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)
- Primary pulmonary inflammatory myofibroblastic tumor (IMT) associated with paraneoplastic pemphigus (PNP) is extremely rare. IMT is an intermediate (rarely metastasizing) mesenchymal neoplasm rather than a conventional sarcoma. We report a case of a 68-year-old female patient who initially presented with generalized skin rash, oral mucosal ulceration, and fever. Chest CT revealed a thoracic mass (initially difficult to determine whether mediastinal or pulmonary in origin). Subsequent thoracotomy and surgical resection with pathological examination confirmed an ALK-rearranged inflammatory myofibroblastic tumor (SQSTM1: ALK fusion) of pulmonary origin. Oral mucosal pathology, combined with clinical findings, supported a diagnosis of PNP. This case aims to provide reference for the diagnosis and treatment of patients with primary pulmonary IMT complicated by PNP. However, the follow-up period was short and systemic immunosuppressive therapy was not administered; this should be regarded as a cautionary note rather than a therapeutic recommendation. - Source: PubMed
Publication date: 2026/06/10
Dong YiGuan YongjieFeng ShuangWang XiaoweiRen XiyuanGao Ke - Autophagy is a conserved catabolic process that degrades damaged proteins and organelles to preserve cellular homeostasis. Autophagy plays two opposing roles during viral infection. On the one hand, it can be subverted by viruses to facilitate replication and immune evasion. On the other hand, it limits viral infection by delivering viral components to lysosomes. The interaction between autophagy and important picornaviruses that infect cattle and poultry, such as SVV, EMCV, FMDV, and DHAV, is the main topic of this paper. However, comprehensive summaries focusing specifically on livestock and poultry remain limited. We summarize current research showing that these viruses evade host protection by manipulating several steps of the autophagic pathway, from initiation to lysosomal fusion, to produce replication-favorable environments. Notably, by directing the breakdown of viral capsid proteins, specific autophagy receptors such as SQSTM1/p62, NDP52, and optineurin (OPTN) serve as antiviral effectors. In response, picornaviruses have developed proteolytic strategies to inactivate these receptors, such as SVV 3C-mediated cleavage of SQSTM1 and OPTN. Moreover, different immune evasion tactics are shown by virus-specific engagement of organelle-selective autophagy, such as ER-phagy (SVV) or mitophagy (DHAV). The development of broad-spectrum antiviral treatments and autophagy-based biomarkers for livestock disease progression may benefit from an understanding of the convergent and different ways picornaviruses take advantage of the autophagic machinery. - Source: PubMed
Publication date: 2026/06/09
Ma HaibinLiu RongchangLiao Ming - Alopecia areata (AA) is a common autoimmune alopecia disease. Evidence suggests that autophagy-related genes (ARGs) may contribute to its pathophysiology. This study aims to explore and identify potential autophagy-related biomarkers and molecular subtypes in AA. In this study, autophagy-related differential expression genes (ARDEGs) in AA were identified by comparing the differentially expressed genes (DEGs) in the GSE68801 dataset with the ARGs. Then, we applied three different machine learning methods to identify key hub genes and further verified them on independent datasets. We used the receiver operating characteristic (ROC) curve to evaluate the diagnostic potential of these hub genes and constructed a predictive nomogram. In addition, this study also used the consensus clustering method to define two AA subtypes and explored their immune characteristics and functional pathways through ssGSEA, MCPcounter and enrichment analysis. Experimental validation included qRT-PCR for four hub genes and Western blotting for critical autophagy markers. Our analysis detected 10 ARDEGs in AA. Applying three machine learning algorithms, we identified four candidate hub genes, , , and , and verified their expression patterns in independent cohorts. The combined four-gene model and nomogram showed potential diagnostic performance. Consensus cluster analysis divided AA cases into two subtypes, each associated with different immune infiltration and functional pathways. Downregulation of and and upregulation of were verified by qRT-PCR. Western blotting further suggested altered autophagy-related protein expression in AA lesions, characterized by a reduced LC3B-II/I ratio and Beclin-1 expression and increased SQSTM1 expression. This study identified four candidate autophagy-related genes and two exploratory molecular subtypes in AA and may provide clues for understanding autophagy-related immune dysregulation and support further validation of candidate diagnostic markers. - Source: PubMed
Publication date: 2026/05/23
Li YufenZhang XiaolinWang JiatingJiang Yiqun - Iron overload disrupts cellular homeostasis and drives ferroptosis through dysregulated iron metabolism. Non-coding RNAs (ncRNAs) are considered as key regulators of various biological functions and targets for a new generation of RNA therapeutics and biomarkers. However, few studies have investigated the regulatory roles of ncRNAs, particularly competitive endogenous RNAs (ceRNAs) in iron overload. This study performed whole-transcriptome sequencing to characterize the ceRNA network in ferric ammonium citrate (FAC)-induced iron-overloaded HT-1080 fibrosarcoma cells. A total of 208 differentially expressed mRNAs, 83 lncRNAs, and 170 circRNAs ( < 0.05) were identified, with hierarchical clustering revealing distinct expression patterns between control and iron-treated groups. KEGG enrichment implicated vitamin B6 metabolism ( < 0.001) and lysine degradation ( < 0.001) as key disrupted pathways. ceRNA network was conducted and further demonstrated lncRNA/circRNA-mediated regulation of ferroptosis genes via shared miRNA response elements. Notably, was implicated in the regulation of both ferritin heavy chain () and sequestosome 1 (), two ferroptosis-associated mRNAs. upregulation mitigates iron toxicity through ferroxidase activity, while modulates lipid peroxidation in ferroptosis. These findings provide a preliminary transcriptomic landscape for hypothesis generation regarding ncRNA-mediated regulatory mechanisms in iron overload-induced ferroptosis and offer a computational foundation for future functional and therapeutic investigations. - Source: PubMed
Publication date: 2026/06/22
Teng YifanZhang QianDing HaoxuanFeng Jie - SQSTM1/p62 is a multifunctional scaffold protein that plays important roles in selective autophagy and cellular redox homeostasis. While phosphorylation-dependent regulation of p62 has been extensively studied, the functional significance of oxidative modification remains incompletely understood. Our previous studies showed that the natural small compound Alternol induces cancer cell-specific killing via a xanthine oxidase-mediated strong oxidative stress. In this study, we investigated p62-associated oxidative responses under Alternol-induced oxidative stress conditions in prostate cancer cells. Using biochemical assays and cell-based models, we found that Alternol treatment was associated with the accumulation of oxidized and high-molecular-weight p62 species, accompanied by altered KEAP1 association and increased Nrf2-associated signaling. Furthermore, Alternol-induced p62 oxidative modification was associated with autophagy-related responses and adaptive cellular survival under oxidative stress conditions. Disruption of the Cys105/113-dependent oxidative modification response attenuated Nrf2-associated transcriptional activity and increased cellular sensitivity to Alternol treatment. Collectively, our findings support an association between p62 oxidative modification and redox-responsive autophagy- and antioxidant-associated signaling pathways under Alternol-induced oxidative stress conditions, providing new insight into adaptive stress responses in prostate cancer cells. - Source: PubMed
Publication date: 2026/06/22
Liu WangZhao JiangLi ChanglinXu HaixiaChen RuibaoZeng XingYang JunZhong CuncongWang XiangweiLi Benyi