Ask about this productRelated genes to: BMP7 antibody
- Gene:
- BMP7 NIH gene
- Name:
- bone morphogenetic protein 7
- Previous symbol:
- -
- Synonyms:
- OP-1
- Chromosome:
- 20q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-05
- Date modifiied:
- 2016-10-05
Related products to: BMP7 antibody
Related articles to: BMP7 antibody
- Extended periods of skeletal unloading cause rapid and severe bone loss, structural weakening, and increased fragility. Unlike postmenopausal osteoporosis, disuse bone atrophy is only partially responsive to pharmacological treatments, making it a critical and unresolved medical challenge in both space- and Earth-based medicine. Here, we investigate and assess the dose-response to P7C3 during the transition of bone-derived mesenchymal stem cells to osteoblasts and adipocytes, and its effect during human preosteoclast differentiation into mature osteoclasts in vitro. We further evaluate the in vivo protective properties of P7C3 against pathological bone atrophy induced by mechanical disuse. Data demonstrates that multifunctional P7C3 selectively promoted osteogenesis while inhibiting osteoclast maturation and activity. Proteomic analyses indicate osteogenic augmentation via ↑FSTL-1 and ↓IL-10Rβ, adipogenic inhibition via ↓ADIPOQ and ↑NAMPT, and osteoclastic inhibition via ↓OPN, ↑BMP-7 and ↑OPG. Enrichment analyses suggest the positive regulation of MAPK, JAK/STAT, and Wnt signaling pathways. Transcriptomic data reveal P7C3-induced cell-selective alterations in transcriptional programs within mitochondrial DNA, potentially promoting ATP generation through NADH activity, and regulating cellular energy metabolism. Hindlimb suspension (HLS) induced rapid pathologic bone loss in vivo, with an overarching drive towards adipogenesis (↑C4.A4, ↑FABP3, ↑ADIPOQ, and ↓Dcn) over osteogenesis (↑activin R2A, ↑LIFR and ↓STAT3) and augmented osteoclastic activity and cellular senescence, potentially via MAPK, JAK/STAT, and Wnt signaling. Despite HLS, P7C3 attenuated oxidative stress, RANKL, osteoclastic activity, bone marrow adiposity, cellular senescence, and pathological bone loss. P7C3 presents as an undiscovered and promising multi-target therapeutic strategy against disuse-induced bone atrophy for both space- and Earth-based applications. - Source: PubMed
Publication date: 2026/10/03
Wei FeiNgo ChristopherNeal Craig JSchwartzman Jonathan DPugazhendhi Abinaya SinduOmer MahmoudWalck Christine DSeal SudiptaCoathup Melanie J - [This corrects the article DOI: 10.3389/fcell.2026.1914540.]. - Source: PubMed
Publication date: 2026/09/17
Li FengXu XingHu Yi-QiuZhang Cheng-PengShen Yi-WeiGeng ChiChu Jia-PengBai Hui-YuGu Xiao-SongLi Hui - Sclerostin (SOST) is a secreted glycoprotein that antagonizes Wnt and BMP signaling, however, the molecular mechanisms regulating its extracellular distribution and growth factor (GF) interactions remain poorly understood. Here, we identify fibrillin microfibrils as high-affinity extracellular binding partners of SOST. Recombinant SOST bound specifically to fibrillin-1 positive fibers in cell culture and localized near the bead region of purified tissue fibrillin microfibrils. Surface plasmon resonance (SPR) mapping revealed that SOST recognizes the N-terminal regions of fibrillin-1 and fibrillin-2 with nanomolar affinity, and deletion analysis identified the fibrillin-unique N-terminal (FUN) domain as the primary SOST binding site. Our findings further extend the SOST binding repertoire to include BMP-10 GF, as well as the prodomains (PDs) and PD-GF complexes (CPLXs) of BMP-7 and BMP-10. Heparin interfered with SOST binding to BMP-7 PDs and CPLXs but not with the SOST-fibrillin-1 interaction. SPR interaction experiments showed that SOST binding to fibrillin-1 occludes the BMP PD targeting site and that fibrillin-1-bound SOST is unable to engage BMP-7 PDs. Molecular docking further supported this competitive mechanism by revealing overlapping interaction interfaces among SOST, BMP-7 CPLX, and fibrillin-1. Together, these findings establish SOST as a multifunctional ECM-associated BMP modulator that links fibrillin microfibril scaffolds to the fine-tuning of BMP and Wnt signaling. - Source: PubMed
Publication date: 2026/09/29
Correns AnnkatrinMarcous FadyLütke SteffenMörgelin MatthiasBarnowski PhilippFurlan Ariane GSchröder Nathalie HLevkau BodoRiek SarahMollenhauer MartinKoch ManuelSengle Gerhard - : Prostate cancer (PCa) is a leading cause of cancer-related mortality worldwide, highlighting the need for improved prognostic tools. The integration of artificial intelligence (AI) and machine learning (ML) with multi-omics data offers new opportunities for biomarker discovery and risk stratification. : We integrated bulk transcriptomic data from GSE116918 (training, = 248) and three cross-cohort consistency evaluation cohorts (TCGA-PRAD, GSE70769, GSE46602), focusing on 1087 epithelial-mesenchymal transition (EMT)-associated genes. Using consensus clustering, weighted gene co-expression network analysis (WGCNA), and 91 machine learning algorithm combinations (including Random Forest, Lasso, and CoxBoost), we constructed a prognostic signature. SHAP analysis was used for model interpretability. Single-cell RNA sequencing (scRNA-seq, GSE268307, 10,672 cells) and spatial transcriptomics (10× Genomics Visium FFPE) provided hypothesis-generating evidence; spatial analysis was based on one tissue section. : A three-gene signature (INHBA, FAP, ITGBL1) effectively stratified patients into high- and low-risk groups, with the high-risk group showing significantly worse metastasis-free survival (HR = 1.61, 95% CI: 1.39-1.87; 4-year AUC = 0.93 in the training cohort; external AUCs ranged from 0.62 to 0.77). CytoTRACE inferred high differentiation potential of COMP+ fibroblasts, and Monocle3 inferred a transcriptional transition from COMP+ toward NELL2+ fibroblasts. BayesPrism deconvolution suggested that high inferred COMP+ fibroblast abundance was associated with poor prognosis and advanced T stage. NicheNet analysis prioritized BMP7 as a key upstream ligand, with downstream targets enriched in TGF-β signaling and stem cell pluripotency pathways. : This study presents a machine learning-based multi-omics framework for prostate cancer risk stratification. The three-gene signature provides a new exploratory prognostic model while inferring a COMP+ to NELL2+ transcriptional transition. These findings may inform future hypothesis-driven studies of treatment sensitivity, pending experimental validation, and demonstrate the value of AI-driven multi-omics integration for precision oncology. - Source: PubMed
Publication date: 2026/08/27
Zhang XueqianZhang WeiWang ZhengShi XinyangZhang ChenghaoGao YanDeng YihengShen TianyuAn ZiyanFu Weijun - Craniosynostosis, resulting from the premature fusion of one or more cranial sutures, often requires invasive surgery for treatment. Currently, the spatiotemporal regulation of calvarial ossification during suture development is largely focused on cellular and molecular patterns. Using physicochemical imaging and nanomechanical mapping, we identified a unidirectional osteo-periosteal interface characterized by calcium phosphate deposition gradient during early postnatal calvarial development. Lineage tracing and dynamic bone formation assays revealed that Mmp13-positive osteoprogenitors, derived from Erg-expressing suture mesenchyme, establish this osteo-periosteal interface and drive asymmetric calvarial osteogenesis in mice. In the Twist1 craniosynostosis model, mineralization patterns initially resembled those of wild-type mice; however, misregulation of the PAK1/MMP13/BMP7 signaling cascade at the dura side triggered bilateral mineralization within the coronal suture, ultimately leading to bone fusion. Importantly, early localized inhibition of MMP13 overactivation, achieved by applying CL-82198 (a small-molecule MMP13 inhibitor) in a thin 20% gelatin methacryloyl (GelMA) hydrogel-based 'Suture Patch', preserved coronal suture patency in Twist1 mutants via a minimally invasive surgical procedure. Our work identifies a unilateral osteo-periosteal interface that is critical for coronal suture patency, reveals the regulatory role of non-cellular components in calvaria development, and proposes a minimally invasive strategy to preserve asymmetric osteogenesis in cranial sutures for the treatment of craniosynostosis. STATEMENT OF SIGNIFICANCE: Craniosynostosis is a premature skull suture fusion that currently requires invasive surgery. We discover a unidirectional mineralization gradient driven by Mmp13 osteoprogenitors. In a craniosynostosis model, this asymmetric process becomes bilateral and pathological. Leveraging this insight, we engineer a 200-μm hydrogel "Suture Patch" that delivers a small-molecule Mmp13 inhibitor locally. A single application in newborn mice preserves suture patency in 80% of treated animals, corrects skull deformity, and restores progenitor pools-without surgery. Our work integrates advanced materials characterization, single-cell biology, and translational bioengineering to provide both a fundamental revision of suture development and a practical, minimally invasive biomaterial therapy for the debilitating pediatric disorder. - Source: PubMed
Publication date: 2026/09/24
Meng HongxuWang XinyiWu BoxuanJiang YingqiDong YuningZhang TianyiChen BingqianLi HanzhangChen TaozehanLi WenyueWang XiaozhaoLan XinZhao TianruiHu HuanHuang WenwenGavara NúriaOuyang HongweiYuan Yuan