SQSTM1 antibody Host rabbit
- Known as:
- SQSTM1 (anti-) Host host: rabbit
- Catalog number:
- 'ARP54262_P050
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SQSTM1 antibody Host rabbit
Related genes to: SQSTM1 antibody Host rabbit
- 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 Host rabbit
Related articles to: SQSTM1 antibody Host rabbit
- Alzheimer's disease (AD) is a neurodegenerative disorder marked by cognitive decline, where females account for 60% of diagnosed cases. AD is featured by β-amyloid deposition, which influences the activity of M1 muscarinic acetylcholine receptors (M1 mAChRs) that are essential for memory and learning. We previously demonstrated that VU0486846, a M1 mAChR positive allosteric modulator, improves cognitive function in AD mice by ameliorating β-amyloid pathology. However, it remains unclear how changes in M1 mAChR signaling and subcellular localization in AD brain influences its mechanism and how this differs between sexes. Nine-month-old male and female APPswe/PSEN1ΔE9 (APP/PS1) and wild-type mice were treated with VU0486846 (10 mg/kg/day) or vehicle via drinking water for 8 weeks. Elevated extracellular signal-regulated kinase 1/2 signaling, a plausible driver for β-amyloid pathology, was observed in female but not male APP/PS1 mice cortices, whereas VU0486846 mitigated this change. Additionally, VU0486846 enhanced the phosphorylation of the neuronal transcription factor cAMP response element-binding protein and increased the level of c-Fos, which regulate neuronal survival, in female wild-type and APP/PS1 mice only. In contrast, only male APP/PS1 mice exhibited increased levels of p62/SQSTM1 and decreased glycogen synthase kinase-3β activity, indicative of impaired autophagic flux, a change that was ameliorated by VU0486846 treatment. In subcellular fractions obtained from mice cortices, VU0486846 only increased cytosolic M1 mAChR level in female wild-type and APP/PS1 mice but not in males. Our findings indicate that M1 mAChR signaling is disrupted in APP/PS1 mice in a sex-dependent manner. VU0486846 enhances prosurvival signaling in females, potentially by increasing the cytosolic pool of M1 mAChRs, while modulating autophagy pathways in males, highlighting a sex-specific mechanism of action and underscoring its therapeutic potential. SIGNIFICANCE STATEMENT: The study highlights the sex-specific role of M1 muscarinic acetylcholine receptor (M1 mAChR) in Alzheimer's disease (AD) pathophysiology, providing evidence that the ability of M1 mAChR positive allosteric modulation to alleviate β-amyloid pathology occurs through distinct mechanisms. It rescues neuronal activity in females, which could be linked to enhanced cytosolic receptor pooling, while restoring autophagic flux in males. The study also reinforces the therapeutic potential of M1 mAChR positive allosteric modulators and supports the development of sex-tailored interventions for AD. - Source: PubMed
Publication date: 2026/07/09
Bassiouni WesamYe EmilyColson Tash-Lynn LFerguson Stephen S GAbd-Elrahman Khaled S - Epithelioid cell histiocytoma (ECH) has been previously classified as a rare variant of fibrous histiocytoma (FH). The epithelioid nature of this lesion imitates the appearance of neoplastic lesions such as melanocytic, dermatofibroma/histiocytoma, non-Langerhans histiocytosis such as reticulohistiocytoma, atypical fibroxanthoma, and rhabdomyosarcoma. Most ECH cases are characterized by Anaplastic lymphoma kinase (ALK) protein rearrangement and overexpression. ALK has several fusion partners, the most common being Sequestosome 1 (SQSTM1) which produces proteins involved in signal transduction and autophagy. A recent detection of ALK protein expression and/or ALK gene rearrangement in ECH suggests that it may be biologically different from conventional FH. The epithelioid nature of the lesion in this case imitates the appearance of neoplastic lesions such as melanocytic, dermatofibroma/histiocytoma, non-Langerhans histiocytosis such as reticulohistiocytoma, atypical fibroxanthoma, and rhabdomyosarcoma. Owing to the unusual morphology and aberrant immunohistochemical staining pattern, the sample was analyzed through next-generation sequencing (NGS), which showed the presence of a fusion of genes Sequestosome 1 (SQSTM1) and Anaplastic lymphoma kinase (ALK). SQSTM1 gene produces proteins involved in signal transduction pathways and autophagy, whereas ALK mainly serves the role of cellular communication and development. The most well-known ALK fusion partners include SQSTM and Vinculin (VCL). The spectrum of neoplasms produced through these fusions is wide as seen in lung adenocarcinoma and renal cell carcinoma (EML4-ALK), epithelioid histiocytoma (SQSTM1::ALK and VCL-ALK), and pediatric renal cell carcinoma (VCL-ALK) among others. We hope this case is a helpful addition to the literature to further aid diagnoses of future ALK fusion cases. - Source: PubMed
Publication date: 2026/07/28
Hong JinpyoGizaw Naomi BThieu Thanh-MaiKominick CarolineHelm Thomas NHelm Klaus F - Paget's disease of bone (PDB) is a moderately common clinical entity that causes bone deformities and focal areas of disorganized new bone formation. It is characterized by abnormal bone remodeling, leading to enlarged and weakened bones. Although often asymptomatic, it can present with localized pain, deformity, or fractures. Elevated alkaline phosphatase (ALP) levels, which are bone-specific, are common biochemical findings of PDB and can be treated with bisphosphonates; however, diagnosing it based on clinical presentation may be challenging due to the asymptomatic nature of the disease, as well as the various factors, causes, and tests required for an accurate diagnosis. We present the case of a 67-year-old male patient who initially presented to the clinic with a right heel fracture and right hip pain, which turned out to be PDB marked by an increased ALP level. A radionuclide bone scan confirmed right pelvic bone deformity and prompted the prescription of zoledronic acid. Lab work was repeated six months later, and a repeat radionuclide bone scan will be performed if the patient experiences any new symptoms. With such cases often being overlooked, especially in primary care settings, this report emphasizes the vital need to monitor biochemical markers, such as ALP. This report highlights the diagnostic process and clinical considerations involved in identifying and managing PDB. - Source: PubMed
Publication date: 2026/06/19
Nandkumar Nikhil AChakrala Aruna - Selective remodeling of nuclear architecture under pharmacological stress remains incompletely characterized in three-dimensional cancer models, particularly at the ultrastructural level. Lithium chloride (LiCl) is widely used as a cellular stressor capable of altering membrane organization, proliferation, and organelle dynamics; however, its effects on nucleus-associated structural remodeling in three-dimensional tumor systems remain unclear. In the present study, Ishikawa endometrial carcinoma spheroids were exposed to LiCl (10 or 50 mM) for up to 96 h, and cellular responses were evaluated using cell cycle analysis, 5-bromo-2'-deoxyuridine (BrdU) incorporation, viability assays, and transmission electron microscopy. LiCl exposure was associated with sustained accumulation of cells in the G/G phase and suppression of DNA synthesis without evidence of a dominant apoptotic or necrotic response under the examined conditions. Ultrastructural analyses showed prominent nuclear envelope elongation, membrane reorganization, and perinuclear double-membraned structures, particularly under prolonged LiCl exposure. These alterations were observed alongside mitochondrial and endomembrane remodeling, supporting the presence of a broader stress-associated ultrastructural adaptation response within LiCl-treated spheroids. Importantly, the present study is morphology-focused and descriptive in scope. Although some ultrastructural features were morphology-compatible with nucleophagy-associated remodeling, no molecular validation using LC3, p62/SQSTM1, LAMP1/lysosomal colocalization, lamin degradation, or autophagic-flux assays was performed. Therefore, the findings should be interpreted as evidence of stress-associated nuclear envelope remodeling rather than mechanistic proof of nucleophagy. Collectively, this study identifies nucleus-associated ultrastructural remodeling as a prominent cellular response to LiCl-induced stress in 3D endometrial cancer spheroids and highlights the utility of three-dimensional tumor models for investigating stress-related architectural adaptations in cancer cells. - Source: PubMed
Publication date: 2026/07/17
Bilir AyhanYıldırım BernaKaralök Mete HakanKulak Kudret - The purpose of this study was to offer a theoretical foundation for the use of curcumin in poultry systems for anti-stress responses. Fourteen-day-old SPF Leghorn embryonic eggs were isolated and digested to produce primary cultured cardiomyocytes for this investigation. The primary cultured cardiomyocytes were divided into three groups: the CK group, serving as the control check; the HS group, which underwent a heat stress challenge; and the HS_Cur group, which was pre-treated with curcumin prior to experiencing heat stress. Twenty hours prior to the heat stress phase, the HS_Cur group received 15 μmol/L of curcumin. The culture medium's cells and supernatant were extracted. Curcumin has been shown to protect cells against heat stress by drastically inhibiting the release of CK-MB and LDH, reducing the generation of MDA, and improving the potential of the mitochondrial membrane. Heat stress may alter cell proliferation, the base repair process, and cause proteotoxic stress, according to pathway enrichment analysis. Several iron metabolism-related pathways were both shown in CK vs. HS and HS vs. HS_Cur comparisons. Curcumin can promote heme synthesis and improve iron storage and antioxidant capacity by suppressing the expression of FTL, MAP1LC3C, and FXN and increasing the expression of SLC7A11, FTH1, FECH, SQSTM1, and NQO1, according to our subsequent analysis of iron metabolism-related DEGs. Curcumin may protect cells from the toxicity of LIP by inhibiting the expression of ferritinophagy-related genes and increasing the expression of heme production, iron storage, and antioxidant-related genes. - Source: PubMed
Publication date: 2026/07/15
Bian MengZeng XiaojuanZhang DingdingBu JiapeiBai Dingping