ArticleStem cell reports2016
Alternative Routes to Induced Pluripotent Stem Cells Revealed by Reprogramming of the Neural Lineage.
Article in Stem cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- The occurrence and development of induced pluripotent stem cells.Frontiers in genetics · 2024Review
- DOT1L interaction partner AF10 controls patterning of H3K79 methylation and RNA polymerase II to maintain cell identity.Stem cell reports · 2023Article
- DOT1L is a barrier to histone acetylation during reprogramming to pluripotency.Science advances · 2023Article
- DOT1L inhibition enhances pluripotency beyond acquisition of epithelial identity and without immediate suppression of the somatic transcriptome.Stem cell reports · 2022Article
- Connecting the DOTs on Cell Identity.Frontiers in cell and developmental biology · 2022Review
- AF10 (MLLT10) prevents somatic cell reprogramming through regulation of DOT1L-mediated H3K79 methylation.Epigenetics & chromatin · 2021Article
- Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2.The EMBO journal · 2020Article
- Defining Reprogramming Checkpoints from Single-Cell Analyses of Induced Pluripotency.Cell reports · 2019Article
- Bromodomain inhibition of the coactivators CBP/EP300 facilitate cellular reprogramming.Nature chemical biology · 2019Article
- DOT1L promotes progenitor proliferation and primes neuronal layer identity in the developing cerebral cortex.Nucleic acids research · 2019Article
- Cellular trajectories and molecular mechanisms of iPSC reprogramming.Current opinion in genetics & development · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the reprogramming of mouse embryonic fibroblasts (MEFs) to induced pluripotent stem cells, the activation of pluripotency genes such as NANOG occurs after the mesenchymal to epithelial transition. Here we report that both adult stem cells (neural stem cells) and differentiated cells (astrocytes) of the neural lineage can activate NANOG in the absence of cadherin expression during reprogramming. Gene expression analysis revealed that only the NANOG+E-cadherin+ populations expressed stabilization markers, had upregulated several cell cycle genes; and were transgene independent. Inhibition of DOT1L activity enhanced both the numbers of NANOG+ and NANOG+E-cadherin+ colonies in neural stem cells. Expressing SOX2 in MEFs prior to reprogramming did not alter the ratio of NANOG colonies that express E-cadherin. Taken together these results provide a unique pathway for reprogramming taken by cells of the neural lineage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.