BMPRIA _ ALK_3 _ CD292 Protein
- Known as:
- BMPRIA _ ALK_3 _ CD292 Protein
- Catalog number:
- 10446-H03H
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- BMPRIA _ ALK_3 CD292 Protein
Related genes to: BMPRIA _ ALK_3 _ CD292 Protein
- Gene:
- BMPR1A NIH gene
- Name:
- bone morphogenetic protein receptor type 1A
- Previous symbol:
- ACVRLK3
- Synonyms:
- ALK3, CD292
- Chromosome:
- 10q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-12
- Date modifiied:
- 2019-04-23
Related products to: BMPRIA _ ALK_3 _ CD292 Protein
Related articles to: BMPRIA _ ALK_3 _ CD292 Protein
- The hypothalamus coordinates energy-balance regulation and is also a neurogenic/plastic region in the adult brain. Tanycytes, a specialized population of radial glial-like cells lining the third ventricle, reside at the critical interface between the blood, cerebrospinal fluid, and hypothalamic parenchyma. This unique positioning enables them to sense metabolic and nutrient-derived signals, and to shuttle molecules between periphery and brain. Tanycytes can respond to glucose and lipids, as demonstrated by a calcium transient down their long processes that extend into the hypothalamic nuclei. Tanycytes are also capable of self-renewal and differentiation after brain injury, supporting their classification as putative neural stem cells in the adult hypothalamus. Bone morphogenetic protein (BMP) signaling regulates neuroplasticity and contributes to metabolic regulation, including appetite and sympathetic drive to adipose. We previously demonstrated that central administration of BMP7 suppresses appetite, and BMP receptor 1A (BMPR1A) in anorectic hypothalamic POMC neurons impacts appetite regulation. BMPR1A is also tightly and highly co-expressed in hypothalamic tanycytes. Here, we attempted to genetically inactivate BMPR1A in adult tanycytes to explore its functional roles. Using the Rax-CreERxBMPR1Aflox mouse line, we tested multiple routes of tamoxifen administration, as well as its metabolite, without success. Cre recombinase activity was successfully induced via dietary tamoxifen (shown by recombination of the BMPR1A locus and fluorescent reporter induction), but efficient BMPR1A knockout in adult tanycytes was not achieved. Similarly, adeno-associated viral (AAV)-mediated BMPR1A knockdown via the Dio2 promoter and intracerebroventricular delivery yielded limited efficiency, despite confirmed Cre activity indicated by reporter expression. We also observed a compensatory increase in BMPR1A in cells not targeted by these knock-out/knockdown systems, as we observed previously with POMC-Cre knockout of BMPR1A, indicating a responsiveness of the hypothalamic niche to manipulation of BMPR1A levels. Together, our findings support that Cre-driven reporter activity doesn't guarantee gene depletion, and demonstrate that current strategies for loss of function of BMPR1A in adult hypothalamic tanycytes remain technically challenging and require careful validation before interpretation of phenotypes. More efficient and reliable methods are required to elucidate the molecular signaling and functional roles of molecules expressed in adult tanycytes. - Source: PubMed
Publication date: 2026/04/24
Tao TianyiLeon-Palmer NoelleDiPietro SabrinaTownsend Kristy L - Bone defect healing failure and osteoporosis pose significant challenges to clinical orthopedics and geriatric medicine, while the structural heterogeneity of natural heparan sulfate (HS) hinders the clarification of the functional role of 6-O-sulfation patterns in osteogenesis and its translational application. To address this gap, we developed a structurally defined 6-O-sulfated heparan sulfate glycopolymer (6-O-HS) via reversible addition-fragmentation chain transfer (RAFT) polymerization and copper(I)-catalyzed azide-alkyne cycloaddition (CuAAC) click chemistry, establishing an engineering-based synthesis strategy with controllable molecular weight and uniform structure. In vitro experiments showed that 6-O-HS (5 µg/mL) significantly enhanced alkaline phosphatase (ALP) activity, osteocalcin (OC) expression, and extracellular matrix mineralization in murine bone marrow mesenchymal stem cells (BMSCs), outperforming conventional HS. RNA sequencing and functional validation revealed that 6-O-HS specifically activated the TGF-β/BMP signaling pathway by upregulating the gene and protein levels of BMP receptors (BMPR1A, BMPR1B, BMPR2) without altering BMP-2 ligand expression. In an ovariectomized (OVX) mouse model, 6-O-HS administration significantly improved bone microarchitecture, increased cortical thickness (Ct.Th) and bone volume fraction (BV/TV), and reduced trabecular separation (Tb.Sp). This study presents a reproducible glycopolymer synthesis and application framework, integrating precision chemical engineering, in vitro mechanistic verification, and in vivo efficacy validation. The framework provides a low-cost, scalable engineering tool for targeted regulation of BMSC osteogenic differentiation, offering novel solutions for bone tissue engineering scaffold development and osteoporosis treatment with broad translational potential in regenerative medicine. - Source: PubMed
Publication date: 2026/04/09
Xu ZhujieLiu YiChen JingxiaoGao AiguoXu Youjia - Bone morphogenetic protein (BMP) signalling plays a pivotal role in bone regeneration by regulating osteoprogenitor cell (OPC) function, and BMPs have been widely used in clinical treatment. However, their limited specificity for OPCs often lead to side effects, highlighting that the regulatory mechanisms of BMP signalling remain to be further elucidated. BMPR1A, a key type I BMP receptor, has emerged as a critical regulator of bone development, yet its precise role in bone regeneration and downstream mechanisms remains unclear. Using OPC-specific conditional knockout (cKO) and constitutively activated (CA) BMPR1A mouse, we found conditional knockout of BMPR1A in OPCs during the first 2 weeks of healing significantly accelerated bone regeneration. At the cellular level, BMPR1A knockout promoted the proliferation of OPCs, thereby accelerating bone regeneration in cKO mice. Mechanistically, BMPR1A knockout reduced ID1 expression, releasing its inhibition of TCF3, which in turn induced GNG4 expression and ultimately activated the PI3K-AKT pathway. Finally, a double-knockdown cell line further demonstrated the role of the BMPR1A-ID1-TCF3-GNG4 signalling axis. This study reveals the function and mechanism of BMPR1A in bone regeneration and provides new insights for more precise BMP-targeted strategies. - Source: PubMed
Publication date: 2026/04/06
Zhou ZihaoZhai YunLiu XiaochenShao JiaojiaoZhou JianiLi ZhaoyangHe JialeLin ShuxianZhang Qi - Pulmonary arterial hypertension (PAH) is a severe disease characterized by elevated pulmonary artery pressure, leading to heart failure and premature death if untreated. Genetic factors significantly contribute to PAH, and several genes have been linked to its development. According to the ClinGen PH-GCEP group, 12 genes have definitive evidence of association with PAH, three have moderate evidence, six have limited evidence, and five remain disputed due to insufficient genetic data. The aim of this study was to analyze variants in genes without definitive evidence in a cohort of 1480 individuals (954 PAH patients and 526 relatives) by next-generation sequencing (NGS). Variants were prioritized through a custom pipeline developed in-house and classification was performed according to ACMG guidelines. A total of 32 different variants were identified in 42 individuals (32 patients and 10 relatives, five of whom developed the disease): Two pathogenic or likely pathogenic variants in ABCC8 and 30 variants of unknown significance (VUS) in 10 genes (ABCC8, AQP1, BMPR1A, BMPR1B, BMP10, FBLN2, NOTCH3, SMAD1, SMAD4 and TET2). On the opposite, no candidate variants were detected in GGCX, KLF2, KLK1 or PDGFD genes. These findings provide further genetic evidence supporting the association of ABCC8 and related genes with PAH, while no candidate variants were detected in GGCX, KLF2, KLK1, or PDGFD. Further research is needed to confirm the functional impact of these variants. - Source: PubMed
Publication date: 2026/03/25
Miranda-Alcaraz LucíaMora-Gómez MónicaGallego-Zazo NataliaCruz-Utrilla AlejandroDel Cerro Marín María JesúsOchoa Parra NuriaMartín de Miguel IreneGutiérrez Ortiz EvaJiménez-Estrada Juan AndrésParra AlejandroCazalla MarioRamos SergioRodríguez-Canó ManuelSilván CristinaVásquez-Amell ValeriaArias PedroNevado Juliánde Jesús Pérez VinicioLapunzina PabloEscribano-Subías PilarTenorio-Castano Jair - Intramuscular fat (IMF) deposition is a key factor for meat quality traits like juiciness, tenderness, and flavor. Although fibro/adipogenic progenitor cells (FAPs) participate in adipogenesis, the roles of other stromal cells in the muscle microenvironment are unclear. This study aimed to characterize cellular heterogeneity in cattle IMF deposition and identify key cell types and molecular mechanisms regulating intramuscular adipogenesis. - Source: PubMed
Publication date: 2026/03/11
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