Polyclonal Rabbit BMP4 Antibody
- Known as:
- Polyclonal Rabbit BMP4 Antibody
- Catalog number:
- abx000714
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Polyclonal Rabbit BMP4 Antibody
Ask about this productRelated genes to: Polyclonal Rabbit BMP4 Antibody
- Gene:
- BMP4 NIH gene
- Name:
- bone morphogenetic protein 4
- Previous symbol:
- BMP2B
- Synonyms:
- -
- Chromosome:
- 14q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-11
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit BMP4 Antibody
Related articles to: Polyclonal Rabbit BMP4 Antibody
- This study elucidates a novel intercellular communication mechanism underlying radiotherapy resistance in cervical cancer, focusing on the functional role of cancer-associated fibroblast-derived exosomes (CAF-Exo) in modulating redox homeostasis and cell death pathways. We demonstrate that CAF-Exo serve as critical vehicles for transferring radioresistant phenotypes to tumor cells through coordinated regulation of antioxidant defense systems and copper-dependent cell death processes. Our findings reveal that CAF-Exo activate the Nrf2-HO-1 signaling axis while simultaneously suppressing key cuproptosis regulators, establishing a dual-pathway mechanism for treatment resistance. Bone morphogenetic protein 4 (BMP4) was identified as the essential molecular cargo within these exosomes, functioning as a master regulator of this protective cellular response. The pathological significance of this pathway was confirmed through comprehensive functional assays showing that BMP4 knockdown effectively restored radiosensitivity in vitro and significantly enhanced radiotherapy efficacy in vivo. These results uncover a previously unrecognized biological axis wherein tumor-stroma interactions mediated by exosomal BMP4 orchestrate a sophisticated defense mechanism against radiotherapy-induced stress. This study elucidates key molecular mechanisms underlying treatment resistance and highlights potential therapeutic targets for cervical cancer, offering a basis for future intervention strategies. - Source: PubMed
Chi ChiXu MindanZhang JieZhang YiHan GuorongLi Min - Ischemic stroke poses a substantial clinical and socioeconomic burden due to limited therapeutic efficacy and poor neurological outcomes. To uncover novel gene targets for intervention, we conducted an integrative analysis combining single-cell RNA sequencing with Mendelian randomization using large-scale genomic datasets from the European Bioinformatics Institute (34,593 cases and 624,214 controls), with validation in an independent European Bioinformatics Institute dataset (86,668 cases and 1,503,898 controls) and the UK Biobank (26,052 cases and 487,214 controls). Colocalization analysis identified four core genes-PEBP1, BMP4, APOA1 and CD86-strongly associated with ischemic stroke risk, with a posterior probability of a shared causal variant greater than 0.8. Among them, PEBP1 was markedly upregulated post-ischemia, particularly in endothelial cells, as confirmed by quantitative PCR and immunofluorescence in a middle cerebral artery occlusion model. Both pharmacological inhibition of PEBP1 with FerroLOXIN-1 and AAV-BI30-mediated shRNA knockdown reduced cerebral infarct volume, enhanced neuronal survival, and improved neurological functional recovery. In vitro, FerroLOXIN-1 enhanced cell proliferation and viability under oxygen-glucose deprivation conditions, with potential off-target effects of the interventions validated. Mechanistically, these effects were mediated through activation of the Akt/p38 MAPK signaling cascade. These findings highlight PEBP1 as a central mediator of ischemia-induced neuronal injury and a potential therapeutic target. The convergence of transcriptomic, genetic and experimental validation supports the translational relevance of PEBP1 inhibition in post-stroke neuroregeneration. - Source: PubMed
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Niu Yu-QianCai Ze-YuZhi Hao-YangZhu Yu-ChunXi Xin-YuanYang ZhenFeng Dong-Fu - Erythroferrone (ERFE), secreted by erythroblasts, is regarded as a classical regulator of iron metabolism through its suppression of hepcidin. Thus, as a consequence of insufficient hepcidin suppression and reduced iron availability, global mice exhibit delayed recovery after phlebotomy. We have shown previously that, apart from erythroblasts, ERFE is notably expressed in osteoblasts. To explore the effect specifically of osteoblast-derived ERFE during stress erythropoiesis, we first created mice, which were then crossed with -Cre mice to generate osteoblast-selective mutants (or -Cre; mice). The induction of stress erythropoiesis in these latter mice by phlebotomy resulted in reduced serum ERFE levels and increased liver (hepcidin) expression. Importantly, -Cre; mice showed a more robust red blood cell (RBC) recovery 6 d postphlebotomy, with no differences in bone marrow relative to mice. Furthermore, despite no differences in the baseline RBC count, reticulocyte count, spleen size, or bone marrow cellularity, osteoblast-selective ERFE loss resulted in enhanced erythropoietin receptor () and bone morphogenetic protein 4 () expression in whole bone in vivo and in osteoblasts ex vivo. Finally, the osteoblast-selective mutants showed erythroid lineage proliferation and enhanced EPO responsiveness in a BMP4-dependent manner. Taken together, we posit that ERFE loss specifically from osteoblasts enhances RBC recovery during stress erythropoiesis-defining mechanisms of regulation in the crosstalk between osteoblasts and erythroblasts. - Source: PubMed
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