SQSTM1 Antibody (C-term S403)
- Known as:
- SQSTM1 Antibody (C-terminus S403)
- Catalog number:
- AP19505b
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SQSTM1 Antibody (C-term S403)
Related genes to: SQSTM1 Antibody (C-term S403)
- Gene:
- RNA5SP403 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 403
- Previous symbol:
- RN5S403
- Synonyms:
- -
- Chromosome:
- 16p13.2
- Locus Type:
- pseudogene
- Date approved:
- 2012-01-30
- Date modifiied:
- 2014-11-19
- Gene:
- SQSTM1 NIH gene
- Name:
- sequestosome 1
- Previous symbol:
- PDB3, OSIL
- Synonyms:
- p62, p60, p62B, A170
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-13
- Date modifiied:
- 2019-03-07
Related products to: SQSTM1 Antibody (C-term S403)
Related articles to: SQSTM1 Antibody (C-term S403)
- Puerarin (Pue), a major isoflavone derived from , has demonstrated neuroprotective potential in multiple neurological disorders; however, its effects on ethanol (EtOH)-induced cortical injury and the associated molecular responses remain incompletely understood. In the present study, network pharmacology was combined with in vivo and in vitro experiments to investigate molecular responses associated with the effects of Pue on EtOH-induced neurotoxicity. Public databases were used to predict targets of Pue and alcohol-related brain injury, followed by protein-protein interaction analysis, Gene Ontology annotation, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment. A total of 101 overlapping targets were identified, among which TNF, AKT1, EGFR, TP53, and PPARG emerged as major hub targets, and PI3K-Akt signaling pathway was among the pathways that remained significantly enriched after FDR correction. In a 4-day binge EtOH rat model, Pue attenuated EtOH-associated increases in oxidative stress, neuronal degeneration, and apoptotic markers in cortical tissue. This was accompanied by attenuation of the EtOH-associated reductions in the p-AKT/AKT and p-mTOR/mTOR ratios, as well as an attenuation of EtOH-associated changes in LC3, ATG5, and Beclin-1 expression. In primary cortical neurons, Pue partially attenuated the EtOH-associated loss of neuronal viability and preserved neurite morphology. Bafilomycin A1 (BafA1)-based analysis of LC3-II and p62/SQSTM1 showed an overall BafA1-sensitive increase in LC3-II without a significant treatment-dependent difference in the BafA1 response. Collectively, these findings suggest that Pue attenuates binge EtOH-induced cortical neurotoxicity in association with changes in AKT/mTOR phosphorylation and autophagy-related responses. - Source: PubMed
Publication date: 2026/09/14
Liu FuHuang ShuyingXiao HongwenZhou YuhongLin LongLiu ZaiqiangLan JumeiChen XiaohongTian Hua - Glioblastoma multiforme (GBM) is the most aggressive primary brain tumor, for which radiotherapy constitutes the key component of standard comprehensive treatment; however, tumor relapse could inevitably arise from intrinsically radioresistant GBM subclones. Radiotherapy exerts biphasic regulatory effects on the tumor immune microenvironment (TIME), with transient activation followed by sustained immunosuppression. Nevertheless, it remains elusive how radioresistant GBM cells remodel such an immunosuppressive TIME to evade immune surveillance. Herein, integrative analyses encompassing clinical specimens, public single-cell RNA-seq datasets, orthotopic glioma models, primary CD8 T cell co-culture systems, and tandem mass tag (TMT) proteomics indicated that CD81 was highly expressed in radioresistant GBM and governed GBM immune evasion. CD81-high tumor cells were surrounded by functionally exhausted CD8 T cells, alongside immunosuppressive signature within neighboring myeloid and NK cells. CD81 depletion promoted selective macroautophagic/autophagic degradation of CD274/PD-L1, increased CD8 T cell infiltration and cytotoxic activity, reduced M2-like tumor-associated macrophages, and suppressed intracranial tumor growth. Moreover, CD81-knockdown augmented the antitumor efficacy of anti-PDCD1/PD-1, yielding a pronounced survival benefit when combined with radiotherapy. Mechanistically, CD81 interacted with CD274 via its large extracellular loop (LEL) and recruited the deubiquitinase USP14 through its cytoplasmic C-terminal tail (CCT). This resultant ternary complex erased K63-linked ubiquitination at the K280 residue of CD274, thereby abolishing SQSTM1/p62-dependent recognition and subsequent autophagy-lysosomal degradation of CD274 to maintain its protein stability. Collectively, our work establishes CD81 as a pivotal bridge connecting radioresistance to immune escape via sustaining CD274 abundance in GBM, highlighting CD81 as a promising therapeutic target to optimize radioimmunotherapy. - Source: PubMed
Publication date: 2026/09/13
Zeng LiangZhou YuchuanCai LinboZheng WangLiu XinglongLiao WeiXiao YuqiJin XiaoyaZhang JialingLai MingyaoLi HainanXu YanwuZhang JianghongPan YanWang YangShao Chunlin - - Source: PubMed
Publication date: 2026/09/13
Moorman HannahCrimmins JenniferGillam JosephTurner ScottMochel Mark C - Bovine mastitis severely compromises dairy cattle health, primarily through oxidative stress and dysregulated autophagy in bovine mammary epithelial cells (BMECs), ultimately impairing lactation performance. While heme oxygenase-1 (HO-1) is well-established as a critical regulator of oxidative stress and autophagy, its interplay with the selective autophagy receptor sequestosome 1 (SQSTM1/p62), as a key mediator linking autophagy to antioxidant responses, remains unclear in the context of mastitis. We hypothesized that p62 modulates HO-1 activity to coordinate cellular defense mechanisms in BMECs. To test this, we established p62 overexpression/knockdown cell lines, treating them with lipopolysaccharide (LPS), exogenous HO-1, nuclear factor erythroid 2-related factor 2 (Nrf2) inhibitor, or autophagy inhibitor. Our results demonstrated that p62 overexpression suppressed autophagy while concurrently activating the Nrf2/HO-1 pathway by binding to kelch-like ECH-associated protein 1 (Keap1). The p62-HO-1 axis and exogenous HO-1 synergistically enhanced antioxidant enzyme expression, attenuated reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and mitigated LPS-induced pro-inflammatory cytokine production. Mechanistically, the p62-HO-1 axis restored mitochondrial membrane potential, elevated adenosine triphosphate (ATP) synthesis, reduced mitochondrial superoxide accumulation, and corrected mitochondrial dynamics imbalances. Crucially, these protective effects were found to be autophagy-independent but Nrf2-dependent. This study elucidates a novel mechanism by which the p62-HO-1 axis safeguards BMECs by integrating antioxidant defenses with mitochondrial homeostasis, offering new insights into the pathogenesis of bacterial mastitis and identifying potential therapeutic targets. - Source: PubMed
Publication date: 2026/09/12
Li HepingZhang XinyiLiu XiaoxiaoYang QilongPeng DaiCao RuiLuo SijiaSun XiangshunSong LeiHan YingqianLiu YangWang Yueying - Autophagy terminates in the degradation of cargo delivered by fusion of the autophagosome with the lysosome, a step tethered by the homotypic fusion and vacuole protein sorting (HOPS) complex. Heterozygous loss-of-function variants in , which encodes a core HOPS subunit, cause autosomal dominant DYT- dystonia. The pathogenicity of missense alleles has remained uncertain due to a lack of mechanistic data from patient-derived cells. We summarize our recent report of the youngest individual with DYT- described to date. This child presented with infantile-onset generalized dystonia caused by a missense variant, p. Ala466Thr. Patient-derived fibroblasts accumulate enlarged, stalled autolysosomes and show concurrent elevation of SQSTM1/p62 and the MAP1LC3B/LC3B-II:LC3B-I ratio, consistent with a block in autophagic flux. We discuss the consequences for variant interpretation, describe a previously unrecognized caudate-predominant neuroimaging correlate, and speculate on why striatal neurons are selectively vulnerable to HOPS dysfunction. HOPS: homotypic fusion and vacuole protein sorting; LOF: loss-of-function; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; SQSTM1: sequestosome 1. - Source: PubMed
Publication date: 2026/09/09
Gonzalez Saez-Diez EnriqueXue XutongEbrahimi-Fakhari Darius