Pub. Date : 2017 Mar 8
PMID : 28154153
11 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which results in dissociation of TACC1 from retinoic acid response elements and leads to transcriptional activation of RA target genes. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 2 | Furthermore, RA triggers GCN5-mediated acetylation of TACC1, which results in dissociation of TACC1 from retinoic acid response elements and leads to transcriptional activation of RA target genes. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 3 | Intriguingly, RA signaling defects caused by in vitro inhibition of GCN5 can be rescued through RA-dependent mechanisms that require RARbeta. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 4 | Intriguingly, RA signaling defects caused by in vitro inhibition of GCN5 can be rescued through RA-dependent mechanisms that require RARbeta. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 5 | Last, we demonstrate that the diencephalic expansion and transcriptional defects seen in (Gcn5hat/hat ) mutants can be rescued with gestational RA supplementation, supporting a direct link between GCN5, TACC1, and RA signaling in the developing diencephalon. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 6 | Together, our studies identify a novel, nonhistone substrate for GCN5 whose modification regulates a previously undescribed, tissue-specific mechanism of RA signaling that is required to restrict diencephalic size during early forebrain development.SIGNIFICANCE STATEMENT Changes in diencephalic size and shape, as well as SNPs associated with retinoic acid (RA) signaling-associated genes, have been linked to neuropsychiatric disorders. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 7 | Together, our studies identify a novel, nonhistone substrate for GCN5 whose modification regulates a previously undescribed, tissue-specific mechanism of RA signaling that is required to restrict diencephalic size during early forebrain development.SIGNIFICANCE STATEMENT Changes in diencephalic size and shape, as well as SNPs associated with retinoic acid (RA) signaling-associated genes, have been linked to neuropsychiatric disorders. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 8 | Together, our studies identify a novel, nonhistone substrate for GCN5 whose modification regulates a previously undescribed, tissue-specific mechanism of RA signaling that is required to restrict diencephalic size during early forebrain development.SIGNIFICANCE STATEMENT Changes in diencephalic size and shape, as well as SNPs associated with retinoic acid (RA) signaling-associated genes, have been linked to neuropsychiatric disorders. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 9 | Here we demonstrate a novel role of the acetyltransferase GCN5 in a previously undescribed mechanism of RA signaling in the developing forebrain that is required to maintain the appropriate size of the diencephalon. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 10 | Together, our experiments identify a novel nonhistone substrate of GCN5, highlight an essential role for both GCN5 and RA signaling in early diencephalic development, and elucidate a novel molecular regulatory mechanism for RA signaling that is specific to the developing forebrain. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |
| 11 | Together, our experiments identify a novel nonhistone substrate of GCN5, highlight an essential role for both GCN5 and RA signaling in early diencephalic development, and elucidate a novel molecular regulatory mechanism for RA signaling that is specific to the developing forebrain. | Tretinoin | K(lysine) acetyltransferase 2A | Mus musculus |