Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Concurrent progress of reprogramming and gene correction to overcome therapeutic limitation of mutant ALK2-iPSC.

Experimental & molecular medicine - 3 Jun 2016

Kim Bu-Yeo, Jeong SangKyun, Lee Seo-Young, Lee So Min, Gweon Eun Jeong, Ahn Hyunjun, Kim Janghwan, Chung Sun-Ku

Abstract excerpt

Fibrodysplasia ossificans progressiva (FOP) syndrome is caused by mutation of the gene ACVR1, encoding a constitutive active bone morphogenetic protein type I receptor (also called ALK2) to induce heterotopic ossification in the patient. To genetically correct it, we attempted to generate the mutant ALK2-iPSCs (mALK2-iPSCs) from FOP-human dermal fibroblasts. However, the mALK2 leads to inhibitory pluripotency...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Activin Receptors, Type I
Share to CRISPR-Cas Systems

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Editing

Share to Genetic Therapy

Share to Induced Pluripotent Stem Cells

Share to Mice, SCID

Share to Myositis Ossificans

Share to Transcriptome

Source

Open in PubMed Open full text

Identifiers

PMID: 27256111
DOI: 10.1038/emm.2016.43
PMCID: PMC4929693

Genes

ACVR1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Concurrent progress of reprogramming and gene correction to overcome therapeutic limitation of mutant ALK2-iPSC.PMID 27256111Read ↗

Pathogenic mutation of ALK2 inhibits induced pluripotent stem cell reprogramming and maintenance: mechanisms of reprogramming and strategy for drug identification.Semantic proximity Read ↗

Generation of an induced pluripotent stem cell line (TRNDi012-B) from Fibrodysplasia Ossificans Progressiva (FOP) patient carrying a heterozygous mutation c. 617G > A in the ACVR1 gene.Semantic proximity Read ↗

Induced Pluripotent Stem Cells to Model Human Fibrodysplasia Ossificans ProgressivaSemantic proximity Read ↗

New Protocol to Optimize iPS Cells for Genome Analysis of Fibrodysplasia Ossificans ProgressivaSemantic proximity Read ↗

iMSC-mediated delivery of ACVR2B-Fc fusion protein reduces heterotopic ossification in a mouse model of fibrodysplasia ossificans progressiva.Semantic proximity Read ↗

BMP-SMAD-ID promotes reprogramming to pluripotency by inhibiting p16/INK4A-dependent senescence.Semantic proximity Read ↗

Disease-causing allele-specific silencing against the ALK2 mutants, R206H and G356D, in fibrodysplasia ossificans progressiva.Semantic proximity Read ↗

Induced pluripotent stem cells from patients with human fibrodysplasia ossificans progressiva show increased mineralization and cartilage formationSemantic proximity Read ↗

Suppression of Heterotopic Ossification in Fibrodysplasia Ossificans Progressiva Using AAV Gene DeliverySemantic proximity Read ↗

Antisense-oligonucleotide mediated exon skipping in activin-receptor-like kinase 2: inhibiting the receptor that is overactive in fibrodysplasia ossificans progressiva.Semantic proximity Read ↗

Recapitulation of pro-inflammatory signature of monocytes with ACVR1 mutation using FOP patient-derived iPSCs.Semantic proximity Read ↗

Suppression of heterotopic ossification in fibrodysplasia ossificans progressiva using AAV gene delivery.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.