Human BMPR-IB / ALK-6 Protein
- Known as:
- Human BMPR-IB / ALK-6 Protein
- Catalog number:
- AL6-H5226
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human BMPR- / ALK-6 Protein
Related genes to: Human BMPR-IB / ALK-6 Protein
- 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 NIH gene
- Name:
- bone morphogenetic protein receptor type 1B
- Previous symbol:
- -
- Synonyms:
- ALK6, CDw293
- Chromosome:
- 4q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-03-19
- Date modifiied:
- 2016-10-05
- 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: Human BMPR-IB / ALK-6 Protein
Related articles to: Human BMPR-IB / ALK-6 Protein
- To determine the prevalence and phenotypes of children with heritable pulmonary arterial hypertension (PAH) and those with pulmonary hypertension (PH) associated with genetic disorders. - Source: PubMed
Publication date: 2026/04/21
Grynblat JulienEyries MélanieAmbar-Akkaoui MarineLevy MarilyneMeot MathildeSzezepanski IsabelleRanchoup JulienCallegari AlessiaKarila-Cohen JulieBonnet CarolineMarijon PierreChamp JeromeCoulet FlorenceOvaert CarolinePerros FrédéricAntigny FabriceMaragnes PascaleVaksmann GuyHumbert MarcMalekzadeh Milani Sophie GuitiMontani DavidBonnet Damien - Pulmonary arterial hypertension (PAH) is a progressive disease characterized by pulmonary microvascular loss and obliterative remodeling driven by endothelial dysfunction. Low penetrance of only BMPR2 mutations causing metabolic shifts in pulmonary microvascular endothelial cells (PMVECs), suggests role of additional genetic modifiers. Genetic screening of PAH PMVECs identified carboxylesterase1 (CES1)-an endoplasmic reticulum (ER) enzyme involved in lipid metabolism and detoxification-as a candidate regulator of endothelial metabolism and angiogenesis. We hypothesize that CES1 loss promotes endothelial dysfunction via metabolic reprogramming, lipotoxicity, and oxidative stress. - Source: PubMed
Publication date: 2026/02/24
Agarwal StutiBankar AnuradhaHeo LyongMitra AnkitaChakraborty AnanyaLiu LichaoHuang FloraSwaminathan GowriAuer NatashaChelladurai PrakashGuardado Eleana StephanieMatos JuanLe CrystalWest JamesSuresh KarthikNair RameshRabinovitch MarleneMorisseau ChristopheHammock Bruce DWu JosephArany ZoltNicolls Mark RDe Jesus Perez Vinicio - Improved understanding of the complex and interconnected mechanisms driving pulmonary arterial hypertension (PAH) has expanded therapeutic development beyond the traditional vasodilator pathways. This review summarizes recently established and emerging signalling pathways that may influence the next generation of targeted PAH therapies. - Source: PubMed
Publication date: 2026/05/05
Budhram BrandonBonnet SébastienWeatherald Jason - 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