to: SQSTM1 Antibody (N-term S24)
Related articles to: SQSTM1 Antibody (N-term S24)
- Pathological cardiac hypertrophy is maladaptive cardiac remodeling induced by chronic adverse stimuli. In this study, the E3 ubiquitin ligase RNF128 was identified as a suppressor of pathological cardiac dysfunction with therapeutic value. - Source: PubMed
Publication date: 2026/08/12
Zhang YujieLiu XuehanYu LiwenLiu ChanghaoLi JingweiHan QingmeiWang XiaohongCao LeiCai LiangyuJiao LinqiSu GuohaiZhang MengZhang Cheng - 6PPD-quinone (6PPD-Q), a transformation product of the tire antioxidant 6PPD, is an emerging traffic-related contaminant with well-documented ecotoxicity in aquatic species. Its recent detection in airborne particulate matter, road dust, and human urine has raised concerns about possible human health effects. However, its cardiotoxicity in mammalian cells remains poorly understood. Here, we integrated network toxicology, molecular modeling, and in vitro experiments to investigate the effects of 6PPD-Q on the human AC16 cardiomyocyte cell line and the underlying mechanisms. Network toxicology identified 144 putative targets associated with 6PPD-Q-induced cardiotoxicity, with TP53 ranked as the top hub gene, followed by TRAF6, MAPK1, SQSTM1, TNF, and IL6. Enrichment analysis highlighted oxidative stress, inflammation, apoptosis, and autophagy regulation as key biological processes. Molecular docking suggested potential interactions between 6PPD-Q and these hub proteins, while molecular dynamics simulation supported the dynamic stability of the predicted 6PPD-Q-p53 complex. Experimentally, 6PPD-Q induced marked ROS accumulation in AC16 cells, with an IC50 of 13.92 μM after 24 h exposure. It also promoted p53 phosphorylation at Ser15 without increasing total p53 protein or TP53 mRNA expression, indicating stress-associated post-translational activation of p53. This response was accompanied by TRAF6 upregulation, enhanced MAPK1 phosphorylation, and increased IL6 and TNF expression and secretion, supporting the activation of inflammatory stress signaling. Functionally, 6PPD-Q triggered mitochondrial apoptosis, as indicated by mitochondrial membrane potential loss, an increased Bax/Bcl-2 ratio, and activation of cleaved caspase-9 and cleaved caspase-3. In addition, 6PPD-Q disrupted autophagy homeostasis, as evidenced by LC3-II accumulation, p62 depletion, reduced SQSTM1 mRNA expression, increased yellow LC3 puncta, and decreased red-only puncta, suggesting autophagosome accumulation with impaired late-stage autophagic flux. Pharmacological inhibition of p53 by Pifithrin-α (PFTα) attenuated 6PPD-Q-induced inflammatory responses, MAPK1 phosphorylation, mitochondrial apoptosis, and SQSTM1 transcriptional suppression, supporting the functional involvement of p53-related stress signaling. Collectively, these findings show that 6PPD-Q induces cardiomyocyte injury through a p53-associated stress network linking oxidative stress, inflammatory signaling, mitochondrial apoptosis, and autophagy dysregulation, providing mechanistic insight into its potential cardiovascular relevance. - Source: PubMed
Publication date: 2026/09/07
Lu AimeiHuang KailinLi MengfanLu YingdongCha SunaZhang YaniHu XiaomengJi XingXue XinyuWu HuanlinLi HongzhengLi Wei - K63-linked ubiquitination (K63) is closely associated with the interaction, intracellular trafficking or activity of tagged proteins. However, its role during metabolic dysfunction-associated steatohepatitis (MASH) is largely unknown. Here we show that UBE2N, a ubiquitin-conjugating enzyme that specializes in creating K63, is downregulated by THAP11 in human and mouse hepatocytes with MASH. While hepatocyte-specific Ube2n deficiency exacerbates western diet-induced MASH and fibrosis via PANoptosis and impaired mitophagy, its overexpression reverses these pathological phenotypes and restores hepatic homeostasis. Mechanistically, UBE2N increases PARKIN-mediated K63-p62 at lysine 420, promoting K63-p62 translocation into damaged mitochondria for mitophagic clearance. Ube2n deficiency, conversely, induces cytoplasmic p62 accumulation and NRF2 hyperactivation, driving PANoptosis. Additional Sqstm1 deletion mitigates Ube2n deletion-induced pathologies, highlighting the importance of p62 accumulation for MASH progression. Thus, our results demonstrate that hepatocyte UBE2N is essential for regulation of metabolic stress-mediated mitophagy and PANoptosis, and that p62 is a proof-of-concept target for treating MASH and fibrosis. - Source: PubMed
Publication date: 2026/09/04
Wang FengLee JinPark Jeong-SuHuang MeizhouMa HwanSui GuoyanZhou ZixiongMatsuda MichitakaKim So YeonTsuchiya TakashiWu XuefengLee HaramOh SoohwanPark HanseulLim Key-HwanPark Chun-WoongHan Sang-BaeHong Jin TaeKarin MichaelRoh Yoon SeokSeki Ekihiro - The pathogenesis of ulcerative colitis (UC) is closely associated with excessive intestinal inflammation and epithelial barrier disruption. Hesperetin possesses natural anti-inflammatory properties, but its protective mechanisms remain unclear. - Source: PubMed
Publication date: 2026/08/25
Xianpeng WeiYuzhou LaiYu ZhanTaiyu ChenHongyuan ZhaoYong WenXuegui Tang
- Source: PubMed