BAG3 antibody
- Known as:
- BAG3 (anti-)
- Catalog number:
- orb101835
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- BAG3 antibody
Related genes to: BAG3 antibody
- Gene:
- BAG3 NIH gene
- Name:
- BCL2 associated athanogene 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 10q26.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-23
- Date modifiied:
- 2019-04-23
Related products to: BAG3 antibody
Related articles to: BAG3 antibody
- Bcl-2-associated athanogene 3 (BAG3) is a mediator of chaperone-assisted selective autophagy, and in the brain, is most highly expressed in astrocytes. However, its role in astrocytes remains poorly defined. Given the genetic and pathological links of BAG3 to proteostasis and neurodegenerative diseases, we investigated how BAG3 contributes to astrocyte function and Alzheimer's disease (AD). To define its function and relevance, we used single-nucleus RNA sequencing to confirm BAG3 enrichment in astrocytes and employed CRISPR/Cas9 editing of human induced pluripotent stem cells followed by proteomic and transcriptomic profiling, which revealed that BAG3 loss caused greater disruption in astrocytes than in neurons. BAG3-deficient astrocytes displayed reduced autophagy, lysosomal abundance and activity, and proteasome function. Coimmunoprecipitation identified BAG3 known binding partners (e.g., HSPB8, proteasome regulators), as well as an interactor in the retromer complex, VPS35. BAG3 deficiency resulted in altered retromer activity as measured by amyloid precursor protein (APP) localization in endosomes. In addition to validating these binding partners, integrative -omics analyses showed that BAG3 regulates AD-relevant proteins (GFAP, BIN1), as well as HSPB8. Functionally, BAG3 knockout astrocytes exhibited impaired amyloid-β proteostasis when cocultured with APP/PSEN1 mutant neurons, directly linking BAG3 to a disease-relevant astrocyte phenotype. Finally, analysis of postmortem human brain revealed that BAG3 expression marks a stress-responsive astrocyte subtype in aged individuals. Together, these findings demonstrate that BAG3 coordinates astrocyte proteostasis through interactions with regulators of autophagy, proteasome activity, and retromer function, positioning it as a potential therapeutic target and central node of astrocytic protein quality control in neurodegeneration. - Source: PubMed
Publication date: 2026/09/28
Augur Zachary MFogo Garrett MBenoit Courtney RKearney Masin ATerzioglu GizemMurphy Zachary RArbery Mason RComandante-Lou NatachaDuong Duc MSeyfried Nicholas TDe Jager Philip LYoung-Pearse Tracy L - Intertidal burrowing bivalves, such as razor clam Sinonovacula constricta, are economically significant aquaculture species in coastal China. However, they exhibit high susceptibility to heat stress under global warming, which poses a substantial challenge to aquaculture sustainability and production. While several studies have identified genes responsive to heat stress in S. constricta, the regulatory mechanisms and core networks underlying these responses remain poorly understood. Non-coding RNAs (ncRNAs) play a crucial role in gene regulation. To investigate the function of ncRNAs and their associated regulatory networks during both heat stress and recovery, this study employed transcriptomic and miRNA transcriptomic analyses, enrichment analysis of key responsive genes, network construction, and dual-luciferase reporter assays. The results showed that, in contrast to other species, more than 7 of the top 10 most significantly responsive genes in S. constricta during heat stress were heat shock protein 70 (HSP70) genes, while the number of HSP genes sharply decreased (to 3 or 0) during recovery. Enrichment analysis revealed that protein stability and folding were critical response processes during heat stress, whereas catabolism dominated during the recovery phase. Network analysis identified Bcl-2-associated athanogene 3 (BAG3), miR-m0017-5p, and lnc9737 as the core genes, in the heat stress response. Dual-luciferase reporter assays demonstrated that lnc9737 might act as a ceRNA in the miR-m0017-5p/BAG3 axis during heat stress. This research enhances our understanding of heat stress responses in these key aquaculture species and identifies molecular targets for selective breeding to improve thermal tolerance in razor clam farming. - Source: PubMed
Publication date: 2026/09/28
Liu YouliLi WenXu HongqiangSun ChangsenLin ZhihuaDong Yinghui - According to the Global Burden of Disease Study 2023, Parkinson's disease (PD) affects an estimated 11.67 million people worldwide, a progressive neurodegenerative condition marked by the accumulation of Lewy bodies containing α-synuclein and the progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Over the past ten years, advances in genetic and molecular research have shown that PD pathogenesis involves interrelated mechanisms such as impaired protein homeostasis, mitochondrial dysfunction, oxidative stress, defects in lysosomal-autophagic pathways, and chronic neuroinflammation, which go beyond dopaminergic neuronal loss. This review summarizes new data about major genes associated with monogenic and polygenic forms of PD, including SNCA, LRRK2, PRKN, PINK1, DJ-1 (PARK7), GBA1, VPS35, ATP13A2, FBXO7, and the GWAS-prioritized risk genes TMEM175, SCARB2, CTSB, RIT2, DYRK1A, and BAG3, together with the molecular pathways disrupted by these genetic alterations in light of current evidence. The polygenic architecture of PD and ancestry-related variation in genetic risk are also discussed. α-synuclein aggregation and proteostasis networks, oxidative stress, autophagy and mitophagy failure, neuroinflammation, mitochondrial quality control, and epigenetic regulation are all given special attention. Apart from traditional dopaminergic treatments, new therapeutic approaches such as immunotherapies targeting α-synuclein, gene therapies mediated by adeno-associated virus (AAV), induced pluripotent stem cell (iPSC)-based methods, and genotype-guided precision medicine are critically examined. A more comprehensive understanding of the molecular mechanisms underlying PD is expected to facilitate the development of reliable biomarkers and accelerate the clinical translation of disease-modifying therapies. - Source: PubMed
Publication date: 2026/09/28
Yildirim Sumeyye - Mechanical stress plays a critical role in regulating cardiomyocyte structure and physiology. However, mechanobiology studies still rely on static systems that failed to capture the progressive nature of native cardiac remodeling. Building on our prior shape memory polymer (SMP)-based platform, the present study integrates microcontact printing onto SMP substrates to achieve single-cell geometric control and on-demand dynamic mechanical modulation. Using CRISPR/Cas9-engineered MYBPC3- and BAG3-mutant hiPSC-CMs along with isogenic wild-type (WT) control, we systematically assessed sarcomere organization and contractile behavior under static and dynamic mechanical conditions. WT hiPSC-CMs displayed robust morphological adaptability and coordinated sarcomere remodeling in response to dynamic mechanical cues, whereas MYBPC3- and BAG3-deficient hiPSC-CMs exhibited mutation-specific defects in sarcomere integrity and contractile behavior that were exacerbated by dynamic mechanical stress. These results demonstrate that this SMP-based platform enables us to systematically compare genotype-based mechanical sensitivity to develop more severe cardiomyopathy phenotypes. - Source: PubMed
Publication date: 2026/09/11
Wang ChenyanMai Nhu YDonelson Fred JMoradi Nasab SusanShi HuaiyuYang HuaxiaoMather Patrick TWang XinruiHenderson James HMa Zhen - Cardiovascular disease (CVD) is a result of complex pathophysiological processes affecting the heart and blood vessels. Heat shock proteins (HSPs) are evolutionarily conserved molecular chaperones that play key roles in maintaining protein homeostasis and cell survival under various stress conditions. Studies have shown the role of HSPs in diseases, including autoimmune disorders, liver, pancreatic, cancer, diabetes, and kidney disorders. Important findings regarding the role of HSPs in cardiovascular diseases include atherosclerosis, ischemic heart disease, atrial fibrillation, cardiomyopathy, heart failure, deep vein thrombosis, and peripheral vascular disease. Several proteins related to HSPs have been identified in various molecular mechanisms, including autophagy, apoptosis, oxidative stress, inflammatory responses, and fibrosis in cardiac disease. This review provides a comprehensive overview of the molecular biology and classification of HSPs, including extracellular HSPs, small HSPs, and co-chaperone molecules. We explored the roles of HSPs in regulated cell death mechanisms and in modulating oxidative stress and inflammatory responses. Furthermore, we demonstrated the pathological and protective roles of specific HSPs by regulating gene expression in response to drugs and cytokines, including geldanamycin and geranylgeranylacetone (GGA), across various cardiovascular conditions, highlighting the potential for HSP-targeted therapies. Promising strategies, including small-molecule inhibitors, inducers, and gene therapies, such as Bcl-2-associated athanogene 3 (BAG3) modulation, are discussed in the context of clinical relevance and therapeutic potential. However, despite promising experimental and clinical evidence, the translational application of HSPs remains limited by their context-dependent biological functions, the lack of standardized biomarker assays, heterogeneous clinical findings, and insufficient large-scale prospective validation. This narrative review was not prospectively registered, and received no external funding. It was conducted by searching PubMed, Scopus, Google scholar and Web of Science for relevant published articles. Understanding the multifaceted roles of HSPs offers new insights into cardiovascular disease mechanisms and paves the way for novel diagnostic and therapeutic approaches. - Source: PubMed
Publication date: 2026/08/19
Naderi NiloofarBolhassani AzamPirani Fatemeh