Proteins BMPR-II , Human
- Known as:
- Proteins BMPR-II , Human
- Catalog number:
- C303
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins BMPR- Human
Related genes to: Proteins BMPR-II , Human
- Gene:
- BMPR1AP1 NIH gene
- Name:
- bone morphogenetic protein receptor type 1A pseudogene 1
- Previous symbol:
- BMPR1APS1
- Synonyms:
- -
- Chromosome:
- 6q22.33
- Locus Type:
- pseudogene
- Date approved:
- 2003-07-21
- Date modifiied:
- 2018-05-23
- Gene:
- BMPR1AP2 NIH gene
- Name:
- bone morphogenetic protein receptor type 1A pseudogene 2
- Previous symbol:
- BMPR1APS2
- Synonyms:
- -
- Chromosome:
- 11q24.1
- Locus Type:
- pseudogene
- Date approved:
- 2003-07-21
- Date modifiied:
- 2018-05-23
- Gene:
- BMPR1B-DT NIH gene
- Name:
- BMPR1B divergent transcript
- Previous symbol:
- BMPR1B-AS1
- Synonyms:
- TCONS_00007797
- Chromosome:
- 4q22.3
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2014-07-14
- Date modifiied:
- 2018-03-21
- Gene:
- BMPR2 NIH gene
- Name:
- bone morphogenetic protein receptor type 2
- Previous symbol:
- PPH1
- Synonyms:
- BRK-3, T-ALK, BMPR3, BMPR-II
- Chromosome:
- 2q33.1-q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-03-19
- Date modifiied:
- 2019-04-23
Related products to: Proteins BMPR-II , Human
Related articles to: Proteins BMPR-II , Human
- Pulmonary arterial hypertension (PAH) is a progressive disease characterized by pulmonary vascular remodeling, right ventricular overload, and premature death. Despite advances achieved through endothelin receptor antagonists, phosphodiesterase type 5 inhibitors, and prostacyclin analogs, these agents primarily act as vasodilators and do not reverse underlying vascular pathology. Sotatercept, a first-in-class activin signaling modulator, restores the balance between pro- and antiproliferative signaling within the pulmonary vasculature via the TGF-β/activin-BMPR2 pathway, offering a novel disease-modifying mechanism. Following encouraging preclinical data, a series of clinical trials, PULSAR, SPECTRA, STELLAR, ZENITH, and HYPERION, demonstrated consistent efficacy across diverse PAH populations. Sotatercept significantly reduced pulmonary vascular resistance, improved exercise capacity, and decreased morbidity and mortality, including in patients receiving maximal background therapy. Across studies, adverse events were generally mild to moderate, with epistaxis, telangiectasia, and increased hemoglobin being the most common treatment-related events. Collectively, these findings establish sotatercept as a major advance in PAH therapy, marking a transition from purely vasodilatory approaches toward targeted modulation of vascular remodeling. By improving pulmonary hemodynamics and right ventricular function, sotatercept represents a new therapeutic option for improving clinical outcomes across different stages of PAH. - Source: PubMed
Publication date: 2026/04/20
Salibe-Filho WilliamZorze Rossetto NathaliaTatagiba Luiza Sarmentode Deus MontAlverne Parente YuriJardim Carlos Viana PoyaresFernandes Caio Julio CesarAlves-Junior José LeonidasSouza Rogerio - Pulmonary arterial hypertension (PAH) involves progressive obstruction of small pulmonary vessels due to vascular remodeling. Although the genetic architecture of PAH is increasingly understood, it remains poorly characterized in Algeria due to limited studies and the absence of molecular diagnostic infrastructure. - Source: PubMed
Publication date: 2026/04/16
Berkane Amel WafaYahiaoui RachidaMethia NadéraDjami-Temim NassimaCoulet FlorenceAntigny FabriceMontani DavidHamouli-Said Zohra - Acute myeloid leukemia (AML) is an aggressive bone marrow disease, characterized by increased levels of bone morphogenetic proteins (BMPs). In this study, the impact of the BMP-enriched leukemia environment was determined on surrounding cells, notably mesenchymal stem cells (MSC). BMP-2, 4, 7, 9, and TGFβ1 were presented via a biomimetic extracellular matrix to healthy and AML-MSC. We have previously shown the existence of a bidirectional cross-talk between BMP receptors and integrins, which tightly connect cell adhesion to cell differentiation. In this study, we investigated how BMPRs and integrins are regulated in the AML microenvironment, in particular in the context of MSC adhesion and differentiation. Smad phosphorylation and cell adhesive responses were assessed for MSC cultured on biomimetic materials with matrix-bound BMPs/TGFβ1 using a recently-developed high-content immunofluorescence method. The specific role of BMP receptors and of integrin beta chains in the activation of pSmad signal, cell adhesion and cell spreading was studied using silencing RNA. 33% of the AML-MSCs exhibited increased receptor levels, with higher variability for BMPR2, β1 and β5 receptors. Notably, AML-MSC exhibited an upregulated and sustained pSmad signaling, associated to ALK5, ALK6 and BMPR2 dysfunctions. AML-MSC adhesion was strongly impaired, associated with a loss of cooperation between BMPR and β integrins. Unexpectedly, β integrins inhibited AML-MSC adhesion, while BMPRI receptors promoted it, notably ALK5. Furthermore, we proved that MSCs from AML patients exhibit an impaired differentiation into osteogenic, chondrogenic and adipogenic lineage. For the first time, we proved here that MSCs present in the AML microenvironment present an altered adhesion and differentiation, due to an altered cross-talk between BMPRs and integrins. This paves the way for future therapeutic strategies taking into account ALK5 and integrin beta chains in AML disease. - Source: PubMed
Publication date: 2026/04/02
Arnaldos-Pérez IreneMachillot PaulGeistlich KevinMarchadier LisaMaguer Satta VéroniqueMigliorini ElisaGuyon LaurentLefort SylvainAlbiges-Rizo CorinnePicart Catherine - 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 - In acute lung injury (ALI), clinical data show that while mortality rates are similar between sexes, women require shorter ventilation times and intensive care unit stays than men, yet preclinical studies show conflicting sex-specific vulnerabilities. We reasoned that a hidden dosing bias may explain the inconsistency, as intratracheal bleomycin is scaled to body weight, even though lung mass grows more slowly than total body mass, so age-matched males, whose body mass outpaces lung growth, inevitably receive more drug per gram of lung than females. - Source: PubMed
Publication date: 2026/03/12
Gillman SamuelNgu AliceLush MichaelKarpuk NikolayHu Kevin MLisco Steven JWang Han-Jun