Results 111 to 120 of about 7,722 (194)

Enhanced Osteogenesis of Adipose-Derived Stem Cells by Regulating Bone Morphogenetic Protein Signaling Antagonists and Agonists. [PDF]

open access: yes, 2016
UnlabelledAlthough adipose-derived stem cells (ASCs) are an attractive cell source for bone tissue engineering, direct use of ASCs alone has had limited success in the treatment of large bone defects.
Aghaloo, Tara L   +11 more
core   +2 more sources

Major transcriptome re-organisation and abrupt changes in signalling, cell cycle and chromatin regulation at neural differentiation in vivo [PDF]

open access: yes, 2014
Here, we exploit the spatial separation of temporal events of neural differentiation in the elongating chick body axis to provide the first analysis of transcriptome change in progressively more differentiated neural cell populations in vivo.
Abranches   +57 more
core   +5 more sources

The role of small RNAs in Paget's associated osteosarcoma [PDF]

open access: yes, 2018
Small RNAs (sRNAs) are a class of non-coding RNA molecules that arekey regulators of gene expression. SRNAs are also specific biomarkersdue to their dysregulation in disease.
Green, Darrell   +2 more
core   +2 more sources

FoxK1 and FoxK2 in insulin regulation of cellular and mitochondrial metabolism [PDF]

open access: yes, 2019
A major target of insulin signaling is the FoxO family of Forkhead transcription factors, which translocate from the nucleus to the cytoplasm following insulin-stimulated phosphorylation.
Albrechtsen, N.   +15 more
core   +2 more sources

Specific detection of methionine 27 mutation in histone 3 variants (H3K27M) in fixed tissue from high-grade astrocytomas [PDF]

open access: yes, 2014
Studies in pediatric high-grade astrocytomas (HGA) by our group and others have uncovered recurrent somatic mutations affecting highly conserved residues in histone 3 (H3) variants. One of these mutations leads to analogous p.Lys27Met (K27M) mutations in
Albrecht, Steffen   +16 more
core   +1 more source

International physician survey on management of FOP: a modified Delphi study

open access: yesOrphanet Journal of Rare Diseases, 2017
Fibrodysplasia ossificans progressiva (FOP), a disabling disorder of progressive heterotopic ossification (HEO), is caused by heterozygous gain-of- function mutations in Activin receptor A, type I (ACVR1, also known as ALK2), a bone morphogenetic protein
Maja Di Rocco   +12 more
doaj   +1 more source

Chitayat syndrome: hyperphalangism, characteristic facies, hallux valgus and bronchomalacia results from a recurrent c.266A>G p.(Tyr89Cys) variant in the ERF gene. [PDF]

open access: yes, 2016
BACKGROUND: In 1993, Chitayat et al., reported a newborn with hyperphalangism, facial anomalies, and bronchomalacia. We identified three additional families with similar findings.
Balasubramanian, M.   +16 more
core   +1 more source

Heterotopic Ossification: Cellular Basis, Symptoms, and Treatment [PDF]

open access: yes, 2012
Heterotopic ossification (HO) is the process by which calcified bone develops in soft tissues. Because of the abnormal calcification, complications such as bone deformation, loss of range of motion, and joint immobility adversely affect patients.
Wolfe, Brian
core  

An Activin Receptor IA/Activin-Like Kinase-2 (R206H) Mutation in Fibrodysplasia Ossificans Progressiva

open access: yesCase Reports in Genetics, 2013
Fibrodysplasia ossificans progressiva (FOP) is an exceptionally rare genetic disease that is characterised by congenital malformations of the great toes and progressive heterotopic ossification (HO) in specific anatomical areas. This disease is caused by
Rafael Herrera-Esparza   +7 more
doaj   +1 more source

Fibrodysplasia ossificans progressiva: mechanisms and models of skeletal metamorphosis

open access: yesDisease Models & Mechanisms, 2012
Fibrodysplasia ossificans progressiva (FOP; MIM #135100) is a debilitating genetic disorder of connective tissue metamorphosis. It is characterized by malformation of the great (big) toes during embryonic skeletal development and by progressive ...
Frederick S. Kaplan   +2 more
doaj   +1 more source

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