BMP4 ELISA kit
- Known as:
- BMP4 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-BMP4-Rb
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- BMP4 ELISA kit
Related genes to: BMP4 ELISA kit
- 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
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- Dioscorea polystachya Turcz. (Chinese yam) is a Traditional Chinese Medicine with a documented history of over 2000 years for nourishing kidney essence and supporting male reproductive health. Despite its broad ethnomedical applications, it has not been comprehensively studied for its efficacy in delaying reproductive aging. - Source: PubMed
Publication date: 2026/08/13
Zhang YiwenFeng JiabaoXie TongdeZhang XinyuePan DaianLiu ShichaoZhao DaqingWang SimingLiu MeichenYu Shiting - Prompted by a fetus with a homozygous pathogenic variant and persistent open eyelids on sonography, suggesting fusion failure, this study marks the first prenatal human description linking to eyelid closure, mirroring waved with open eyelids 2(woe2) and waved 3 (wa3) mouse models. Eyelid morphogenesis involves complex epidermal-dermal interactions. We reviewed the literature to understand embryonic/fetal development and identify molecular pathways crucial for proper eyelid morphology. Known signaling pathways in eyelid closure and reopening include NF-κB, p53, Wnt, TGF-β, BMP4, MAPK, SMAD, ECM-receptor interaction, and integrin signaling. Open-eye phenotypes are associated with pathogenic variants affecting the Wnt/β-catenin pathway, p63, and the TGFβ family. Notably, SMAD molecules are common to all these pathways. Eyelid closure seems regulated by SMAD protein activation in the supraorbital epithelium and underlying mesenchyme, promoting cell proliferation and adhesion. Physiological SMAD1 downregulation is crucial for eyelid reopening. Given SMAD signaling's importance in development, its disruption likely impacts eyelid closure or reopening. - Source: PubMed
Publication date: 2026/08/04
Shalata ZaherMintz HilaHaddad SamiOsman KhaledMahroum MohammadHadid YarinShalata Adel - Liver sinusoidal endothelial cells (LSECs) regulate nutrient flux and immune surveillance within the hepatic niche, yet how they function as metabolic stress sensors that instruct adaptive immune remodeling during metabolic dysfunction-associated steatotic liver disease (MASLD) remains unclear. Here, single-nucleus transcriptomics of human MASLD reveals stage-dependent activation of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling in LSEC comparable to that in macrophage, with endothelial activation showing greater responsiveness to metabolic stress. Endothelial-specific STING deletion attenuates steatohepatitis and fibrosis in mice. Mechanistically, LSEC-intrinsic STING activation reprograms the angiocrine landscape through NF-κB-mediated transcriptional repression of the endothelial-derived factor BMP4. Loss of BMP4 disrupts the tolerance-supporting sinusoidal immunometabolic niche, skewing CD4⁺ T cell differentiation toward pathogenic Th17 states while destabilizing Treg, collectively exacerbating hepatic metabolic failure. In human MASLD, endothelial STING activity inversely correlates with BMP4 expression at single-cell resolution. Targeted delivery of a STING inhibitor to LSECs using peptide-functionalized nanoparticles restores hepatic metabolic-immune balance at one-tenth the systemic dose. Together, these findings establish endothelial STING as a metabolically responsive vascular immune checkpoint that links chronic metabolic stress to adaptive immune remodeling and fibrotic progression. - Source: PubMed
Publication date: 2026/08/06
Lin Zhi-BinZou PengMa Xian-YiSong Jun-BoZhang HongDu WeiWei DanSong PingHong XinLiu JingjingFang Zhi-QiangXu HaoHe FeiDuan Juan-LiDou Ke-FengWang Lin - Trachea is a wide tube with smooth luminal epithelia that enables efficient ventilation. In this study, we provide the evidence that the mitotic angles of most tracheal epithelial cells exhibit ordered and transverse orientations, which allows the tracheal lumen to grow along the anterior-posterior (AP) axis, with its circumference being higher than length. We show that the BMP4 signaling antagonist follistatin-like 1 (Fstl1) is a critical regulator for tracheal morphogenesis. Mice with deletion exhibit wider trachea with enlarged lumen as a result of the increased proportion of mitotic cells with their spindles nearly vertical to the tracheal longitudinal axis. Mechanistically, Fstl1 regulates BMP4 signaling by antagonizing -Smad1/5/8 in tracheal epithelial cells. Reducing BMP4 signaling activity rescues lumen enlargement and normalizes the spindle angle distribution in -deficient tracheas. Therefore, we provide evidence to demonstrate that Fstl1 modulates the oriented cell division and tracheal morphogenesis, in part, through BMP4 signaling. - Source: PubMed
Publication date: 2026/07/30
Jin YueyueZhang YueLiu YingyingYao MaolinZhang ChenjieLi ShuziDing YiboNiu ZhuanHan YueGeng YanLi LianLiu XueNing Wen - The current evidence suggests that the formation of pulp stones (PS) has a genetic background. Therefore, the present study aimed to evaluate the association between PS in orthodontically treated patients and single nucleotide polymorphisms (SNPs) in the mineralization-related genes ( [, , , and [). - Source: PubMed
Publication date: 2026/08/06
Hemming Danielde Mattos de Araujo Bianca MarquesKirschneck ChristianScariot RafaelaPerin Camila PaivaSousa-Neto Manoel DFonseca-Souza GabrielaMattos Natanael Henrique RibeiroMeger Michelle NascimentoBaratto-Filho FlaresKüchler Erika Calvano