SQSTM1 Antibody (N-term S24)
- Known as:
- SQSTM1 Antibody (N-terminus S24)
- Catalog number:
- AP19120a-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SQSTM1 Antibody (N-term S24)
Related genes to: SQSTM1 Antibody (N-term S24)
- Gene:
- CHMP3 NIH gene
- Name:
- charged multivesicular body protein 3
- Previous symbol:
- VPS24
- Synonyms:
- NEDF, CGI-149
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-11
- Date modifiied:
- 2014-11-19
- Gene:
- HSPA4 NIH gene
- Name:
- heat shock protein family A (Hsp70) member 4
- Previous symbol:
- -
- Synonyms:
- HS24/P52, HSPH2
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-26
- Date modifiied:
- 2015-11-19
- Gene:
- KLRK1 NIH gene
- Name:
- killer cell lectin like receptor K1
- Previous symbol:
- D12S2489E
- Synonyms:
- NKG2D, KLR, NKG2-D, CD314
- Chromosome:
- 12p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-12
- Date modifiied:
- 2016-10-05
- Gene:
- MRPS24 NIH gene
- Name:
- mitochondrial ribosomal protein S24
- Previous symbol:
- -
- Synonyms:
- MRP-S24, HSPC335
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-26
- Date modifiied:
- 2016-10-05
- Gene:
- RNA5SP24 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 24
- Previous symbol:
- RN5S24
- Synonyms:
- -
- Chromosome:
- 13q12.11
- Locus Type:
- pseudogene
- Date approved:
- 2011-08-08
- Date modifiied:
- 2012-08-07
Related products to: SQSTM1 Antibody (N-term S24)
Related articles to: SQSTM1 Antibody (N-term S24)
- Inorganic arsenic (As) exposure is known to induce pulmonary fibrosis, yet the underlying mechanisms remain incompletely understood. This study investigated the crosstalk between sequestosome 1 (SQSTM1/p62) and nuclear factor erythroid 2-related factor 2 (Nrf2) in regulating cellular senescence and epithelial-mesenchymal transition (EMT) in As-exposed alveolar type II (AT2) cells. RNA sequencing analysis initially suggested that As exposure promotes EMT and senescence in MLE-12 cells. Subsequent experiments demonstrated that As exposure progressively decreased the epithelial marker E-cadherin while increasing the mesenchymal marker N-cadherin in MLE-12 cells, a mouse AT2 cell line, and murine lung tissues. In addition, elevated expression of transforming growth factor (TGF)-β and α-smooth muscle actin (SMA) was observed. Meanwhile, As exposure increased the number of SA-β-galactosidase (SA-β-gal)-positive MLE-12 cells and enhanced the transcriptional activity of senescence-associated secretory phenotype (SASP)-related genes, including Cxcl1, Cxcl11, Cxcl16, Ccl20, Mcp-1, Tgf-β, and Gm-csf. Moreover, the expression of senescence-associated markers p16 and p21 was upregulated in both As-exposed MLE-12 cells and murine lungs. Notably, Nrf2 knockdown exacerbated cellular senescence, as evidenced by increased SA-β-gal-positive cells, enhanced SASP gene expression, and elevated p16 and p21 levels, along with augmented EMT marker expression. To further verify the protective role of Nrf2, As-exposed MLE-12 cells were treated with the Nrf2 activator dimethyl fumarate (DMF). DMF activates Nrf2 by modifying Keap1, thereby disrupting Keap1-mediated Nrf2 degradation and promoting Nrf2 stabilization and nuclear translocation. DMF markedly reversed As-induced senescence, as shown by decreased SASP-related gene, p16, and p21 expression, while attenuating EMT, evidenced by restored E-cadherin and reduced N-cadherin and α-SMA. Moreover, pharmacological disruption of the p62-Keap1 interaction using K67 restored Keap1-mediated suppression of Nrf2 and further aggravated senescence and EMT phenotypes. Collectively, these findings demonstrate that As exposure induces cellular senescence and EMT in MLE-12 cells and murine lungs. The p62-Keap1-Nrf2 positive feedback loop functions as an essential cytoprotective axis that attenuates As-evoked senescence and EMT in AT2 cells, underscoring its potential as a therapeutic target for arsenic-associated pulmonary fibrosis. - Source: PubMed
Publication date: 2026/10/05
Guo XinyangMa XinyuQin LiyiLi YibingHan XinyueWang MeiqiWei XiaoxiGong ShuwenSu WeiCheng DeminJin YulanShen FuhaiZhao XinyuanGuo ZhiweiLi Jinlong - Acute pancreatitis (AP) is one of the most common gastrointestinal emergencies, with a fatality rate reaching 30%. Many studies reported defective autophagy in AP. Trehalose, a disaccharide, has been shown to reduce inflammatory injury by restoring autophagy; however, few studies have examined its ability to enhance autophagy in L-arginine-induced AP. Twenty-four adult male Swiss albino mice were assigned to 3 groups: a control group, an L-arginine group, and an L-arginine + trehalose group (2 g/kg once daily for 12 days). Seventy-two hours after the last treatment, all mice were dissected, and blood samples were collected for pancreatic enzyme assessment. Histological assessment and histopathological scoring for pancreatic tissues were performed. To assess autophagic machinery, an immunohistochemical study using antibodies against LC3-II and P62/SQSTM1 was performed, and mRNA expression of the Beclin-1 and LC3-II genes in pancreatic tissues was assessed. The L-arginine group demonstrated significant increases in serum pancreatic lipase and amylase levels (P < 0.001), distortion of the exocrine acini, inflammatory cell infiltration, areas of necrosis, and many autophagic vacuoles. Immunohistochemical analysis showed a significant increase in the percentage of areas occupied by LC3-II and P62 (P < 0.001) and in the gene expression of Beclin-1 and LC3-II compared with the control group (P < 0.001). Compared to the L-arginine group, the L-arginine + trehalose group revealed a significant reduction in serum pancreatic lipase and amylase levels (P < 0.001), intact exocrine acini, and minimal inflammatory cell infiltration, with a significant reduction in the immunohistochemical area percentages of LC3-II and P62 (P < 0.001), and in Beclin-1 and LC3-II gene expressions (P < 0.001). In conclusion, trehalose therapy significantly mitigates pancreatic injury by restoring effective autophagy. - Source: PubMed
Publication date: 2026/10/01
Arafat Eetmad AElsayed Hassan Reda HassanNasr AhmedAlghamdi Mansour AElhessy Heba MEl-Desoky Manal MMostafa NoraShabaan Dalia A - Impaired local perfusion, excessive oxidative stress, persistent inflammation, and apoptosis can compromise cutaneous wound healing. Licochalcone D (LCD), a licorice-derived flavonoid, has antioxidant and anti-inflammatory properties, but its effects on cutaneous repair remain incompletely characterized. This study evaluated LCD in a rat full-thickness excisional wound model. Thirty-two male Sprague-Dawley rats were randomly assigned to vehicle control or LCD treatment at 5, 25, or 50 mg/kg/day by oral gavage. Wound closure, local perfusion, histological repair, oxidative stress, inflammatory mediators, apoptosis-related proteins, antioxidant signaling-related proteins, and selected mitochondrial protein markers were evaluated. LCD accelerated wound closure, enhanced perfusion, increased VEGF expression, reduced inflammatory-cell infiltration, and improved collagen organization. LCD also increased SOD activity, reduced MDA and 4-HNE levels, and decreased TNF-α, IL-1β, and IL-6. Nrf2, HO-1, and NQO1 expression increased after LCD treatment, supporting an association with enhanced antioxidant responses. Apoptosis-related proteins shifted toward an anti-apoptotic pattern. LCD treatment was additionally accompanied by changes in PINK1, Parkin, LC3B, SQSTM1/p62, and COX IV expression; however, these single-time-point measurements do not establish altered mitophagic flux or a causal mitochondrial mechanism. Overall, orally administered LCD improved multiple wound-healing-related outcomes, with more pronounced effects in the medium- and high-dose groups. - Source: PubMed
Publication date: 2026/09/26
Liu YunmianZhang YekaiWang Junkai - Alzheimer's disease (AD) is characterized by progressive cognitive decline driven by the convergence of tauopathy, impaired proteostasis, and chronic neuroinflammation. Emerging evidence identifies the immunoproteasome (iP), particularly the β5i/LMP7 subunit, as a central regulator linking these pathological processes. Unlike the constitutive proteasome, the iP is markedly induced in microglia, neurons, and astrocytes under inflammatory conditions through interferon-γ and NF-κB signaling. This review discusses the dual and context-dependent role of the iP in AD pathogenesis. In microglia, chronic iP activation promotes degradation of NRF2, leading to oxidative stress, NLRP3 inflammasome activation, and the development of a senescence-associated secretory phenotype that exacerbates neuroinflammation and tau propagation. In neurons, moderate iP activity facilitates the clearance of phosphorylated tau; however, sustained overactivation generates aggregation-prone tau fragments that enhance trans-synaptic tau spreading. We further highlight the cross-talk between the iP and autophagy pathways through TFEB and p62/SQSTM1 signaling and discuss how gut microbiota-derived inflammatory mediators may prime central iP activation through the gut-brain axis. Importantly, recent preclinical studies support the concept of partial immunoproteasome modulation rather than complete inhibition, with selective LMP7 targeting restoring proteostatic balance, reducing microglial senescence, and attenuating tau pathology. Collectively, the iP emerges as a promising immunopharmacological target and a potential therapeutic rheostat in AD. - Source: PubMed
Publication date: 2026/10/03
Shokr Mustafa MAbdelaziz Ahmed M - Cellular senescence drives aging and age-related diseases, posing a critical barrier to stem cell-based regeneration. While selective elimination of senescent cells (senolysis) remains a theoretically promising strategy, safe natural senotherapeutic agents are limited. Human exfoliated deciduous tooth stem cells (SHED) possess high regenerative potential yet are vulnerable to senescence, compromising their therapeutic utility. - Source: PubMed
Publication date: 2026/09/17
Yang KangluLiu LanyiboLi CaifengDeng ShiwenCao JunxianChen JunqiWang ShaopingChen QiangpuChen Peng