BMP_2
- Known as:
- BMP_2
- Catalog number:
- ANT-183
- Product Quantity:
- 100µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- BMP_2
Related genes to: BMP_2
- 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: BMP_2
A-hum bone morphogen (BMP) moALK3 (BMP R1A) Anti-Human Host: Mouse ALK3; SKR5; CD292; ACVRLK3; 10q23del, bone morphogenetic protein receptor, type IAALK3 (BMP R1A), Host: Mouse, Species: Anti-Human, Synonyms: ALK3; SKR5; CD292; ACVRLK3; 10q23del, bone morphogenetic protein receptor, type IAALK6 (BMP R1B) Anti-Human Host: Mouse BMPR1B; ALK6; ALK-6; CDw293ALK6 (BMP R1B), Host: Mouse, Species: Anti-Human, Synonyms: BMPR1B; ALK6; ALK-6; CDw293Anti- Bone Morphogenetic Protein-2 4 (BMP-2 4) AntibodyAnti- Bone Morphogenetic Protein-2/4 (BMP-2/4) AntibodyAnti-BMP-1 (Bone Morphogenic Protein-1, ProCollagen C-endopeptidase, PCP, mTld); Aminoterminal end AntibodyAnti-BMP-1 (Bone Morphogenic Protein-1, ProCollagen C-endopeptidase, PCP, mTld); Carboxyterminal end long form AntibodyAnti-BMP-1 (Bone Morphogenic Protein-1, ProCollagen C-endopeptidase, PCP, mTld); CUB-2 domain AntibodyAnti-BMP-1 Bone Morphogenic Protein-1 ProCollagen C-endopeptidase PCP mTld; Aminoterminal end antibodyAnti-BMP-1 Bone Morphogenic Protein-1 ProCollagen C-endopeptidase PCP mTld; Carboxyterminal end long form antibodyAnti-BMP-1 Bone Morphogenic Protein-1 ProCollagen C-endopeptidase PCP mTld; CUB-2 domain antibodyanti-BMP-2anti-BMP-2 anti-Bone Morphogenic Protein-2 mouse, monoclonal Related articles to: BMP_2
- 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 - Glaucoma represents a predominant cause of irreversible blindness globally, characterized by the association of elevated intraocular pressure (IOP) and retinal ganglion cell loss with dysfunction of the trabecular meshwork (TM), the principal tissue regulating conventional aqueous humor outflow. Emerging evidence suggests that this dysfunction is not exclusively driven by genetic variation or mechanical stress; rather, it is significantly influenced by epigenetic mechanisms that integrate factors such as aging, hypoxia/oxidative stress, glucocorticoid exposure, and other environmental challenges into enduring alterations in TM phenotype. This review synthesizes current understanding of the primary epigenetic mechanisms involved in glaucomatous TM remodeling, encompassing DNA methylation, histone modifications, non-coding RNAs (including microRNAs and long non-coding RNAs), and RNA N⁶-methyladenosine (m⁶A) methylation. In this study, we elucidate the role of aberrant DNA methylation in the regulation of profibrotic genes, such as TGF-β1 and GDF7, elasticity-modifying genes like LOXL1, and repetitive elements, which collectively contribute to extracellular matrix (ECM) accumulation, tissue stiffening, and increased outflow resistance. Furthermore, we explore how dysregulated miRNA-lncRNA networks and histone acetylation/methylation influence central signaling pathways, including TGF-β/BMP-Smad, Wnt/β-catenin, RhoA/ROCK, PI3K-Akt, and NF-κB. These pathways are crucial in orchestrating trabecular meshwork (TM) fibrosis, cytoskeletal remodeling, cellular senescence, and impaired stress responses. Additionally, we investigate the emerging roles of m⁶A regulators, such as METTL3, YTHDF2, and YTHDC2, at the intersection of outflow pathway fibrosis and retinal ganglion cell vulnerability. We propose that epigenetic modifiers, ncRNA-based therapies, and partial epigenetic reprogramming could offer innovative, TM-targeted, and neuroprotective strategies beyond conventional IOP-lowering treatments. Collectively, our findings support an integrated model wherein diverse epigenetic modifications converge to produce a stereotypical glaucomatous TM phenotype, thereby presenting novel opportunities for mechanism-based diagnosis and therapeutic intervention in glaucoma. - Source: PubMed
Publication date: 2025/12/21
Liu ZhihaoZheng YajuanZhao Jing - Intrauterine adhesions (IUA) are a leading cause of acquired female infertility that predominantly arises following surgical intrauterine interventions. Clinical strategies are available for managing IUA, however, the molecular pathogenesis of IUA, particularly the role of immune dysregulation in endometrial repair processes, has not been fully characterized, necessitating comprehensive mechanistic studies. - Source: PubMed
Publication date: 2025/10/03
Lv FengqingLuo SangXu FengjuanDu YueBai YiyunZhang JingyiZou XiaojieLiu Dan - Curcumin, a major phytochemical derived from Curcuma longa, has been shown to enhance the efficacy of chemotherapeutic agents such as doxorubicin, 5-fluorouracil, and cisplatin by overcoming drug resistance, making it a promising adjunct in the treatment of glioblastoma. However, the global gene-expression changes triggered by curcumin in glioblastoma remain underexplored. In this study, we investigated the effects of curcumin on human glioblastoma (U87 MG) cells, where it significantly reduced cell viability and proliferation in a dose- and time-dependent manner and induced apoptosis without affecting senescence. Transcriptomic analysis revealed 5036 differentially expressed genes, with pathway enrichment identifying 13 dysregulated cancer-associated pathways. Notably, curcumin modulated several key regulators involved in MAPK, Ras, TGF-β, Wnt, Cytokine, and TNF signaling pathways. Several apoptosis and cell cycle-associated genes, including PRKCG, GDF7, GDF9, GDF15, GDF5, FZD1, FZD2, FZD8, AIFM3, TP53AIP1, CRD14, NIBAN3, BOK, BCL2L10, BCL2L14, BNIPL, FASLG, GZMM, TNFSF10, TNFSF11, and TNFSF4, were significantly altered. Several pro-apoptotic and anti-BCL, cell-cycle-regulated genes were modulated following curcumin treatment, emphasizing its potential role in curcumin-mediated anti-tumor effects. This study provides insight into the molecular mechanisms underlying curcumin's action against glioblastoma. - Source: PubMed
Publication date: 2025/05/09
Mashozhera Nicole TendayiReddy Chinreddy SubramanyamRanasinghe Yevin NenukaNatarajan PurushothamanReddy Umesh KHankins Gerald