scholarly article | Q13442814 |
P819 | ADS bibcode | 2013PLoSO...869096S |
P356 | DOI | 10.1371/JOURNAL.PONE.0069096 |
P932 | PMC publication ID | 3701692 |
P698 | PubMed publication ID | 23861958 |
P5875 | ResearchGate publication ID | 249967833 |
P50 | author | Peter A.C. 't Hoen | Q57190543 |
Dwi U Kemaladewi | Q59692180 | ||
Annemieke Aartsma-Rus | Q42215747 | ||
P2093 | author name string | Peter ten Dijke | |
Jie Cai | |||
David J J de Gorter | |||
Gonzalo Sanchez-Duffhues | |||
Songting Shi | |||
Willem M H Hoogaars | |||
P2860 | cites work | A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva | Q24321505 |
BMP-2/4 and BMP-6/7 differentially utilize cell surface receptors to induce osteoblastic differentiation of human bone marrow-derived mesenchymal stem cells | Q24328930 | ||
BMP type I receptor inhibition reduces heterotopic [corrected] ossification | Q24611307 | ||
Antisense-mediated exon skipping: a versatile tool with therapeutic and research applications | Q24682555 | ||
Overactive bone morphogenetic protein signaling in heterotopic ossification and Duchenne muscular dystrophy | Q26864900 | ||
Characterization of bone morphogenetic protein-6 signaling pathways in osteoblast differentiation | Q28145299 | ||
ALK2 R206H mutation linked to fibrodysplasia ossificans progressiva confers constitutive activity to the BMP type I receptor and sensitizes mesenchymal cells to BMP-induced osteoblast differentiation and bone formation | Q28265302 | ||
Abnormal angiogenesis but intact hematopoietic potential in TGF-beta type I receptor-deficient mice | Q28361871 | ||
Lack of the bone morphogenetic protein BMP6 induces massive iron overload | Q28510138 | ||
Dorsomorphin inhibits BMP signals required for embryogenesis and iron metabolism | Q29617479 | ||
Classic and atypical fibrodysplasia ossificans progressiva (FOP) phenotypes are caused by mutations in the bone morphogenetic protein (BMP) type I receptor ACVR1 | Q30373949 | ||
Identification of progenitor cells that contribute to heterotopic skeletogenesis | Q30436925 | ||
Molecular consequences of the ACVR1(R206H) mutation of fibrodysplasia ossificans progressiva. | Q33991272 | ||
Systemic administration of PRO051 in Duchenne's muscular dystrophy | Q34172661 | ||
Conversion of vascular endothelial cells into multipotent stem-like cells | Q35532554 | ||
BMP2 activity, although dispensable for bone formation, is required for the initiation of fracture healing. | Q52002102 | ||
BMP2 is required for early heart development during a distinct time period. | Q52170375 | ||
Targeted exon skipping as a potential gene correction therapy for Duchenne muscular dystrophy. | Q52547202 | ||
Deregulated bone morphogenetic protein receptor signaling underlies fibrodysplasia ossificans progressiva. | Q54508841 | ||
BMP-9-induced muscle heterotopic ossification requires changes to the skeletal muscle microenvironment. | Q54587581 | ||
Local dystrophin restoration with antisense oligonucleotide PRO051 | Q80412961 | ||
Bone morphogenetic protein-2 converts the differentiation pathway of C2C12 myoblasts into the osteoblast lineage | Q36235105 | ||
An Acvr1 R206H knock-in mouse has fibrodysplasia ossificans progressiva | Q36566730 | ||
Fibrodysplasia ossificans progressiva | Q37105402 | ||
Splice modulating therapies for human disease | Q37994280 | ||
BMP signaling in vascular diseases | Q38019702 | ||
Renal uptake of an 18-mer phosphorothioate oligonucleotide | Q38290811 | ||
Exonic sequences provide better targets for antisense oligonucleotides than splice site sequences in the modulation of Duchenne muscular dystrophy splicing | Q38345010 | ||
Guidelines for antisense oligonucleotide design and insight into splice-modulating mechanisms | Q38360555 | ||
In vitro analyses of the dysregulated R206H ALK2 kinase-FKBP12 interaction associated with heterotopic ossification in FOP. | Q38542691 | ||
Disease-causing allele-specific silencing against the ALK2 mutants, R206H and G356D, in fibrodysplasia ossificans progressiva | Q39255284 | ||
Biphasic effects of transforming growth factor β on bone morphogenetic protein-induced osteoblast differentiation | Q39536713 | ||
BMP antagonists enhance myogenic differentiation and ameliorate the dystrophic phenotype in a DMD mouse model | Q39645240 | ||
Murine endothelial cell lines as models of tumor endothelial cells | Q40574091 | ||
Exposure of KS483 cells to estrogen enhances osteogenesis and inhibits adipogenesis | Q40746983 | ||
Subcloning of three osteoblastic cell lines with distinct differentiation phenotypes from the mouse osteoblastic cell line KS-4. | Q41154242 | ||
Restoration of normal BMP signaling levels and osteogenic differentiation in FOP mesenchymal progenitor cells by mutant allele-specific targeting | Q41994816 | ||
Comparative analysis of antisense oligonucleotide analogs for targeted DMD exon 46 skipping in muscle cells | Q44960581 | ||
Bone morphogenetic protein (BMP) type II receptor is required for BMP-mediated growth arrest and differentiation in pulmonary artery smooth muscle cells | Q46879441 | ||
P275 | copyright license | Creative Commons Attribution 4.0 International | Q20007257 |
P6216 | copyright status | copyrighted | Q50423863 |
P433 | issue | 7 | |
P407 | language of work or name | English | Q1860 |
P921 | main subject | fibrodysplasia ossificans progressiva | Q1410831 |
P304 | page(s) | e69096 | |
P577 | publication date | 2013-07-04 | |
P1433 | published in | PLOS One | Q564954 |
P1476 | title | Antisense-oligonucleotide mediated exon skipping in activin-receptor-like kinase 2: inhibiting the receptor that is overactive in fibrodysplasia ossificans progressiva | |
P478 | volume | 8 |
Q38184276 | Antisense-mediated exon skipping: taking advantage of a trick from Mother Nature to treat rare genetic diseases |
Q34512444 | Bone Morphogenetic Protein (BMP) signaling in development and human diseases |
Q33587847 | Identification and characterization of regulatory elements in the promoter of ACVR1, the gene mutated in Fibrodysplasia Ossificans Progressiva. |
Q34502398 | Molecular, phenotypic aspects and therapeutic horizons of rare genetic bone disorders |
Q33635469 | Nonsense-mediated decay as a terminating mechanism for antisense oligonucleotides |
Q58725014 | Recent Topics in Fibrodysplasia Ossificans Progressiva |
Q38639065 | Shared ACVR1 mutations in FOP and DIPG: Opportunities and challenges in extending biological and clinical implications across rare diseases |
Q35110776 | Targeted excision of VCP R155H mutation by Cre-LoxP technology as a promising therapeutic strategy for valosin-containing protein disease |
Q92738367 | Targeting heterotopic ossification by inhibiting activin receptor‑like kinase 2 function (Review) |
Q52340220 | The Horizon of a Therapy for Rare Genetic Diseases: A "Druggable" Future for Fibrodysplasia Ossificans Progressiva. |
Q26752839 | The biological function of type I receptors of bone morphogenetic protein in bone |
Q92152712 | The role of Activin A in fibrodysplasia ossificans progressiva: a prominent mediator |
Q42370380 | Towards a cure for Fibrodysplasia ossificans progressiva. |
Search more.