SQSTM1 Antibody (Phospho S403)
- Known as:
- SQSTM1 Antibody (Phospho S403)
- Catalog number:
- AP3802a
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SQSTM1 Antibody (Phospho S403)
Related genes to: SQSTM1 Antibody (Phospho S403)
- Gene:
- RNA5SP403 NIH gene
- Name:
- RNA, 5S ribosomal pseudogene 403
- Previous symbol:
- RN5S403
- Synonyms:
- -
- Chromosome:
- 16p13.2
- Locus Type:
- pseudogene
- Date approved:
- 2012-01-30
- 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 (Phospho S403)
Related articles to: SQSTM1 Antibody (Phospho S403)
- Dual-specificity protein kinase CLK4 plays a pivotal role in regulating alternative mRNA splicing, DNA repair, and various cellular processes through precise phosphorylation. In this study, we analyzed 3825 global human cellular phosphoproteome studies, identifying 430 qualitative profiles and 55 quantitative differential datasets featuring high-confidence Class-1 phosphosites (localization probability ≥ 75%; A-score ≥ 13). Notably, S136 and S138 emerged as predominant phosphorylation sites outside the kinase domain. These sites showed frequent detection and differential expression in liver, lung, and head and neck cancers, as documented in PhosphositePlus. We identified a high-confidence set of co-regulated phosphoproteins, including SQSTM1, SRRT, RPS6, TP53BP1, TNKS1BP1, THUMPD1, OTUD4, and TCEA1. These proteins link CLK4 to critical pathways, including RNA splicing, autophagy, DNA damage response, and cancer progression. Binary interactors, including SRRM2, Interacts with SPT6 1 (IWS1), RBBP6, ZC3H18, BUD13, and DYRK1A, further connect CLK4 to RNA processing and splicing. Predicted downstream substrates, such as CCNL2, CDK11B, PRDX6, YTHDC1, RBM15, SRRM1, SFSWAP, HNRNPU, and DOCK7, highlight CLK4's broad regulatory scope. Upstream kinases were also predicted for S136 and S138. Site-resolved analyses revealed tumor-specific dysregulation of CLK4 phosphorylation at key residues. Co-occurring phosphosite alterations and nearby somatic mutations suggest disrupted CLK4 regulation in cancer. Overall, this study provides a comprehensive phosphoproteomic resource that maps CLK4's co-regulatory networks, paving the way for mechanistic investigations and targeted cancer therapies. - Source: PubMed
Publication date: 2026/07/22
Pai ApoorvaDcunha LeonaGopalakrishnan Athira PerunellyUmmar SamseeraRajeev Athira CRaju Rajesh - Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia/lymphoma (ATLL) and the neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax regulatory protein plays a critical role in HTLV-1 persistence and pathogenesis; however, the underlying mechanisms are poorly understood. Here we show that Tax dynamically regulates mitochondrial reactive oxygen species (ROS) and membrane potential to trigger mitochondrial dysfunction. Tax is recruited to damaged mitochondria through its interaction with the IKK regulatory subunit IKBKG/NEMO and directly engages the ubiquitin-dependent PINK1-PRKN/parkin pathway to induce mitophagy. Tax also recruits autophagy receptors CALCOCO2/NDP52 and SQSTM1/p62 to damaged mitochondria to induce mitophagy. Furthermore, Tax requires PRKN to limit the extent of CGAS-STING1 activation and suppress type I interferon (IFN) induction. HTLV-1-transformed T-cell lines and PBMCs from HAM/TSP patients exhibit hallmarks of chronic mitophagy, and inhibition of PRKN in HTLV-1-transformed cell lines downregulates p19 Gag expression and induces cell death. Collectively, our findings suggest that Tax manipulation of the PINK1-PRKN mitophagy pathway represents a new HTLV-1 immune evasion strategy important for maintaining viral gene expression and cell survival. - Source: PubMed
Publication date: 2026/07/22
Mohanty SuchitraSuklabaidya SujitMnatsakanyan NelliJacobson StevenHarhaj Edward W - Non-alcoholic fatty liver disease (NAFLD), a common metabolic disorder, is increasingly linked to impaired male reproductive health. This study investigates the therapeutic potential of adipose-derived mesenchymal stem cells (AD-MSCs) and their exosomes (AD-MSCs-Exo) in ameliorating NAFLD-induced testicular dysfunction in a murine model. Male C57BL/6 mice were divided into four groups: [n = 8 per group: control, high-fat diet (HFD), HFD + AD-MSCs, and HFD + AD-MSCs-Exo]. Sperm parameters according to the WHO Laboratory Manual, hormonal profiles via ELISA, and expression of genes involved in autophagy and spermatogenesis were assessed using qRT-PCR. HFD-induced NAFLD significantly reduced sperm count (P = 0.036), motility (P < 0.0001), viability (P = 0.023), and normal morphology (P = 0.015) while increasing DNA fragmentation (P = 0.004). Moreover, in the HFD group, LH and total testosterone levels decreased significantly (P = 0.0002 and P < 0.0001), whereas estradiol levels increased significantly (P = 0.0001) compared with controls. Expression of STAR was significantly downregulated (P = 0.0001); conversely, the relative fold changes of BECN1 (P = 0.0003), MAP-LC3b-a (P = 0.0002), and SQSTM-1/p62 (P = 0.005) were significantly enhanced in the HFD group compared to the controls. Treatment with AD-MSCs or AD-MSCs-Exo improved sperm quantity and quality and balanced hormonal levels. AD-MSCs showed slightly greater modulation of key autophagy genes (BECN1, MAP-LC3b-a, and SQSTM1/p62), whereas exosomes were more effective in hormonal restoration (especially testosterone) and in enhancing genes related to steroidogenesis (especially INHBB). AD-MSCs and their exosomes improve sperm-related abnormalities, hormonal imbalance, and testicular autophagy dysregulation in the NAFLD model. These findings support their potential as therapeutic agents for NAFLD-induced male infertility, highlighting translational relevance while noting the need for further clinical validation. - Source: PubMed
Publication date: 2026/07/21
Mirani MaryamMoayedfard ZahraBahmyari SedighehMasjedi FatemehNekooeian Ali AkbarBahmanpour SoghraHeidarian RonakDara MahintajKoohpeyma FarhadAzarpira Negar - Receptor tyrosine kinases (RTKs) are core cancer therapeutic targets, yet their integral membrane localization hinders efficient degradation by traditional ubiquitin-proteasome system (UPS)-based targeted protein degradation (TPD) strategies. Herein, we describe the structure-guided development of p62/SQSTM1-directed autophagy-targeting chimera (AUTOTAC) degraders targeting RTKs. Medicinal chemistry optimization yielded two potent AUTOTACs, and , which selectively degrade EGFR and VEGFR2, respectively. Mechanistic studies confirmed that these degraders act via p62 recruitment and autophagy-lysosome pathway activation in a UPS-independent manner. and exhibited robust antiproliferative, proapoptotic, and antimigratory effects , and further demonstrated significant antitumor efficacy with good tolerability in xenograft models. This study validates AUTOTAC technology for RTK degradation, offering a new approach to address TKI resistance and broaden the TPD landscape. - Source: PubMed
Publication date: 2026/07/21
Wu DefaWu YongyaZhao MinLi YangTang HaolinChen WenqingDuan MaolinFeng GuotaiZheng LangWang ShuoZhang YiwenLiu JieOuyang LiangSun Qiu - Cisplatin (CP) chemotherapy can elicit clinically meaningful cardiac injury, and the additional use of effective cardioprotective agents is a pressing need. This study investigated the protective effects and mechanisms of gastrodin against CP-induced cardiotoxicity, through redox-, inflammatory-, apoptotic-, and Nrf2-axis mechanisms. - Source: PubMed
Publication date: 2026/07/20
Alqudah AbdelrahimQnais EsamBsieso YousraHamdallah Amjad EGammoh OmarShilbayeh Sireen Abdul RahimAljabali Alaa A A