SQSTM1 predesign siRNA
- Known as:
- SQSTM1 predesign small interfearing RNA
- Catalog number:
- RI15074
- Product Quantity:
- 5 OD
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SQSTM1 predesign siRNA
Related genes to: SQSTM1 predesign siRNA
- 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 predesign siRNA
Related articles to: SQSTM1 predesign siRNA
- Amyotrophic lateral sclerosis (ALS) is considered a highly complex, heterogeneous, fatal disease with a high unmet medical need that affects multiple pathophysiological pathways and has no known singular cause. Oxidative stress, however, is implicated as a central player in the progression of ALS and other neurodegenerative diseases. To date, only two FDA-approved drugs, Edaravone, an antioxidant, and Riluzole, an antiglutamatergic, have been widely used clinically, albeit with modest effects on the clinical course of ALS disease progression. Additionally, preclinical studies of both drugs in ALS mouse models have not shown any significant survival benefit, although some abatement in disease progression is observed and translated from preclinical animal models to clinical human studies. - Source: PubMed
Publication date: 2026/07/26
Sanghai NiteshKelley RhondaLao YingMadlangsakay M Immanuel ReyesPaul PrasantaLlanes-Cuesta M AlejandraWang Jun-FengZahedi René PKong JimingTranmer Geoffrey K - Phenethyl isothiocyanate (PEITC), isolated from cruciferous vegetables, exhibits anticancer activity against various human cancer cells. Our previous studies demonstrated that PEITC suppresses the growth of glioblastoma multiforme (GBM) 8401 cells in vitro and in vivo. In this study, we investigated the effects of PEITC on autophagy and its underlying molecular mechanisms in GBM 8401 cells. PEITC altered the morphology of GBM 8401 cells and triggered acidic vesicular organelle and autophagosome formation, as confirmed by acridine orange (AO) and monodansylcadaverine (MDC) staining, respectively. PEITC-treated cells transfected with green fluorescent protein (GFP)-microtubule-associated protein 1 A/1B-light chain 3 (LC3) exhibited punctate autophagosomes, and autophagosome formation was further confirmed via transmission electron microscopy (TEM). Treatment with chloroquine (CQ) inhibited autophagy, resulting in a decrease in the number of autophagosome puncta. CQ also enhanced PEITC-induced cytotoxicity in GBM 8401 cells. Furthermore, the expression of autophagy-associated proteins including GβL, mTOR, mTOR, Raptor, Rictor, and, Beclin 1 was decreased, whereas the expression of AMPKα, AMPKα1/AMPKα2, PI3K class III, VPS34, autophagy protein 5 (Atg5), Atg7, Atg12-Atg5, Atg16L1, Atg3, sequestosome 1 (SQSTM1/p62), and LC3 II was increased. Confocal laser scanning microscopy further revealed decreased Beclin 1 and increased LC3 levels following PEITC treatment. After CQ pre-treatment, the expression levels of SQSTM1/p62 and LC3 II were elevated. PEITC induces protective autophagy via the adenosine monophosphate-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) signaling pathway in GBM 8401 cells. Elucidation of the molecular mechanism of PEITC in GBM 8401 cells in vitro may provide a potential therapeutic approach for glioblastoma in the future. - Source: PubMed
Publication date: 2026/07/26
Peng Shu-FenLiu Hsin-ChungChueh Fu-ShinLee Hsu-TungHsu Sheng-YaoChen Jaw-ChyunChung Jing-GungChou Yu-Cheng - The goat milk industry is expanding, yet the toxic effects of bis(2-ethylhexyl) phthalate (DEHP) on goat mammary glands remain understudied despite extensive in vivo research in mice and humans. This study used mammary epithelial cells to investigate the mechanisms of DEHP-induced damage. Mitochondrial and endoplasmic reticulum damage was observed, accompanied by reactive oxygen species accumulation, indicating oxidative stress. At the transcriptional level, the mitogen-activated protein kinase (MAPK) signalling pathway played a critical role, while protein analysis highlighted the involvement of the ribosome, ferroptosis, and p53 signalling pathways. These findings suggest that DEHP-induced reactive oxygen species (ROS) indirectly activate p53, promoting lipid peroxidation and affecting ferroptosis and ribosome function. Joint analysis identified 22 significantly upregulated and 91 significantly downregulated genes (proteins), with GCLC, SQSTM1, and ATF3 closely related to cell proliferation, apoptosis, and oxidative stress. This study elucidated the health risks to goat mammary epithelial cells caused by DEHP based on cell phenotype and genes (proteins) expression. Our results provide insights for selecting dairy goat breeds resilient to environmental pollutants and ensuring a safer milk supply for human consumption. - Source: PubMed
Publication date: 2025/08/22
Xu XiaolongLuo MuhuaHu JiaxiangWang HaifengWang XuganBu JiaqiLi JiayuanYan HanbingAn Xiaopeng - Huntington disease (HD) is a progressive neurodegenerative disease caused by an expanded CAG repeat in the () gene, leading to the accumulation of mutant HTT (mHTT). IL17A (interleukin 17A), a proinflammatory cytokine primarily secreted by Th17 and γδ T cells, has been implicated in immune-mediated neurodegeneration. However, the role of IL17A in the pathogenesis of HD remains poorly understood. Here, we identify IL17A as a critical pathogenic factor in HD that promotes neuroinflammation, mHTT aggregation, and autophagy-lysosomal dysfunction. IL17A disrupts autophagic flux by downregulating CTSB and CTSD, inducing SQSTM1/p62 and MAP1LC3B-II/LC3-II accumulation, and impairing lysosomal reformation. Mechanistically, IL17A suppresses lysosomal biogenesis by inhibiting the nuclear translocation of TFE3. This regulation occurs via a novel GSK3B/GSK-3β-TFE3 signaling pathway. Therapeutic neutralization of IL17A with a monoclonal antibody (IL17A mAb) ameliorates disease phenotypes in R6/2 HD mice, improving motor performance, extending survival, and reducing gliosis. IL17A mAb also attenuates mHTT aggregation and enhances neuroprotective signaling, as evidenced by increased expression of DLG4/PSD-95, phosphorylated CREB1, and BDNF. Moreover, IL17A mAb restores autophagy-lysosomal function by facilitating the clearance of protein aggregates and upregulating lysosomal enzymes and biogenesis markers, including CTSB, CTSD, PIP5K1A, and LAMP2. These findings establish IL17A as a key modulator of HD pathophysiology and highlight IL17A inhibition as a promising therapeutic strategy for targeting autophagy-lysosomal dysfunction in HD. - Source: PubMed
Publication date: 2026/07/23
Chen Kai-PoJu Tz-Chuen - Breastfeeding anchors infant immunity and long-term health, but its benefits are threatened by () mastitis, an increasingly prevalent condition driven by antimicrobial resistance and therapeutic limitations. Beyond compromising maternal wellness, mastitis threatens the safety and continuity of breast milk, highlighting a critical need for innovative intervention strategies. Herein, we demonstrated that α‑ketobutyrate (α-KB), a metabolite of the transsulfuration pathway, mitigated ‑induced inflammation, oxidative stress, and blood-milk barrier (BMB) disruption both and . α‑KB enhanced macroautophagic/autophagic responses, marked by increased ATG5, BECN1 (beclin 1), and LC3-II:LC3-I conversion and reduced SQSTM1/p62, through a RIPK1-lactate-TFEB axis. Specifically, it directly bound and stabilized RIPK1, elevated lactate production, and drove TFEB nuclear translocation to activate macroautophagy/autophagy and promote intracellular bacterial clearance. Molecular docking and molecular dynamics simulations suggested stable α‑KB and RIPK1 binding via hydrophobic and hydrogen bond interactions; RIPK1 knockout abolished α‑KB-induced autophagy and lactate generation, effects rescued by lactate supplementation. This study identifies a novel immunometabolic circuit linking a metabolite to RIPK1-lactate-TFEB-mediated autophagy, offering therapeutic potential against antibiotic‑resistant mastitis and presenting a new paradigm for safeguarding breastfeeding quality and infant health. - Source: PubMed
Publication date: 2026/07/23
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