SQSTM1 Antibody (Phospho S403) Blocking Peptide
- Known as:
- SQSTM1 Antibody (Phospho S403) Blocking Peptide
- Catalog number:
- BP3802a
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SQSTM1 Antibody (Phospho S403) Blocking Peptide
Related genes to: SQSTM1 Antibody (Phospho S403) Blocking Peptide
- 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) Blocking Peptide
Related articles to: SQSTM1 Antibody (Phospho S403) Blocking Peptide
- Mitophagy-mediated mitochondrial quality control is essential for normal cardiac physiology. In this study, we observed that cardiac RNF10 expression was induced by multiple chronic stressors, including aging, angiotensin II (Ang II) exposure, and obesity. Cardiac-specific RNF10 knockout (RNF10-CKO) mice developed cardiac hypertrophy with aging, characterized by cardiomyocyte enlargement, exacerbated myocardial fibrosis, and impaired cardiac function. Aged RNF10-CKO mice exhibited elevated reactive oxygen species (ROS) levels and reduced mitochondrial membrane potential in cardiomyocytes. Transmission electron microscopy revealed mitochondrial rounding, matrix expansion, and cristae disorganization. Similarly, compared with control mice, Ang II-exposed RNF10-CKO mice exhibited cardiomyocyte hypertrophy, increased fibrosis, and cardiac dysfunction, accompanied by mitochondrial membrane potential depolarization, ROS accumulation, and mitochondrial morphological abnormalities equivalent to those in aged RNF10-CKO mice. Mechanistically, chronic stressors upregulated RNF10 expression, which subsequently mediated the K63-linked polyubiquitination of the mitochondrial outer membrane protein mitofusin 2 (MFN2). This modification stabilized MFN2 on mitochondria and facilitated Parkin recruitment. The accumulated Parkin in mitochondria further promoted the robust recruitment of the autophagy adaptor sequestosome 1 (SQSTM1/p62), leading to increased LC3-II lipidation and the initiation of mitophagy. Notably, this RNF10-mediated mitophagy is dependent on MFN2. However, the effects of RNF10 are independent of those of PINK1. This study identifies RNF10 as a critical regulator of cardiac mitophagy, suggesting that targeting cardiac RNF10 may represent a therapeutic strategy for treating cardiac pathologies. - Source: PubMed
Publication date: 2026/07/15
Song Jia-NiQiu Tong-TongZhang LeiHuang Jin-CanZhang Yu-JieZhang Yin-LiangChang Yong-Sheng - Skin aging is driven by oxidative stress and ultraviolet (UV) exposure, leading to extracellular matrix degradation and loss of skin elasticity. This study aimed to identify the most biologically active species using a bioassay-guided approach and evaluate its potential for dermal applications. - Source: PubMed
Publication date: 2026/07/01
Swilam NohaNematallah Khaled AAlbohy AmgadBadawi Noha MGad Sameh SShouman Maha MAl-Ghamdi Saeed SAlzahrani Abdullah RAyoub Nahla - Sepsis-induced myocardial injury (SIMI) contributes substantially to sepsis mortality. We investigated whether low-dose esmolol is associated with improved autophagy-related homeostasis and restored PI3K/Akt phosphorylation in SIMI. - Source: PubMed
Publication date: 2026/07/14
Zhang XianfenFu QizhiZhang HengzheSong HaosenHao HaoboLi YingyangSun Yun - Spinal Muscular Atrophy (SMA) is a neuromuscular genetic disorder resulting from the mutation or deletion of the Survival Motor Neuron 1 (SMN1) gene and the reduction of the Survival Motor Neuron (SMN) protein. As a result, SMN level in SMA depends on the almost identical copy gene SMN2, which produces a small amount of functional SMN due to a silent mutation in exon 7. SMN deficiency critically impairs spinal cord motoneuron (MN) function, causing progressive degeneration. Advances in SMA therapeutics have significantly improved clinical management and prognosis. However, therapeutic outcomes vary among SMA patients, resulting in broad heterogeneity in phenotypes and clinical trajectories; consequently, more focused investigation on the underlying disease mechanisms is essential. One of the FDA-approved treatments is nusinersen, an antisense oligonucleotide (ASO) designed to enhance SMN2 exon 7 splicing and increase SMN protein. The present study used non-SMA and SMA MNs differentiated from human induced Pluripotent Stem Cells (hiPSCs) to analyze the effect of a nusinersen-like ASO treatment on intracellular pathways altered in SMA MNs. ASO treatment efficiently increased SMN, prevented MN degeneration, and decreased apoptotic markers in SMA MNs. Furthermore, treatment increased Gemin3 protein and the NF-κB members, IKKβ and RelA. Nevertheless, ASO did not revert alterations of the autophagy markers LC3-II and p62/SQSTM1, and the calpain activation product α-fodrin 145/150 kDa. Our observations indicate that nusinersen-like ASO treatment might be insufficient to counteract the full spectrum of intracellular alterations occurring in SMN-reduced MNs. Therefore, supplementary compounds targeting these unrecovered pathways might supply additional protective effects on degenerating MNs. - Source: PubMed
Publication date: 2026/07/13
Miralles Maria PGimenez-Fernandez IsabelBeltran MariaSansa AlbaMartínez-España LauraCalderó JordiPortero-Otín ManuelSoler Rosa MGarcera Ana - Heart failure (HF) presents a persistent clinical challenge. While SUMOylation and mitochondrial function are vital for cardiomyocyte health, their combined influence on HF remains elusive. Two HF-related datasets were downloaded from GEO. The overlapping genes were obtained from all genes in the training set, SUMO-related genes, and mitochondrial-related genes. Three machine learning algorithms were applied to identify diagnostic key genes. Subsequently, diagnostic models were constructed and evaluated based on these genes. Besides, the immune microenvironment in HF versus healthy controls was assessed using CIBERSORT, MCP-counter, and ssGSEA. The differences in immune infiltration between HF and healthy controls were analyzed. Drug prediction and molecular docking were performed to identify potential drug candidates targeting these genes. Finally, qPCR was employed to validate gene expression levels in clinical samples. A total of 113 common genes with notable enrichment in mitochondrial regulation were identified. Five key genes, namely NFKB1, MYEF2, NSUN2, SQSTM1, and FKBP4, were identified by three machine learning algorithms. Functional enrichment analyses linked these genes to immune response, RNA processing, and cell cycle regulation. Moreover, immune infiltration profiling revealed that neutrophil infiltration contributes to dysregulated immune responses in HF. Molecular docking revealed that the small-molecule drug IMX-942 has a favorable binding affinity with SQSTM1 (-5.8 kcal/mol). qPCR validation supported the bioinformatics results. NFKB1, MYEF2, NSUN2, SQSTM1, and FKBP4 were identified as key genes linking SUMOylation and mitochondrial function in HF. These findings provide new insights into HF pathophysiology and may contribute to the development of novel diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/06/26
Chen ZheZhao JinXiao NaZhang Fu'eZhao ShujianYin Hongshan