SQSTM1 Antibody (Center S207) Blocking Peptide
- Known as:
- SQSTM1 Antibody (Center S207) Blocking Peptide
- Catalog number:
- BP19360c
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SQSTM1 Antibody (Center S207) Blocking Peptide
Related genes to: SQSTM1 Antibody (Center S207) Blocking Peptide
- Gene:
- RNA5SP207 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 207
- Previous symbol:
- RN5S207
- Synonyms:
- -
- Chromosome:
- 6p21.1
- Locus Type:
- pseudogene
- Date approved:
- 2011-11-04
- 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 (Center S207) Blocking Peptide
Related articles to: SQSTM1 Antibody (Center S207) Blocking Peptide
- Regulation of Duck Tembusu virus (DTMUV) non-structural protein 1 (NS1) remains unclear. Exogenous and endogenous co-immunoprecipitation (Co-IP) assays demonstrated an association between the T-complex protein 1 subunit 2 (CCT2) and NS1. Further experiments mapped the NS1 region required for assembly of this complex to amino acid residues 172-352 of NS1.DTMUV increased CCT2 expression; CCT2 overexpression increased NS1 accumulation, whereas CCT2 knockdown delayed NS1 and envelope (E) protein accumulation. Although NS1 also associated with chaperonin-containing T-complex protein 1 subunit 6 (CCT6), CCT6 knockdown did not significantly alter NS1 messenger RNA (mRNA) or clearly change NS1 protein abundance. NS1 underwent lysine 48 (K48)- and lysine 63 (K63)-linked polyubiquitination. Increasing tripartite motif-containing protein 21 (TRIM21) reduced NS1 abundance and enhanced NS1-associated ubiquitin signals; the proteasome inhibitor MG132 promoted NS1 accumulation, which was highest with CCT2 co-expression, supporting proteasome-related turnover and CCT2-associated stabilization without establishing direct TRIM21 ubiquitination. CCT2 interacted with microtubule-associated protein 1 light chain 3C (LC3C), and DTMUV infection was associated with reduced late-stage lipidated LC3 (LC3-II) abundance and SQSTM1 mRNA expression. In dose-gradient Co-IP experiments, increasing NS1 expression was associated with a dose-associated reduction in CCT2 recovery in LC3C immunoprecipitates; the concomitant reduction in immunoprecipitated LC3C across the NS1 dose gradient precludes conclusions regarding direct competition or a binding capacity-dependent mechanism. These findings indicate that CCT2 is a DTMUV-associated host factor capable of stabilizing intracellular NS1 protein and promoting the production of infectious DTMUV progeny. CCT2 contributes to the homeostasis of NS1 protein. - Source: PubMed
Publication date: 2026/09/17
Yang ZekunFeng HaixiaWang QiongjieXiang ChengweiHan YinXu FeiJing MengyaoLi HongmeiLiang JianhuaHe XianmingChen RuiaiXiong Ting - The neonicotinoid insecticide imidacloprid (IMD), widely used in agriculture, poses potential risks to aquatic ecosystems, yet its hepatotoxic mechanisms in freshwater fish remain poorly understood. This study investigates the roles of ferroptosis, mitochondrial dysfunction, inflammation, and the miR-153c/SQSTM1-mediated ferritinophagy pathway in IMD-induced hepatotoxicity in carp () hepatocytes. Using the CCK-8 assay, 0.6 μM IMD was selected for subsequent experiments. IMD exposure triggered ferroptosis, evidenced by increased intracellular Fe accumulation, upregulated pro-ferroptotic gene and protein expression, and downregulated ferroptosis inhibitors (SLC7A11 and GPX4). Mitochondrial dysfunction was confirmed by reduced ATP content, decreased mtDNA levels, and a lowered NADPH/NADP ratio, along with aberrant expression of mitochondrial fission (Fis1 and Drp1) and fusion (Mfn1 and TFAM) genes. Additionally, IMD induced oxidative stress (elevated ROS and MDA; decreased T-AOC, CAT, and SOD activities) and a pronounced inflammatory response with upregulated pro-inflammatory cytokines. Mechanistically, IMD downregulated miR-153c, with concomitant upregulation of SQSTM1 at both the mRNA and protein levels, and dual-luciferase assays validated SQSTM1 as a direct target of miR-153c. miR-153c overexpression attenuated IMD-induced ferritinophagy, ferroptosis, and inflammation via the miR-153c/SQSTM1 axis. Collectively, these findings demonstrate that IMD induces hepatotoxicity in carp by triggering ferroptosis, mitochondrial dysfunction, and inflammation through the miR-153c/SQSTM1-mediated ferritinophagy pathway, providing mechanistic insights and potential targets for mitigating IMD's ecological risks. - Source: PubMed
Publication date: 2026/09/13
Chen HuijieWang YitongYao ZhenkaiLi JingLi PengDiao Lei - Long-term exposure to polystyrene nanoplastics (PS-NPs) causes neurotoxicity, but the underlying mechanisms remain unclear. We combined network toxicology, molecular docking, and in vivo experiments to investigate the role of MTOR-TFEB-regulated autophagy in PS-NP-induced neurotoxicity. Potential targets related to PS-NPs and neurodegenerative diseases were screened from public databases. Enrichment analysis indicated involvement of neurodegenerative and autophagy pathways. Protein-protein interaction and docking simulations prioritized as a candidate target. Sprague-Dawley rats were gavaged with PS-NPs (0.15 or 1.5 mg/kg) for 60 days. Morris water maze tests showed impaired spatial learning and memory. Western blotting of hippocampal tissues revealed increased p-MTOR/MTOR ratios, decreased total cytoplasmic and nuclear TFEB, reduced lysosomal proteins (LAMP2, CTSD, and CTSB), elevated autophagy markers SQSTM1 and MAP1LC3B-II, and altered apoptosis regulators (BAX up and BCL2 down). Collectively, PS-NPs disrupt the MTOR-TFEB axis, impair lysosomal function and autophagic clearance, and promote apoptosis, leading to neurocognitive deficits. These findings provide mechanistic insights into the MTOR-TFEB axis and highlight it as a candidate pathway warranting further evaluation as a potential intervention target. - Source: PubMed
Publication date: 2026/09/09
Tang NaWang ChunZhang MengLi YajieLiang YongkangZhang JingjingNiu Qiang - Pancreatic cancer cells adapt to nutrient stress by activating metabolic pathways that facilitate survival and proliferation within the tumor microenvironment, a phenomenon known as austerity. Targeting this resilience presents a strategy for developing chemotherapeutic agents with anti-austere properties. Phytochemical investigation of petals led to the isolation of six alkaloids: three benzylisoquinolines (-), two aporphines (, ), and one proaporphine (). Preferential cytotoxicity under nutrient deprivation was evaluated. The most active compound was further analyzed in MIA PaCa-2 cells using proliferation, migration, colony formation, and three-dimensional spheroid growth assays, with additional selective cytotoxicity assessment in KLM-1 cells. Mechanistic studies examined MAPK family signaling, autophagy-associated alterations, and apoptosis. (-)--nornuciferine () exhibited considerable preferential cytotoxicity against MIA PaCa-2 cells (PC = 0.53 µM) and KLM-1 cells (PC = 1.11 µM). Under nutrient-rich conditions, suppressed the proliferation, migration, colony formation, and spheroid growth of MIA PaCa-2 cells. Under nutrient deprivation, increased MAPK phosphorylation and LC3-II accumulation while reducing p62/SQSTM1 levels. Chloroquine (CQ) further increased LC3-II accumulation, particularly at 10 µM , compared with CQ alone. However, autophagy inhibitors did not rescue -induced loss of viability, and the pan-caspase inhibitor Z-VAD-FMK also failed to significantly mitigate cytotoxicity. No detectable PARP or caspase-3 cleavage was observed. (-)--nornuciferine () exhibits anti-austere and anticancer activities in pancreatic ductal adenocarcinoma (PDAC) models, accompanied by MAPK phosphorylation and autophagy-related changes under nutrient deprivation conditions. Conventional caspase-dependent apoptosis is unlikely to be the main contributor to this process. - Source: PubMed
Publication date: 2026/09/14
Nguyen Hung HongManeenet JuthamartOmar Ashraf MMori TomoyaDaodee SupawadeeMonthakantirat OrawanBoonyarat ChantanaKhamphukdee CharinyaSumanont YaowaredFujii TsutomuAwale Suresh - Perfluorooctanoic acid (PFOA) is a persistent per- and polyfluoroalkyl substance that undergoes active renal handling, yet the molecular response of proximal tubular cells remains poorly resolved. We integrated network toxicology with matched RNA sequencing and untargeted LC-MS metabolomics in PFOA-exposed HK-2 cells, then compared the resulting model with an external rat kidney transcriptome, public perturbation signatures and cellular assays. The network analysis yielded 657 kidney-relevant candidates. RNA sequencing identified 407 upregulated and 443 downregulated genes, with induction of ATF4-DDIT3-TRIB3 and redox-related genes and repression of E2F, G2-M, mitotic-spindle and DNA-replication programs. Annotation-audited metabolomics retained 61 exploratory responsive features (7 increased and 54 decreased), showing nominal shifts involving nucleotide, amino-acid and carbon-energy intermediates. Cross-platform prioritization highlighted TRIB3, CDKN1A, SLC7A11, ATF3, DDIT3, HMOX1 and SQSTM1. External WGCNA and perturbation-signature analyses showed partial transcriptomic concordance with the main stress, metabolic and cell-cycle patterns. In concentration-group validation experiments, PFOA increased apoptosis, G0/G1 accumulation and lipid peroxidation, lowered EdU incorporation and the GSH/GSSG ratio, and induced the prioritized genes. These data define a PFOA-responsive proximal-tubule stress program accompanied by redox imbalance, exploratory metabolic shifts and proliferative restraint. - Source: PubMed
Publication date: 2026/09/25
Shang YiweiLuo QikaiZhou YourouHe WenfangWang ShaotingHe RanHe QingHe QiangJin JuanWang Yunguang