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An ES-like pluripotent state in FGF-dependent murine iPS cellsMitochondrial-associated cell death mechanisms are reset to an embryonic-like state in aged donor-derived iPS cells harboring chromosomal aberrationsThe LARGE principle of cellular reprogramming: lost, acquired and retained gene expression in foreskin and amniotic fluid-derived human iPS cellsGatekeeper of pluripotency: a common Oct4 transcriptional network operates in mouse eggs and embryonic stem cellsMolecular insights into reprogramming-initiation events mediated by the OSKM gene regulatory network.Human stromal (mesenchymal) stem cells from bone marrow, adipose tissue and skin exhibit differences in molecular phenotype and differentiation potential.Mitochondrial DNA deletions and chloramphenicol treatment stimulate the autophagic transcript ATG12.Transcriptome based identification of mouse cumulus cell markers that predict the developmental competence of their enclosed antral oocytes.Induced pluripotent stem cell-derived neuronal cells from a sporadic Alzheimer's disease donor as a model for investigating AD-associated gene regulatory networks.The return of metabolism: biochemistry and physiology of the pentose phosphate pathwayA large-scale genetic association study to evaluate the contribution of Omi/HtrA2 (PARK13) to Parkinson's disease.Annexin A1 sustains tumor metabolism and cellular proliferation upon stable loss of HIF1A.A transcriptional roadmap to the induction of pluripotency in somatic cells.Human induced pluripotent stem cells--from mechanisms to clinical applications.OCT4 and the acquisition of oocyte developmental competence during folliculogenesis.Mitochondrial function in pluripotent stem cells and cellular reprogramming.Metabolic restructuring and cell fate conversion.Induced pluripotent stem cells (iPSCs) for modeling mitochondrial DNA disorders.A mitochondrial strategy for safeguarding the reprogrammed genome.Human induced pluripotent stem cells harbor homoplasmic and heteroplasmic mitochondrial DNA mutations while maintaining human embryonic stem cell-like metabolic reprogramming.Modulation of mitochondrial biogenesis and bioenergetic metabolism upon in vitro and in vivo differentiation of human ES and iPS cells.Comparative analysis of human embryonic stem cell and induced pluripotent stem cell-derived hepatocyte-like cells reveals current drawbacks and possible strategies for improved differentiation.Mitochondrial DNA deletions induce the adenosine monophosphate-activated protein kinase energy stress pathway and result in decreased secretion of some proteins.Aging vs. rejuvenation: reprogramming to iPSCs does not turn back the clock for somatic mitochondrial DNA mutationsPrimate-specific endogenous retrovirus-driven transcription defines naive-like stem cells.Assessing the bioenergetic profile of human pluripotent stem cells.Mitochondrial DNA deletions inhibit proteasomal activity and stimulate an autophagic transcript.Erratum: Induced pluripotent stem cell-derived neuronal cells from a sporadic Alzheimer's disease donor as a model for investigating AD-associated gene regulatory networks.Alpha-synuclein nitration and autophagy response are induced in peripheral blood cells from patients with Parkinson disease.The senescence-related mitochondrial/oxidative stress pathway is repressed in human induced pluripotent stem cells.Human mesenchymal factors induce rat hippocampal- and human neural stem cell dependent oligodendrogenesis.HIF1α modulates cell fate reprogramming through early glycolytic shift and upregulation of PDK1-3 and PKM2.Mitochondrial metabolism in early neural fate and its relevance for neuronal disease modeling.Pluripotent stem cells for uncovering the role of mitochondria in human brain function and dysfunction.Human iPSC-Derived Neural Progenitors Are an Effective Drug Discovery Model for Neurological mtDNA Disorders.Efficient genetic reprogramming of unmodified somatic neural progenitors uncovers the essential requirement of Oct4 and Klf4.A Glycolytic Solution for Pluripotent Stem Cells.A mitochondrial view of cell fate.A movement disorder with dystonia and ataxia caused by a mutation in the HIBCH gene.Author Correction: Isolation and cultivation of naive-like human pluripotent stem cells based on HERVH expression
P50
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P50
name
Alessandro Prigione
@ast
Alessandro Prigione
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Alessandro Prigione
@es
Alessandro Prigione
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type
label
Alessandro Prigione
@ast
Alessandro Prigione
@en
Alessandro Prigione
@es
Alessandro Prigione
@nl
prefLabel
Alessandro Prigione
@ast
Alessandro Prigione
@en
Alessandro Prigione
@es
Alessandro Prigione
@nl