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
- Acute myeloid leukemia (AML) remains a therapeutic challenge due to complex oncogenic networks, including the often-undruggable MYC pathway. Here, we present an integrated in silico framework combining transcriptomic analysis, machine learning, and molecular dynamics (MD) simulations to explore potential therapeutic approaches targeting vault RNA1-1 (VTRNA1-1) in AML. RNA-seq profiling revealed that VTRNA1-1 depletion is associated with a profound disruption of the MYC and FOXM1 regulatory axes. To highlight compounds capable of recapitulating this transcriptomic signature, we developed a machine learning pipeline utilizing a Random Forest classifier trained on a fully compiled L1000FWD database subset. Virtual screening of approved drugs predicted the anthelmintic niclosamide as a top candidate (98.17% mimic probability). Explainable AI further rationalized this prediction by highlighting specific fragments within niclosamide's salicylanilide core. Furthermore, a 200 ns MD simulation indicated favorable computational stability of niclosamide bound to the p62 (SQSTM1) ZZ domain. The complex showed rapid structural convergence (ligand RMSD plateauing at 1.65 nm) without dissociation, while maintaining strict receptor compactness (steady Radius of Gyration and solvent-accessible surface area) and a persistent interaction network of ~73 close atomic contacts. These findings suggest that niclosamide may function as a stable physical "lid" over the p62 ZZ domain, occluding its N-degron-binding cleft. Taken together, our computational framework highlights niclosamide as a promising candidate for AML drug repurposing, providing a hypothesis-generating foundation that warrants rigorous experimental validation. - Source: PubMed
Publication date: 2026/08/04
Hatayama YukiShimohiro HisashiKawamura Koji - Endometriosis is a chronic inflammatory disorder characterized by the ectopic growth of endometrial-like tissue, leading to pelvic pain and infertility. Although cepharanthine has well-established anti-inflammatory properties, its therapeutic potential and underlying mechanisms in endometriosis remain largely unexplored. In this study, the effects of cepharanthine were evaluated using a surgically induced mouse model and immortalized human endometrial stromal cell models. Cepharanthine treatment significantly reduced the calculated lesion volume, whereas wet lesion weight did not differ significantly between the groups. Cepharanthine was also accompanied by reduced spleen weight and alterations in the CD4+ helper T-cell population in vivo. In immortalized human ovarian endometriotic stromal cells (ihOESCs), cepharanthine significantly decreased cell viability, induced apoptosis, and disrupted cell-cycle progression. Cepharanthine altered autophagy-related signaling, accompanied by increased acidic vesicle-associated signals and accumulation of LC3B-II and p62/SQSTM1; however, the direction of autophagic flux remains unclear. These changes were associated with elevated reactive oxygen species production, intracellular Ca redistribution, and mitochondrial dysfunction. Collectively, these findings indicate that cepharanthine reduces calculated lesion volume in vivo and alters mitochondrial function, autophagy-related signaling, apoptosis and cell-cycle progression in ihOESCs, supporting its potential as a therapeutic candidate. - Source: PubMed
Publication date: 2026/08/05
Kim MijiPark WonhyoungKim Hee SeungLim WhasunSong GwonhwaPark Sunwoo - Lipopolysaccharide (LPS)-induced acute kidney injury (AKI) is associated with high morbidity and mortality. The molecular mechanisms underlying sepsis-associated renal injury remain incompletely understood. Sinapic acid (SA), a bioactive phenolic compound, exhibits antioxidant, anti-inflammatory, and cytoprotective properties, but its nephroprotective role in LPS-induced AKI has not been clarified. We evaluated the protective effects of SA in an LPS-induced AKI rat model and examined its associations with autophagy-related, apoptotic, inflammatory, and oxidative stress markers. AKI was induced by a single intraperitoneal injection of LPS (5 mg/kg) following 7 days of oral SA pretreatment (40 mg/kg/day). LPS administration caused marked renal tubular injury and significantly increased serum BUN, CREA, and UA levels. SA pretreatment significantly attenuated these alterations. Moreover, LPS increased renal BECN1 immunoreactivity and circulating SQSTM1/p62 levels, indicating alterations in autophagy-related markers, together with increased renal TNF-α and Caspase-3 immunoreactivity. SA pretreatment significantly attenuated the LPS-induced increases in these markers. LPS also increased renal MDA levels and serum total oxidant status. SA pretreatment significantly reduced renal MDA without significantly altering SOD, GPx, or total antioxidant status, indicating attenuation of lipid peroxidation rather than a generalized enhancement of antioxidant defenses. Furthermore, SA attenuated the LPS-induced reductions in serum albumin and total protein and the increase in LDH. Collectively, these findings suggest that SA pretreatment attenuates LPS-induced AKI and that this protective effect is accompanied by changes in autophagy-related markers, reduced renal TNF-α and Caspase-3 immunoreactivity, and decreased renal lipid peroxidation. - Source: PubMed
Doğan SerdarOkuyan Hamza MalikCoşkun AyçaAyçiçek Özen Şeyda ÖznurDoğan MehmetKaraboğa İhsanKulaksızoğlu Sibel - Hepatocellular carcinoma (HCC) remains a formidable worldwide health challenge, characterized by inadequate treatment efficacy and unsatisfactory clinical prognosis. Our previous study implicated LINC01607 in lenvatinib resistance, but its role in HCC progression and ferroptosis-associated vulnerability remains unclear. LINC01607 expression was examined in HCC patient samples and The Cancer Genome Atlas datasets. Cellular, animal, and patient-derived organoid (PDO) models were used to evaluate its biological function. RNA sequencing, ferroptosis-related assays, rescue experiments, and drug-sensitivity analyses were performed to explore associated downstream pathways. LINC01607 was upregulated in HCC tissues and associated with aggressive clinicopathological features and poor survival. Functional assays showed that LINC01607 promoted HCC cell proliferation, migration, invasion, tumor growth, and metastasis. LINC01607 depletion induced ferroptosis-associated changes, including increased lipid peroxidation, glutathione depletion, and Fe accumulation under ferroptotic stress, which were partially reversed by ferroptosis inhibitors. LINC01607 knockdown also enhanced sensitivity to RSL3 and sorafenib, while ferrostatin-1 partially rescued the increased sorafenib sensitivity. RNA sequencing and rescue experiments suggested involvement of the p62-Keap1-Nrf2 pathway. LINC01607 depletion was associated with reduced SQSTM1/p62, Nrf2, and ferroptosis-resistance proteins, whereas p62 overexpression partially reversed these effects and Nrf2 knockdown abrogated the rescue. In xenograft and PDO models, LINC01607 depletion improved the response to sorafenib. LINC01607 contributes to HCC progression and ferroptosis-associated therapy resistance, at least in part through the p62-Keap1-Nrf2 pathway, supporting further investigation of LINC01607 as a potential therapeutic target. - Source: PubMed
Publication date: 2026/07/17
Zhang YuxinXu WeiqiCheng FanglingZhu JinghanLu YuanxiangCai GuangzhenLi JiangZhang Yujie - Upon exposure to stress, cells activate a variety of stress-response and quality-control mechanisms to maintain homeostasis. Dysregulation of these processes is implicated in numerous diseases, including cancer, liver disorders, and neurodegenerative diseases. p62/Sequestosome 1 (SQSTM1) is a multifunctional protein that plays a central role in protein homeostasis and stress responses by regulating autophagy and signal transduction pathways. Through its multiple protein-interacting domains, p62 functions both as a scaffold for selective autophagic degradation and as a signaling hub. Since our previous review of p62 a decade ago, substantial progress has been made in elucidating its molecular functions and physiological roles. Notably, p62 undergoes liquid-liquid phase separation with ubiquitinated proteins to form membraneless condensates, termed p62 bodies, when cells are exposed to proteotoxic stress. By sequestering specific proteins, p62 bodies act as platforms for autophagy-dependent degradation and stress signaling. These findings have substantially revised our view of p62 function, which was previously considered primarily as a receptor simply linking ubiquitinated substrates to autophagic membranes and connecting signaling molecules. This conceptual shift from one-to-one molecular interactions to multivalent, multimolecular, higher-order assemblies has fundamentally redefined the functional landscape of p62. In this review, we highlight how p62 bodies integrate selective autophagy and stress signaling, with a particular emphasis on their emerging roles in disease pathogenesis and their potential as therapeutic targets. - Source: PubMed
Publication date: 2026/08/11
Sakamaki Jun-IchiKomatsu Masaaki