Zobrazeno 1 - 10
of 49
pro vyhledávání: '"Martin Gering"'
Publikováno v:
Cell Reports, Vol 13, Iss 11, Pp 2539-2552 (2015)
Axon injury leads to rapid depletion of NAD-biosynthetic enzyme NMNAT2 and high levels of its substrate, NMN. We proposed a key role for NMN in Wallerian degeneration but downstream events and their relationship to other mediators remain unclear. Her
Externí odkaz:
https://doaj.org/article/818ca742f39140a4bf16b8ada17dd2cb
Publikováno v:
Frontiers in Cell and Developmental Biology, Vol 6 (2018)
5-methylcytosine (5mC) is the best understood DNA modification and is generally believed to be associated with repression of gene expression. Over the last decade, sequentially oxidized forms of 5mC (oxi-mCs) have been discovered within the genomes o
Externí odkaz:
https://doaj.org/article/d3c4f5fe2768491eaba7aa959d9f7c66
Publikováno v:
PLoS ONE, Vol 8, Iss 6, p e65170 (2013)
The importance of microRNAs in development is now widely accepted. However, identifying the specific targets of individual microRNAs and understanding their biological significance remains a major challenge. We have used the zebrafish model system to
Externí odkaz:
https://doaj.org/article/f2dfd071db164275a8e102dfac5438ed
Publikováno v:
PLoS ONE, Vol 8, Iss 11 (2013)
Externí odkaz:
https://doaj.org/article/9f34134c22ff427da5538c6c3e6d28a4
Autor:
Peter Jessop, Martin Gering
Publikováno v:
Methods in Molecular Biology ISBN: 9781071608753
5-methylcytosine (5mC) is an epigenetic modification to DNA which modulates transcription. 5mC can be sequentially oxidized to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC). Collectively, these marks are referre
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::a12d849d80d0b9fa4c6b200bd50851e8
https://doi.org/10.1007/978-1-0716-0876-0_16
https://doi.org/10.1007/978-1-0716-0876-0_16
Autor:
Peter, Jessop, Martin, Gering
Publikováno v:
Methods in molecular biology (Clifton, N.J.). 2198
5-methylcytosine (5mC) is an epigenetic modification to DNA which modulates transcription. 5mC can be sequentially oxidized to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC). Collectively, these marks are referre
Autor:
Roshana Sutharshini Thambyrajah, Maryam J. Jalali, Martin Gering, Yasmin Hough, Deniz Ucanok, Kathryn McMahon, Robert N. Wilkinson, Christopher I. Moore
Publikováno v:
Developmental Biology
A transposon-mediated gene trap screen identified the zebrafish line qmc551 that expresses a GFP reporter in primitive erythrocytes and also in haemogenic endothelial cells, which give rise to haematopoietic stem and progenitor cells (HSPCs) that see
Publikováno v:
Cell Reports, Vol 13, Iss 11, Pp 2539-2552 (2015)
Axon injury leads to rapid depletion of NAD-biosynthetic enzyme NMNAT2 and high levels of its substrate, NMN. We proposed a key role for NMN in Wallerian degeneration but downstream events and their relationship to other mediators remain unclear. Her
Autor:
Yan Chen, Sunir Malla, Fei Sang, Stone Elworthy, Robert N. Wilkinson, Martin Gering, Deniz Ucanok, Joanna L. Richens, Christopher I. Moore, Yasmin Hough
The transcriptional repressors G\ud fi\ud 1(a) and G\ud fi\ud 1b are epigenetic regulators with unique and\ud overlapping roles in hematopoiesis. In different contexts, G\ud fi\ud 1 and G\ud fi\ud 1b restrict or promote\ud cell proliferation, prevent
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4ebc0f74febd6427609258af7d2dd5ca
https://europepmc.org/articles/PMC6199651/
https://europepmc.org/articles/PMC6199651/
Autor:
Michele, Di Stefano, Andrea, Loreto, Giuseppe, Orsomando, Valerio, Mori, Federica, Zamporlini, Richard P, Hulse, Jamie, Webster, Lucy F, Donaldson, Martin, Gering, Nadia, Raffaelli, Michael P, Coleman, Jonathan, Gilley, Laura, Conforti
Publikováno v:
Current biology : CB. 27(6)
Axons require the axonal NAD-synthesizing enzyme NMNAT2 to survive. Injury or genetically induced depletion of NMNAT2 triggers axonal degeneration or defective axon growth. We have previously proposed that axonal NMNAT2 primarily promotes axon surviv