Ask about this productRelated genes to: BMP4 protein
- 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: BMP4 protein
Related articles to: BMP4 protein
- Birds and mammals exhibit extraordinary facial diversity, reflecting adaptations to distinct ecological niches and feeding strategies. While core face-building developmental programs are conserved and orchestrated by interactions between ectodermal organizers and the underlying mesenchyme, mechanisms driving facial shape variation remain poorly understood. Here, we integrate single-cell transcriptomic and chromatin accessibility profiling of mouse and chicken developing face to construct a comparative regulatory map. Although both ectodermal and mesenchymal populations display distinct regulatory features in each species, the mesenchyme exhibits markedly greater divergence, pointing to its central role in shaping facial morphology. We further reveal unexpected molecular complexity in the main face-shaping organizer, including a mouse-specific expression domain. At key morphogen loci (, , and ), conserved and lineage-specific enhancers exhibit spatially restricted activity patterns that mirror divergent signaling domains. These findings demonstrate how cis-regulatory evolution modulates conserved developmental programs to generate morphological novelty, providing a valuable resource for studying vertebrate facial evolution. - Source: PubMed
Publication date: 2026/05/06
Kyomen StellaSeton Louk W GCook Laura EEscamilla-Vega ElioMurillo-Rincón Andrea PJacobsen AlexanderDamatac AmorFortmann-Grote CarstenFuss JaninaVisel AxelKaucká Markéta - Bronchopulmonary dysplasia (BPD) represents the most prevalent chronic pulmonary complication in preterm infants, with incompletely understood pathophysiological mechanisms. Hyperoxia exposure constitutes a major risk factor for BPD development, inducing cellular senescence that impairs alveolar maturation. While senescence is predominantly mediated by the p53/p21 signaling pathway, upstream regulatory mechanisms remain inadequately defined. This study aimed to identify critical genes through bioinformatics and elucidate the molecular mechanisms by which the Noggin-BMP4 signaling axis mediates cellular senescence in BPD pathogenesis. Integrating BPD transcriptomic datasets with aging-related databases via WGCNA, Noggin was identified as a hub gene linking BPD and cellular senescence (AUC = 0.80). In HPMECs exposed to 85% hyperoxia, Noggin expression increased approximately 2.5-fold (mRNA) and 2.0-fold (protein), while BMP4 decreased to 50% of controls, accompanied by elevated p53 and p21 expression and positive SA-β-gal staining. Noggin silencing restored BMP4 expression and significantly attenuated hyperoxia-induced p53/p21 upregulation, suggesting that Noggin promotes senescence by suppressing BMP4. In a neonatal rat hyperoxia-induced BPD model, alveolar simplification was observed alongside a threefold increase in Noggin mRNA, a reduction of BMP4 to 30% of controls, and elevated p53/p21 at day 14, corroborating the findings. These findings suggest that hyperoxia upregulates Noggin to antagonize BMP4 signaling, thereby activating p53/p21-mediated senescence and contributing to alveolar developmental arrest. The Noggin-BMP4 axis may represent a potential therapeutic target for BPD. - Source: PubMed
Publication date: 2026/04/20
Zhang JiaxinQuan JiaLuo YifanZhang ZongliLi TaoXi Shibing - The myotendinous junction (MTJ) is the critical interface connecting muscle to tendon, enabling force transmission for movement and serving as the primary site of muscle injuries. Despite research into MTJ repair, treatment outcomes are suboptimal, partly due to the absence of a comprehensive synthesis of its structural components, cellular diversity, and developmental mechanisms, which impedes the rational selection of materials, cells, and regulatory factors for effective regeneration. This review synthesizes current knowledge on the cytoskeletal and extracellular matrix (ECM) architecture of the MTJ, the cell types involved in its development and repair, and the key molecular regulators governing its formation. We describe the hierarchical architecture of the MTJ and the key molecular complexes that mediate the mechanical connection between the muscle and the tendon. We also describe the roles of Col22a1-expressing muscle nuclei and various resident stem/progenitor cells in MTJ maintenance and healing. We discuss essential regulatory signaling pathways, including Slit, LRT, and BMP4. Furthermore, we evaluate existing MTJ repair strategies. Based on a review of MTJ development and injury repair, we observe that current treatment approaches largely fail to incorporate key insights from MTJ development, particularly regarding stem/progenitor cells and regulatory signals. Therefore, we propose that tissue engineering techniques, by integrating MTJ-resident stem/progenitor cells such as CD106CD24muscle-tendon progenitors (MTPs) and Hic1Col22a1 progenitors, key MTJ developmental regulatory signals like Slit, Lrt, and BMP4, as well as MTJ decellularized ECM scaffolds or biomimetic 3D-printed scaffolds, will substantially enhance the efficacy of MTJ repair therapies. - Source: PubMed
Publication date: 2026/04/27
Yang KunYin ZiFan Chunmei - 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
Publication date: 2026/04/30
Niu Yu-QianCai Ze-YuZhi Hao-YangZhu Yu-ChunXi Xin-YuanYang ZhenFeng Dong-Fu