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
- In Alzheimer's disease (AD), senescent astrocytes fuel neuroinflammation and neuronal damage via the senescence-associated secretory phenotype (SASP). Calcium signaling plays a crucial role in this process, but the underlying molecular mechanisms remain elusive. We retrieved scRNA-seq data from the Gene Expression Omnibus (GEO) for AD and control brains. After cell-type annotation, we resolved astrocyte sub-clusters. Pseudotime trajectory and differential-expression analyses identified SORBS1 as a key senescence-related gene, which we followed with gene-set enrichment analysis. Next, we established an in vitro AD model by treating astrocytes with amyloid-β (Aβ). We evaluated astrocyte senescence using SA-β-gal staining, qRT-PCR, Western blot (WB) for senescence markers, and ELISA for SASP cytokines. We measured concentration of Ca with Fluo-4 AM probes. Subsequently, bioinformatic screening predicted FBXO22 as an interactor of SORBS1 and BAG3 as a ubiquitination substrate of FBXO22. We validated these interactions using Co-IP and in vitro ubiquitination assays. Finally, we constructed an astrocyte-neuron co-culture model. We detected neuronal cell viability, AChE activity, AD phenotype-related protein expression, apoptosis, and levels of inflammatory factors using MTT assay, specific kits, WB, flow cytometry, and ELISA, respectively, to assess neuronal damage. ScRNA-seq analysis revealed a marked reduction in astrocyte expression in AD brains, which may result from cellular senescence. The SASP gene SORBS1 was selectively up-regulated in astrocytes and significantly enriched in calcium-signaling pathways. Functional assays confirmed that SORBS1 accelerated astrocyte senescence. Mechanistically, SORBS1 interacted with FBXO22 to promote the ubiquitin-dependent degradation of BAG3, thereby amplifying calcium signaling, accelerating astrocyte senescence, and contributing to AD-related neuronal damage. We uncover a novel mechanism by which the SORBS1/FBXO22/BAG3 axis drives astrocyte senescence through the regulation of calcium signaling, thereby influencing AD-related neuronal damage. This finding provides a potential therapeutic target for AD treatment by targeting astrocyte senescence. - Source: PubMed
Publication date: 2026/06/17
Li YanHe Xindong - Ischemia-reperfusion injury (IRI) significantly impacts post-kidney transplantation (KTx), leading to delayed graft function (DGF) and potential graft loss. Current biomarkers and therapies for DGF and graft survival are inadequate. Immune cell infiltration after renal IRI is crucial in driving inflammation and injury. - Source: PubMed
Zhang YifeiLi YuqingQiu XuemengWu JiyueBi QingCao PengZhang JiandongWang Wei - Metastatic dissemination remains a major cause of mortality in colorectal cancer (CRC), yet the transcriptional basis of epithelial plasticity is not fully understood. Here, we identified Forkhead Box P4 (FOXP4) as a transcription factor associated with CRC progression. Integrated analyses across multiple patient cohorts, together with single-cell transcriptomic data, showed that FOXP4 is preferentially upregulated in malignant epithelial cells and is associated with poor patient survival. FOXP4 depletion impaired malignant phenotypes in vitro and reduced tumor growth, angiogenesis, and liver metastatic burden in vivo. Mechanistically, FOXP4 bound to the promoter region of the co-chaperone BAG3 and regulated its transcription. Consistent with this, BAG3 restoration or silencing partially reversed the phenotypic changes induced by FOXP4 perturbation. These findings suggest that FOXP4 promotes EMT-associated cellular plasticity, at least in part, through BAG3. Together, these results support a FOXP4-BAG3 regulatory axis linked to EMT-related transcriptional programs in CRC. This study provides additional insight into the molecular basis of epithelial plasticity in CRC and supports further investigation of this pathway. - Source: PubMed
Publication date: 2026/06/11
Wang JiayunYu TengLiu LinHui KaiyuanYuan ChunluanYu ZienWang YilinLi XiumingShen XiaozhuJiang XiaodongLiu Bin - Tumor-associated macrophages (TAMs) are key components of the hepatocellular carcinoma (HCC) microenvironment, but their spatial heterogeneity remains incompletely characterized. We aimed to assess the biological and prognostic relevance of a -associated TAM program in HCC. Public single-cell RNA sequencing (scRNA-seq) datasets were analyzed to characterize TAM heterogeneity, and an integrated validation scRNA-seq dataset was used to assess reproducibility. Spatial transcriptomics was used to provide spatial context in a small treatment-exposed cohort. Pseudotime, regulatory network, and cell-cell communication analyses were performed to characterize state transitions and microenvironmental interactions. Survival modeling evaluated the prognostic relevance of the -associated program. Five TAM subsets were identified, including MARCO, MT RTM-, MMP9, UBE2C, and BAG3 TAMs. Among them, BAG3 TAMs, a less well-characterized subset, exhibited coordinated stress-adaptive, proteostasis-related, and matrix-remodeling programs that were reproduced in the validation dataset. Pseudotime analysis suggested a continuum of TAM states, with BAG3 TAM stress-remodeling features enriched toward late pseudotime. Communication analysis centered on BAG3 TAMs suggested crosstalk between inflammatory stress cues and angiogenic, stromal-remodeling, and immunomodulatory programs; this pattern was primarily supported by HBV-derived samples and recurrently involved the MIF-CD74 axis. Spatial mapping further supported BAG3 TAM-enriched niches with elevated AP-1, EGR1, and NFKB1 activity. A -associated risk score derived from a 10-gene signature remained an independent prognostic factor for overall survival after clinical adjustment. These findings characterize a -associated TAM program with spatial, immunoregulatory, and prognostic relevance in HCC, and support its further evaluation in biomarker and mechanistic studies. - Source: PubMed
Publication date: 2026/05/11
Zhang RuixiangWei YifangYu JundaLi YuanshengYou ZumingXie ChenxiXu SiqiZhou Jiyuan - More than 360,000 Americans experience sudden cardiac arrest (SCA) annually. A subgroup is caused by rare genetic variants, but existing studies are not population based and have been limited to nonsurvivors. - Source: PubMed
Publication date: 2026/04/06
Kransdorf Evan PMathias MarcoNakamura KotokaChugh HarpriyaNguyen DavidTyrer JonathanPharoah Paul DReinier KyndaronAkdemir ZeynepBoerwinkle EricYu BingChugh Sumeet S