Constitutively active ALK2 receptor mutants require type II receptor cooperation

scientific article published on 09 April 2013

Constitutively active ALK2 receptor mutants require type II receptor cooperation is …
instance of (P31):
scholarly articleQ13442814

External links are
P356DOI10.1128/MCB.01595-12
P932PMC publication ID3700091
P698PubMed publication ID23572558
P5875ResearchGate publication ID236189140

P50authorPaul B YuQ42413083
Nicholas W MorrellQ60960702
Panagis FilippakopoulosQ28320317
Petra KnausQ28324737
P2093author name stringHideyuki Beppu
Alex N Bullock
Petra Knaus
Yuji Mishina
Donna Y Deng
Ivan Alfano
Ashley J Vonner
Carol S C Lai
Jan Börgermann
Jana Bagarova
Kelli A Armstrong
P2860cites workConstitutively active receptors as a disease-causing mechanismQ40686419
Hyperactive BMP signaling induced by ALK2(R206H) requires type II receptor function in a Drosophila model for classic fibrodysplasia ossificans progressivaQ41903017
The mode of bone morphogenetic protein (BMP) receptor oligomerization determines different BMP-2 signaling pathways.Q42823613
High frequency of BMPR2 exonic deletions/duplications in familial pulmonary arterial hypertensionQ43173796
Bone morphogenetic protein (BMP) type II receptor deletion reveals BMP ligand-specific gain of signaling in pulmonary artery smooth muscle cellsQ46481363
Bone morphogenetic protein (BMP) type II receptor is required for BMP-mediated growth arrest and differentiation in pulmonary artery smooth muscle cellsQ46879441
Generation of a mouse with conditionally activated signaling through the BMP receptor, ALK2.Q50734070
Generation of a floxed allele of the mouse BMP type II receptor gene.Q51535561
Stoichiometric imbalance in the receptor complex contributes to dysfunctional BMPR-II mediated signalling in pulmonary arterial hypertensionQ57148975
Identification of type I receptors for osteogenic protein-1 and bone morphogenetic protein-4Q72000906
Functional modeling of the ACVR1 (R206H) mutation in FOPQ80486365
Functional analysis of bone morphogenetic protein type II receptor mutations underlying primary pulmonary hypertensionQ24298704
A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressivaQ24321505
Bone morphogenetic protein receptor complexes on the surface of live cells: a new oligomerization mode for serine/threonine kinase receptorsQ24548576
BMP type I receptor inhibition reduces heterotopic [corrected] ossificationQ24611307
Structure of the bone morphogenetic protein receptor ALK2 and implications for fibrodysplasia ossificans progressivaQ24623325
Size-Distribution Analysis of Macromolecules by Sedimentation Velocity Ultracentrifugation and Lamm Equation ModelingQ27860847
Specific activation of Smad1 signaling pathways by the BMP7 type I receptor, ALK2Q28283345
BMP signaling is required for septation of the outflow tract of the mammalian heartQ28592358
The type II activin receptors are essential for egg cylinder growth, gastrulation, and rostral head development in miceQ28592388
Targeted disruption of Cbfa1 results in a complete lack of bone formation owing to maturational arrest of osteoblastsQ29547605
Classic and atypical fibrodysplasia ossificans progressiva (FOP) phenotypes are caused by mutations in the bone morphogenetic protein (BMP) type I receptor ACVR1Q30373949
Kinase mutations in cancer: chinks in the enemy's armour?Q34477061
Somatic mutations of the EGF receptor and their signal transducers affect the efficacy of EGF receptor-specific tyrosine kinase inhibitorsQ34987162
Fibrodysplasia ossificans progressivaQ37105402
Constitutively activated ALK2 and increased SMAD1/5 cooperatively induce bone morphogenetic protein signaling in fibrodysplasia ossificans progressiva.Q37119764
Constitutive activation of G protein-coupled receptors and diseases: insights into mechanisms of activation and therapeuticsQ37157903
The fibrodysplasia ossificans progressiva R206H ACVR1 mutation activates BMP-independent chondrogenesis and zebrafish embryo ventralizationQ37403100
P433issue12
P407language of work or nameEnglishQ1860
P921main subjectcooperationQ380962
P304page(s)2413-2424
P577publication date2013-04-09
P1433published inMolecular and Cellular BiologyQ3319478
P1476titleConstitutively active ALK2 receptor mutants require type II receptor cooperation
P478volume33

Reverse relations

cites work (P2860)
Q54248766ACVR1R206H receptor mutation causes fibrodysplasia ossificans progressiva by imparting responsiveness to activin A.
Q28066886Activin receptor-like kinases: a diverse family playing an important role in cancer
Q35035999Adult-specific systemic over-expression reveals novel in vivo effects of the soluble forms of ActRIIA, ActRIIB and BMPRII.
Q58543870An Adult Zebrafish Model of Fibrodysplasia Ossificans Progressiva
Q48302210Animal models of fibrodysplasia ossificans progressiva.
Q39439904Application of human induced pluripotent stem cells to model fibrodysplasia ossificans progressiva
Q35625198Apyrase as a novel therapeutic inhibitor of heterotopic ossification
Q34293026BMP type II receptors have redundant roles in the regulation of hepatic hepcidin gene expression and iron metabolism
Q91879175BMPR2 acts as a gatekeeper to protect endothelial cells from increased TGFβ responses and altered cell mechanics
Q46612046BmpR1A is a major type 1 BMP receptor for BMP-Smad signaling during skull development
Q34512444Bone Morphogenetic Protein (BMP) signaling in development and human diseases
Q36578816Common mutations in ALK2/ACVR1, a multi-faceted receptor, have roles in distinct pediatric musculoskeletal and neural orphan disorders
Q39271127Conserved signaling pathways underlying heterotopic ossification
Q36981608Granting immunity to FOP and catching heterotopic ossification in the Act.
Q57161028Injury of Adult Zebrafish Expressing Acvr1l Does Not Result in Heterotopic Ossification
Q64058749Insights into the biology of fibrodysplasia ossificans progressiva using patient-derived induced pluripotent stem cells
Q35212915Molecular and cellular mechanisms of heterotopic ossification
Q38944117Mutant activin-like kinase 2 in fibrodysplasia ossificans progressiva are activated via T203 by BMP type II receptors
Q36394399Neofunction of ACVR1 in fibrodysplasia ossificans progressiva
Q41215881New Protocol to Optimize iPS Cells for Genome Analysis of Fibrodysplasia Ossificans Progressiva.
Q58543834Pharmacologic Strategies for Assaying BMP Signaling Function
Q58543855Phenotypic Analyses of Genetically Modified Mice for BMP Receptors
Q38666840Recent advances in understanding contextual TGFβ signaling
Q47378323Regulation of continuous but complex expression pattern of Six1 during early sensory development.
Q38915720Signaling Receptors for TGF-β Family Members
Q50152313Stem cells and heterotopic ossification: Lessons from animal models
Q34313807Structure-activity relationship of 3,5-diaryl-2-aminopyridine ALK2 inhibitors reveals unaltered binding affinity for fibrodysplasia ossificans progressiva causing mutants
Q26798172TGF-β/BMP signaling and other molecular events: regulation of osteoblastogenesis and bone formation
Q33751426The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma
Q38669186The obligatory role of Activin A in the formation of heterotopic bone in Fibrodysplasia Ossificans Progressiva.
Q52343928The orphan GPR50 receptor promotes constitutive TGFβ receptor signaling and protects against cancer development.
Q92152712The role of Activin A in fibrodysplasia ossificans progressiva: a prominent mediator
Q40459563Two tissue-resident progenitor lineages drive distinct phenotypes of heterotopic ossification.
Q36561184Unique genetic and epigenetic mechanisms driving paediatric diffuse high-grade glioma
Q47447929Variable signaling activity by FOP ACVR1 mutations
Q50144496Variant BMP receptor mutations causing fibrodysplasia ossificans progressiva (FOP) in humans show BMP ligand-independent receptor activation in zebrafish

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