Polyclonal Antibody (Concentrated): SQSTM1
- Known as:
- Polyclonal Antibody (Concentrated): SQSTM1
- Catalog number:
- PA1955
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Bouster Immunoleader
- Gene target:
- Polyclonal Antibody (Concentrated): SQSTM1
Related genes to: Polyclonal Antibody (Concentrated): SQSTM1
- 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: Polyclonal Antibody (Concentrated): SQSTM1
Related articles to: Polyclonal Antibody (Concentrated): SQSTM1
- Ubiquitination plays a critical role in hepatocellular carcinoma (HCC) pathogenesis and is closely linked to ferroptosis. This study investigates the function of OTUB1, a deubiquitinase overexpressed in HCC, in regulating autophagy-dependent ferroptosis. Using integrated bioinformatics, biochemical assays, and xenograft models, we demonstrated that OTUB1 is upregulated in HCC and correlates with poor prognosis. Functionally, OTUB1 knockdown suppressed proliferation and induced ferroptosis, whereas its overexpression promoted malignancy. Mechanistically, OTUB1 competitively binds to p62/SQSTM1, thereby suppressing autophagic flux. Crucially, we identified that OTUB1 stabilizes p62 via non-canonical, D88-dependent deubiquitination by specifically removing K48-linked polyubiquitin chains. This stabilization hinders the initiation of autophagy-dependent ferroptosis. Pharmacological inhibition of autophagy abrogated the ferroptosis induced by OTUB1 knockdown. Furthermore, inhibiting OTUB1 sensitized HCC tumors to Lenvatinib, resulting in synergistic anti-tumor efficacy in vivo. Collectively, these findings reveal that OTUB1 drives HCC progression by stabilizing p62 to block autophagy-dependent ferroptosis. Targeting the OTUB1-p62 axis represents a novel therapeutic strategy to overcome drug resistance and improve outcomes in advanced HCC. - Source: PubMed
Publication date: 2026/07/22
Zhao PengchengWang YongxinSaeidi NimaZhang Ping - N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6-PPD) is a widely used tire antiozonant that has recently emerged as a global environmental concern. Although its aquatic toxicity is well documented, its respiratory toxicity in mammals remains poorly understood. We aimed to characterize the temporal progression of 6-PPD-induced pulmonary injury and elucidate the underlying molecular mechanisms, with a focus on mitochondrial homeostasis. A single exposure to 6-PPD (10 or 25mg/kg) in mice induced rapid-onset pulmonary edema and neutrophilic inflammation, peaking within 24-48h. Although 6-PPD was rapidly cleared from lung tissue within 24h and extrapulmonary organs showed only transient or no significant changes, pulmonary injury persisted. Lung weight remained significantly elevated, and foamy alveolar macrophages were observed up to 168h. Mechanistically, 6-PPD induced a state of mitochondrial dysfunction characterized by sustained Drp1-mediated fission and impaired autophagic degradation, evidenced by persistent accumulation of p62 (SQSTM1) and LC3-II up to 336h. Despite these structural alterations, ATP levels and antioxidant enzyme activities remained stable, indicating maintained metabolic function despite disrupted mitochondrial quality control. A single respiratory exposure to 6-PPD induced persistent lung injury that outlasted the presence of the parent compound. This effect was associated with disruption of mitochondrial quality control, highlighting mitochondrial dysfunction as a key mechanism of toxicity. These findings provide important insights for assessing inhalation risks of tire-derived pollutants and support the need for further studies under environmentally relevant exposure conditions. - Source: PubMed
Publication date: 2026/09/22
Kim Je-HeinKang Min-SungLee Ju HongJi MoongiNoh WonChoi Jin SooKim In-HyeonPark Se-WoongChoi Jae-HyeogMoon YeongyuPaik Man-JeongSuh Han NaKim Sung-HwanHyun Moonjung - Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive loss of upper and lower motor neurons, yet it is unknown whether diverse genetic risks converge on a shared pathogenic pathway. Here we identify a common mechanism linking TBK1 insufficiency to inflammatory cell death across distinct ALS genotypes. Whole-exome sequencing of 8 familial ALS patients revealed that 3 of them carried pathogenic variants, namely TBK1 (R573H), TDP-43 (G298V)/GARS (I44M)/SETX (L1304W), or SOD1 (G94R)/SQSTM1 (G262R). Motor neurons differentiated from patient iPSCs, despite their different mutations, consistently exhibited axonal and neurite shortening, reduced TBK1 activity, increased phosphorylated TDP-43 with cytoplasmic aggregation, and co-assembly of caspase-8/7 with the pyroptosis executor gasdermin E (GSDME). Neuroinflammatory stimulation further enhanced caspase-8/7 and GSDME cleavage, increased RIPK1 phosphorylation and suppressed TBK1 activation in patient-derived motor neurons, whereas TBK1 knockdown in SH-SY5Y cells recapitulated these phenotypes. Furthermore, a generated humanized TBK1 R573H knock-in mouse developed progressive motor deficits accompanied by spinal motor-neuron loss, neuroinflammation, and TDP-43 pathology. In these mice, LPS challenge produced increased cleavage of GSDME and caspase-7, along with a marked upregulation of p-TDP-43 expression in vulnerable neurons. Together, these data identify TBK1 loss of function as an upstream driver of a caspase-8/7-GSDME pyroptotic program in motor neurons and provide a mechanistic bridge between neuroinflammation, TDP-43 proteinopathy, and neurodegeneration. Targeting the TBK1-caspase-GSDME axis may offer a tractable strategy for disease modification in ALS. - Source: PubMed
Publication date: 2026/09/21
Qi ZihanLiu XueheGeng LuLiu XiaoniDong SiqiLi JiatongHua WenyiDeng YifanLai SuomeiWang YuhaoXia YuhongHan YuyunZhu DongqingZhang XiangLi JinsongLi JixiChen Xiangjun - Hyperbilirubinemia arises from disrupted bilirubin homeostasis, which can lead to bilirubin encephalopathy (BE). Unconjugated bilirubin (UCB)-induced neuroinflammation plays a pivotal role in the pathogenesis and progression of BE. - Source: PubMed
Publication date: 2026/09/21
Liu ShashaLi LingLi JingLi SiyuChen JiaqiSun QianZhang YanHua Ziyu - We describe the generation and characterization of two induced pluripotent stem cell (iPSC) lines: one derived from an ALS patient carrying the heterozygous SQSTM1 c.1175C > T (p.Pro392Leu) mutation, identified as cell line 047, and another one (cell line 053) derived from a patient carrying the heterozygous TBK1 c.1760 + 4_1760 + 7delAGTA likely pathogenic variant, predicted to result in a premature stop codon +, together with the ERBB4 c.2402A > T (p.His801Leu) variant of unknown significance (VUS). - Source: PubMed
Publication date: 2026/09/15
Santangelo SerenaCasarotto VeronicaCampelli LorenzoLeoni SerenaCabras SaraMatteoni EnricoMarco Giovanni DeCanosa AntonioBasso ManuelaBonetto ValentinaTrojisi FrancescaBossolasco PatriziaSilani VincenzoChiò AdrianoTicozzi NicolaCalvo AndreaRatti Antonia