Human BMP_2 ELISA kit
- Known as:
- Human BMP_2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50501
- Product Quantity:
- 1×96T
- Category:
- Peptides
- Supplier:
- Abfron
- Gene target:
- Human BMP_2 ELISA kit
Related genes to: Human BMP_2 ELISA kit
- Gene:
- BMP2 NIH gene
- Name:
- bone morphogenetic protein 2
- Previous symbol:
- BMP2A
- Synonyms:
- -
- Chromosome:
- 20p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-11
- Date modifiied:
- 2016-10-05
- 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 BMP_2 ELISA kit
Related articles to: Human BMP_2 ELISA kit
- Recent studies have shown that UFMylation plays an important role in cancer, but its specific function in gastric cancer (GC) remains to be fully elucidated. This study aimed to develop a prognostic signature based on UFMylation-related genes (URGs) for survival prediction in GC. - Source: PubMed
Publication date: 2026/07/27
Chen GuohaoGao XianDai LingchenDeng ShukangWang HaoyangHuang XinkunFeng Ying - Intervertebral disc degeneration (IVDD) is characterized by excessive inflammation and extracellular matrix (ECM) degradation in the nucleus pulposus (NP), with limited current therapeutic options. Specialized pro-resolving mediators (SPMs) such as Maresin 1 (MaR1) have emerged as key regulators of inflammation resolution and tissue repair. Here, we report that MaR1 and its receptor LGR6 are significantly downregulated in degenerated human NP tissues, suggesting a loss of endogenous resolution capacity. Exogenous MaR1 administration effectively attenuated IL-1β-induced inflammation and ECM degradation in human NP cells and alleviated IVDD progression in rat models. Mechanistically, MaR1 simultaneously suppressed the catabolic AP-1/MMP pathway and activated the pro-anabolic OSR1/GDF7 axis, rebalancing ECM homeostasis. Notably, the therapeutic efficacy of MaR1 was completely abrogated in Lgr6-knockout mice, demonstrating that LGR6 is the indispensable mediator of MaR1's protective effects in vivo. Our findings identify the MaR1-LGR6 axis as a critical regulator of disc homeostasis and highlight MaR1 supplementation as a novel and promising strategy for IVDD treatment. - Source: PubMed
Publication date: 2026/08/07
Wang HuiLi XiangyuYan TaoHe PanweiYao JunxiangWang JinhuiSu LeleWu AiminJin ShengweiWang JianguangLv Chen - House dust mite (HDM) is a major global inducer of allergic asthma, yet its epigenetic impact on airway tissues remains poorly understood. The aim of this study was to perform an exploratory, hypothesis-generating screening of the DNA methylation changes that occur in lung tissue of mice with robust allergic inflammation compared to saline-exposed controls. - Source: PubMed
Publication date: 2026/07/02
Llinás-Caballero KevinAcevedo NathalieMerid Simon KebedeDonado KarenEspinoza HectorMondol ErnestoReina RandyRegino RonaldBenedetti InésZakzuk JosefinaPuerta LeonardoMelén ErikCaraballo Luis - Glaucoma, a leading cause of irreversible blindness, is a complex polygenic disease where significant clinical and genetic heterogeneity do not explain all glaucoma cases, highlighting the need for a deeper understanding of molecular mechanisms like epigenetics. This review examines the emerging role of key epigenetic mechanisms, specifically DNA methylation, histone modifications, and non-coding RNAs in glaucoma pathogenesis and their potential as biomarkers and therapeutic targets. We discuss how aberrant DNA methylation (e.g., hypomethylation/ hypermethylation) promotes trabecular meshwork fibrosis and increases optic nerve vulnerability, contributing to disease development and/or progression. The histone methylation linked to retinal ganglion cell death at normal eye pressure, and disease-specific microRNA profiles further support the role of epigenetic involvement in glaucoma. The proof-of-concept studies of GDF7 neutralization in primate models and the OSK-factor reprogramming in aged and glaucoma mice models, show that epigenetic changes are reversible and can restore visual functions. DNA methylation-based epigenetic clocks identify glaucoma as an accelerated molecular aging process. Although promising, the current evidences are largely preclinical and long-term human data are still lacking. Nonetheless, the inherent reversible nature of epigenetics offers significant translational potential. Methylation, epigenetic clocks, and circulating microRNA profiles could enable early, non-invasive biomarkers for diagnosis and prognosis. Future efforts are needed to validate biomarkers in large cohorts and develop targeted epigenetic therapies. In conclusion, epigenetics is redefining our current understanding of glaucoma from a pressure-based disease to a modifiable link between genes and environment paving the way for personalized care for vision preservation beyond pressure-lowering treatments. - Source: PubMed
Publication date: 2026/02/23
Kondkar Altaf ASultan TahiraAzad Taif AAl-Obeidan Saleh A - Non-syndromic cleft lip with or without cleft palate (ns-CL/P) is one of the most common craniofacial anomalies with a multifactorial etiology. To investigate the contribution of rare variants to disease risk, we performed whole-exome sequencing (WES) in 58 patients with ns-CL/P from a homogeneous Polish population, excluding from analysis 423 previously investigated cleft candidate genes. After stringent filtering, prioritization, and segregation analysis, we identified 31 likely pathogenic (LP) variants across 30 genes, significantly enriched in categories related to developmental processes. Notably, 29% of variants occurred in genes not previously linked to clefting, including , , , , , , , , and . Three were de novo: FOXA2_p.Arg260Pro, MAML1_p.Gln65Ter, and ZNF319_p.Gln64Ter. Most of the remaining variants were inherited from unaffected parents, suggesting incomplete penetrance and possible modifier effects consistent with the heterogeneous etiology of ns-CL/P. Additionally, analysis of common variants in the 30 loci harboring rare LP variants revealed nominal associations with ns-CL/P for , , , and loci. These results support the candidacy of these genes and suggest contributions from both rare and common variants. In conclusion, we report novel LP variants expanding the spectrum of candidate genes and providing new insights into the genetic landscape of orofacial clefts. - Source: PubMed
Publication date: 2025/12/16
Biedziak BarbaraDąbrowska JustynaBogdanowicz AgnieszkaKarbowska KarolinaMostowska Adrianna