Human Bone Morphogenetic Protein 4 ELISA , BMP4
- Known as:
- Human Bone Morphogenetic Protein 4 Enzyme-linked immunosorbent assay test , BMP4
- Catalog number:
- E01B0543
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Bone Morphogenetic Protein 4 ELISA BMP4
Related genes to: Human Bone Morphogenetic Protein 4 ELISA , BMP4
- 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: Human Bone Morphogenetic Protein 4 ELISA , BMP4
Related articles to: Human Bone Morphogenetic Protein 4 ELISA , BMP4
- Keloid is a refractory fibroproliferative skin disorder with unclear molecular pathogenesis. Here, we delineated FOXM1's role in regulating BMP4/Smad1/5/8 signaling and keloid fibroblast (KF) behavior via integrated bioinformatics and experiments. Bioinformatics analysis of GSE145725 identified differentially expressed genes and co-expression modules. PPI network analysis and module-trait correlation pinpointed BMP4 as a central hub gene. KnockTF 2.0 prediction and luciferase assays confirmed FOXM1 directly binds BMP4 promoter sites to repress its transcription. In vitro assays showed BMP4 overexpression inhibited KF proliferation, migration, and extracellular matrix synthesis by activating Smad1/5/8 phosphorylation. FOXM1 overexpression abrogated these effects via reduced Smad1/5/8 phosphorylation, which was validated by functional rescue experiments. In summary, our findings unravel a novel FOXM1-BMP4-Smad1/5/8 regulatory circuitry in keloid pathogenesis, providing new mechanistic insights and highlighting FOXM1 as a promising therapeutic target for this recalcitrant disorder. - Source: PubMed
Publication date: 2026/05/14
Zhang LuyangLiu AnzhuXue YiJi YiWang GedunSun LetianShi Ting - The dermal papilla (DP) is essential to hair follicle development and regeneration. Isolation of human DPs still largely depends on manual microdissection and human DP cells (DPCs) lose their intrinsic properties in vitro. Establishing a culture condition that maintains the biological properties of DPCs allows for identification of cell surface markers that enable cell sorting of living human DPCs. A new DPC culture condition was developed using the combination of a WNT activator, CHIR99021, and recombinant FGF9 (CH + F9). Global gene expression profiling and bioinformatic analyses of DPCs grown under this condition were conducted to identify DPC surface markers enabling live DPC isolation. Compared to a conventional culture condition, CH + F9 increased the expression of the representative DPC biomarkers WNT5A, LEF1 and BMP4 by 3.4-, 3.8- and 60.5-fold (p < 0.01) and better maintained their expression levels after long-term serial passaging. Aggregated CH + F9-treated DPCs unevenly upregulated DP biomarkers further, suggesting that highly potent DPCs can be enriched using a marker for such cells. Bioinformatics analysis of CH + F9-treated and control DPCs identified cell marker candidates, including roundabout guidance receptor 2 (ROBO2). Importantly, ROBO2 DPCs expressing the representative DP biomarkers WNT5A, VCAN, NOG were successfully sorted from mixed cell suspensions of keratinocytes, fibroblasts and DPCs mimicking enzymatically dissociated human skin. These findings suggest that the new culture condition and cell surface marker for human DPCs established in this study provide useful tools for drug discovery and regenerative medicine to address hair loss diseases. - Source: PubMed
Hayakawa ReinaTakahashi RyoFukuyama MasahiroTsukashima AkiKimishima MomokoYamazaki YoshimiOhyama Manabu - The salmon trout or rainbow trout (Oncorhynchus mykiss) is a teleost fish are characterized by the presence of lingual teeth. The objective of this study is to investigate their development, particularly in relation to the expression of genes associated with mammalian odontogenesis. Sixty fry were reared in a freshwater aquarium at 7°C. Specimens at developmental stages ranging from D0 (hatching) to D35 were collected and subjected to histological (Masson's trichrome) and immunohistochemical analysis, including the expression of proteins associated with the Pitx2, Shh, MSX1, Pax9, Bmp4 and β-catenin genes. The developmental patterns of the lingual teeth are similar to those of the maxillary and mandibular teeth. These are not giant papillae or pseudoteeth. The initiator gene Pitx2 is expressed in the epithelium during early stages but subsequently diminishes. Bmp4, Shh and β-Cat exhibit a pattern similar to that of mammals, except for the absence of the enamel node. Surprisingly, however, we observe expression of Msx1 and Pax9 in the dental mesenchyme as well as in the epithelium, a phenomenon unknown in mammals. The second week marks an increase in the expression of these two proteins and of Shh, while Bmp4 does not appear in large quantities until 10 days. Incidentally, the mucous glands (cement glands) express Shh, Pitx2, Msx1, Pax9 and β-catenin. In conclusion, tongue teeth are 'classical' teeth; their gene expression patterns are similar to those in mammals, except that Msx1 and Pax9 are expressed in both epithelial and mesenchymal tissues in this species. - Source: PubMed
Louryan StéphaneDuterre MyriamVanmuylder Nathalie - Corneal neovascularization (CNV) and corneal lymphangiogenesis (CL) disrupt corneal immune privilege after injury and drive transplant rejection. This study investigated how the bone morphogenetic protein 4 (BMP4)-Smad pathway regulates both vascular arms of the corneal wound response. Bioinformatic analysis of a rat corneal suture-injury dataset showed that sustained injury induced a coordinated inflammatory, angiogenic, lymphangiogenic, and BMP/TGFβ-Smad transcriptional program, with predicted SMAD5-binding motifs in vascular- and lymphatic-related gene promoters. In vitro, BMP4 inhibited the proliferation and migration of human umbilical vein endothelial cells (HUVEC) and human lymphatic endothelial cells (HLEC) and downregulated CD31, VEGFA, LYVE-1, and VEGFC, whereas the BMP antagonist Noggin reversed these effects. BMP4 increased phosphorylated Smad1/5/8 (p-Smad1/5/8) and promoted its nuclear translocation, confirming canonical pathway activation. In a rat corneal suture model, BMP4 reduced inflammatory-cell infiltration and suppressed CNV and CL, as demonstrated by slit-lamp examination, lineage-resolved CD31/CD45 and LYVE-1/Prox1 co-staining, transmission electron microscopy, and molecular assays; Noggin antagonized each effect. BMP4 further activated corneal p-Smad1/5/8 signaling and induced endogenous BMP4 expression in a Noggin-sensitive manner, suggesting a self-amplifying loop. Together, these findings indicate that BMP4 coordinately restrains the vascular and lymphatic arms of the corneal immune response through canonical BMP4-Smad1/5/8 signaling and may help preserve corneal immune privilege during injury repair. - Source: PubMed
Publication date: 2026/06/11
Guo YuxiaoNiu YanZhu QiHe RuoyunYang QingJin ZhaoHe Yuxi - Activation of Estrogen receptors (ER) signaling in adult male rats leads to sub-fertility, and whole genome bisulfite sequencing revealed large-scale genome-wide changes in sperm DNA methylation. In this study, we further probed the developmental consequences of altered sperm methylome. An enrichment map analysis of the differentially methylated genes revealed that clusters related to embryo development and its regulation were most enriched. Genes differentially methylated in sperm and implicated in embryo development were selected for validation in sperm by pyrosequencing. DNA methylation and expression levels of these developmental genes were evaluated in resorbed and normal embryos and placental tissues. The aberrant sperm DNA methylation pattern in developmental genes Cdkn1c, Tgfb1, Bmp4, Gab1, Peg3, Myc, Wt1, Sfmbt2, Sox5 and Hoxa3 was reflected in that of the resorbed embryos, along with their deregulated expression after paternal ER agonist treatment. Whereas, the methylation pattern and expression in normal embryos and placenta for most genes were comparable to those of the controls. Additionally, several key developmental pathways, including MAPK, Tgfβ, Wnt, Notch, Hedgehog, and Scf-cKit signaling, were also found to be affected in resorbed embryos sired by ERα agonist-treated male rats. The results indicate that activation of estrogen signaling during spermatogenesis causes aberrant sperm DNA methylation in developmental genes. These defects could be transmitted to embryos, altering the expression of these genes and pathways and thereby impeding embryonic development and reducing litter size and subfertility. The study provides a mechanism by which ERs epigenetically regulate male fertility and subsequent embryogenesis. - Source: PubMed
Publication date: 2026/06/11
Khambata KushaanRaut SanketaBalasinor Nafisa H