SQSTM1 antibody
- Known as:
- SQSTM1 (anti-)
- Catalog number:
- orb137277
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- SQSTM1 antibody
Related genes to: SQSTM1 antibody
- 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
Related articles to: SQSTM1 antibody
- Y320, initially identified as an immunomodulator, has been reported to reverse multidrug resistance to chemotherapeutic agents in breast and liver cancers. However, its antitumor activities and underlying mechanisms remain poorly elucidated. In this study, we first investigated the antitumor effects and mechanisms of Y320 in non-small cell lung cancer (NSCLC). Y320 exerted potent antitumor activities against NSCLC both in vitro and in vivo. It induced excessive autophagy, as evidenced by increased autophagosome and autolysosome formation, reduced sequestosome 1 (SQSTM1) protein levels, and conversion of microtubule-associated protein 1 light chain 3 beta (LC3B) from type I to type II. Concurrently, Y320 significantly triggered pyroptosis via the caspase-3/GSDME pathway, as indicated by cellular swelling, membrane blebbing, lactate dehydrogenase (LDH) release, increased propidium iodide (PI) uptake, and elevated levels of cleaved caspase-3 and GSDME-NT. Y320-induced pyroptosis depended on autophagy, and blockade of autophagy at the early stage reversed the occurrence of pyroptosis. Additionally, Y320 downregulated cellular FLICE-like inhibitory protein (c-FLIP) expression through the proteasomal pathway. Importantly, we were the first to verify that knockdown of c-FLIP induced pyroptosis via activation of the caspase-3/GSDME axis. Overexpression of c-FLIP reversed Y320-induced autophagy-dependent pyroptosis. Thus, Y320 induced excessive autophagy-dependent pyroptosis in NSCLC cells by downregulating c-FLIP, ultimately leading to cell death. In conclusion, our study identifies Y320 as a promising therapeutic candidate for NSCLC and elucidates that autophagy-dependent pyroptosis are involved in its anti-tumor mechanism. - Source: PubMed
Publication date: 2026/07/09
Xi ShuohanWang WendieShang YueZeng ChaoyangLiu QinZhang XiyanSu LingChen Shu-Zhen - Mild cognitive impairment (MCI) lacks approved disease-modifying therapies. Classical multicomponent prescriptions may act on convergent neurobiological nodes. We combined network pharmacology with testing to evaluate Yizhi Dihuang Decoction (YZDHD). Constituents were curated from traditional chinese medicine systems pharmacology database and analysis platform (TCMSP) and high-throughput experiment- and reference-guided database of Traditional Chinese Medicine (HERB under blood-brain barrier-aware SwissADME criteria. Targets were inferred, intersected with MCI genes, organized into STRING and MCODE networks, and examined by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment. Structure-based docking evaluated ligand-protein interactions across network-identified hub targets and ranked complexes by predicted binding energy. Predictions were tested in a D-galactose mouse model using the Morris water maze and novel object recognition, hippocampal histology with hematoxylin and eosin and Nissl staining, transmission electron microscopy, and molecular readouts by Western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR), including PI3K, p-AKT/AKT, p-mTOR/mTOR, LC3-II/LC3-I, and p62/SQSTM1. We identified 152 bioavailable compounds and 381 overlapping targets that converged on hub kinases including AKT1, PIK3CA, PIK3CD, and mTOR; docking supported feasible engagement. , YZDHD improved spatial learning and recognition memory, preserved hippocampal cytoarchitecture and mitochondrial integrity, increased LC3-II/LC3-I, decreased p62/SQSTM1, and reduced activation indices of AKT and mTOR. YZDHD ameliorates MCI-like deficits by rebalancing PI3K-AKT-mTOR signaling and restoring autophagy-related activity. Signals for mitogen-activated protein kinase (MAPK), hypoxia-inducible factor 1 (HIF-1), epidermal growth factor receptor (EGFR), and toll-like receptor 4 (TLR4) broaden the mechanistic hypothesis space and warrant targeted follow-up. - Source: PubMed
Publication date: 2026/07/09
Hao ZhihuaMeng TianweiLi SongzheBu YifanQie RuiChen Jing - Paget Disease of Bone (PDB) is a chronic metabolic disorder characterized by accelerated, disorganized bone remodeling resulting in structural enlargement and mechanical weakness. This review synthesizes 38 historical cases drawn from a three-journal convenience sample restricted to English-language literature; observed geographic patterns should therefore be interpreted with caution, as they may reflect research and publication bias rather than the true paleopathological distribution of the disease. Within our sampled literature, modern clinical cases are declining in prevalence while the archeological record suggests a spike in medieval Northwest Europe characterized by more severe, polyostotic manifestations - though this apparent concentration may partly reflect the geographic focus of the journals searched rather than a true biological pattern. Crucially, a microscopically confirmed case from Byzantine Jordan and a pre-contact case from Ontario demonstrate that PDB existed outside Europe in antiquity, and the apparent rarity of non-European ancient PDB almost certainly reflects under-research of non-European assemblages and non-English-language literature rather than true biological absence. Historically, subjective macroscopic identification of "pumice-like" textures has proven unreliable. Current best-practice protocols require interdisciplinary integration of radiography to identify "blade of grass" lesions and histology to confirm pathognomonic mosaic cement lines. While the SQSTM1 protein was detected with abnormalities in medieval remains, the modern familial point mutations were absent - raising the possibility of a distinct ancient pathogenic mechanism. We speculate, as a hypothesis requiring further molecular evidence across broader geographic and temporal samples, that PDB may have undergone a fundamental etiological shift over the past millennium; this interpretation remains provisional and should not be read as a confirmed conclusion. - Source: PubMed
Publication date: 2026/06/24
Dagrosa Mackenzie AVan Schaik Katherine D - Antibodies are known to prevent infection by binding to pathogens extracellularly and blocking their entry into cells. What is less well known is that a proportion of pathogens, called the persistent fraction, still succeed in entering cells despite the antibodies bound to their surface. Fortunately, all mammalian cells express a dedicated cytosolic antibody receptor called TRIM21 that intercepts these incoming antibody-bound pathogens as soon as they enter the cytosol. Once it has detected an infection event, TRIM21 uses its E3 ubiquitin ligase activity to target pathogens for degradation. Our early work showed that TRIM21-mediated neutralization was both a fast and efficient process, capable of causing the degradation of incoming viral particles within hours. What was less clear was how TRIM21 achieves this degradation. In a recent study, we reveal that TRIM21 mediates a system of selective autophagy to direct incoming pathogens into the lysosome.:TRIM21:Tripartite-motif containing protein 21; VCP: Valosin-Containing Protein. CRISPR: Clustered Regularly Interspaced Short Palindromic Repeats; FACS: fluorescence activated cell sorting; GFP: green fluorescent protein; LC3: Microtubule-associated Protein 1 Light Chain 3; TBK1: TANK-binding kinase 1; FIP200: FAK family kinase-interacting protein of 200 kDa; ULK1: Unc-51-like autophagy activating kinase 1; PI3K: Phosphoinositide 3-Kinase; ATG: autophagy-related gene; TMEM41B: transmembrane protein 41B; VPS37A: Vacuolar Protein Sorting-Associated Protein 37A; RBSN: Rabenosyn-5; EPG5: Ectopic P-Granules 5 Autophagy Tethering Factor; NDP52: Nuclear Dot Protein 52; ADX: antibody-dependent xenophagy; p62/SQSTM1: Protein 62/ Sequestosome 1; LPS: Lipopolysaccharide. - Source: PubMed
Publication date: 2026/07/08
Rhinesmith TAlbecka AJames L C - Metabolic reprogramming represents a hallmark feature of hepatocellular carcinoma (HCC). As a crucial branch of the polyol pathway, the biological functions and clinical implications of sorbitol metabolism in HCC progression remain to be fully elucidated. - Source: PubMed
Publication date: 2026/07/07
Yang XianchunCheng YiJiang XingLi YinyuJiang ShuoYang JieLi ChaorongWu Lichun