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Daniel R. Fuentes
Researcher at Stanford University
Publications - 7
Citations - 2112
Daniel R. Fuentes is an academic researcher from Stanford University. The author has contributed to research in topics: Transcription factor & Cellular differentiation. The author has an hindex of 5, co-authored 7 publications receiving 1823 citations.
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Journal ArticleDOI
Induction of human neuronal cells by defined transcription factors
Zhiping P. Pang,Nan Yang,Thomas Vierbuchen,Austin Ostermeier,Daniel R. Fuentes,Troy Q. Yang,Ami Citri,Vittorio Sebastiano,Samuele Marro,Thomas C. Südhof,Marius Wernig +10 more
TL;DR: The data demonstrate that non-neural human somatic cells, as well as pluripotent stem cells, can be converted directly into neurons by lineage-determining transcription factors.
Journal ArticleDOI
Hierarchical mechanisms for direct reprogramming of fibroblasts to neurons.
Orly L. Wapinski,Thomas Vierbuchen,Kun Qu,Qian Yi Lee,Soham Chanda,Daniel R. Fuentes,Paul G. Giresi,Yi Han Ng,Samuele Marro,Norma F. Neff,Daniela Drechsel,Ben Martynoga,Diogo S. Castro,Ashley E. Webb,Thomas C. Südhof,Anne Brunet,François Guillemot,Howard Y. Chang,Howard Y. Chang,Marius Wernig +19 more
TL;DR: A precise match between pioneer factors and the chromatin context at key target genes is determinative for transdifferentiation to neurons and likely other cell types.
Journal ArticleDOI
Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates
Moritz Mall,Michael S. Kareta,Soham Chanda,Henrik Ahlenius,Nicholas Perotti,Bo Zhou,Sarah Grieder,Xuecai Ge,Sienna Drake,Cheen Euong Ang,Brandon M. Walker,Thomas Vierbuchen,Daniel R. Fuentes,Philip Brennecke,Kazuhiro R. Nitta,Arttu Jolma,Lars M. Steinmetz,Jussi Taipale,Jussi Taipale,Thomas C. Südhof,Marius Wernig +20 more
TL;DR: By studying the reprogramming of mouse fibroblasts to neurons, it is found that the pan neuron-specific transcription factor Myt1-like (Myt1l) exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program.
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Systematic perturbation of retroviral LTRs reveals widespread long-range effects on human gene regulation.
TL;DR: CARGO is employed, a recent method for CRISPR gRNA multiplexing, to facilitate targeting of LTR5HS, an ape-specific class of HERVK (HML-2) LTRs that is active during early development and present in ~700 copies throughout the human genome.
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Inappropriate p53 activation during development induces features of CHARGE syndrome
Jeanine L. Van Nostrand,Colleen A. Brady,Heiyoun Jung,Daniel R. Fuentes,Margaret M. Kozak,Thomas M. Johnson,Chieh Yu Lin,Chien Jung Lin,Donald L. Swiderski,Hannes Vogel,Jonathan A. Bernstein,Tania Attié-Bitach,Ching Pin Chang,Joanna Wysocka,Donna M. Martin,Laura D. Attardi +15 more
TL;DR: In this paper, a knock-in mutant mouse strain that expressed a stabilized and transcriptionally dead variant of the tumour-suppressor protein p53 (p53(25,26,53,54)), along with a wild-type allele of p53, was found to be associated with a host of phenotypes that are characteristic of CHARGE syndrome, including coloboma, inner and outer ear malformations, heart outflow tract defects and craniofacial defects.