Publication for Pou3f4 and Zic1
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| mmu | Pou3f4 | POU domain, class 3, transcription factor 4 | 18994 | [link] | ||
| mmu | Zic1 | zinc finger protein of the cerebellum 1 | 22771 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 23606270 | 0.98 | Zic genes, like Tbx1 and Brn4, could be required for proper epithelial-mesenchymal signaling. |
| 0.97 | Brn4 is regulated by SHH signaling, and Zic genes regulate SHH signaling in vitro, so the expression of Zic genes in the same regions where Tbx1 and Brn4 are expressed could mean that the Zic genes are involved in the SHH-dependent expression of Tbx1 and Brn4. | |
| 0.89 | Zic+ cells are most likely periotic mesenchyme, a subset of which is condensing cartilage (that will later form the otic capsule), because they expressed either Tbx1 or Tbx1 and Brn4 (Fig. 8B, 8C, 8E, 8F). | |
| 0.87 | Brn4 expression could be independent of Zic expression, suggesting a different role for the Zic genes. | |
| 0.85 | Brn4, Tbx1, and Sox10 in sections at similar levels through the otocyst at E10.5 to attempt to characterize the Zic-expressing cells in the mesenchyme outside of the neuroepithelium and otic epithelium. | |
| 0.79 | Brn4 and Tbx1, markers of condensing mesenchyme and periotic mesenchyme, in the regions where we found Zic-expressing cells. | |
| 20107439 | 0.98 | Brn4, Myt1l, Zic1, and Olig2) substantially potentiated the neuron-inducing activity of Ascl1 (Supplementary Fig. 2a-b). |
| 21336820 | 0.98 | Zic1 has been identified as a neuronal cell-fate inducing gene in mouse fibroblasts; in a screen for genes that induce neural cell fate, five genes (Pou3f2, Pou3f4, Myt1l, Zic1, and Olig2) were found to substantially potentiate the neuron-inducing activities of Ascl1. |
| 23724002 | 0.98 | Zic1 is a transcription factor of the Zic family that potentiates (with Ascl1, Pou3f2, Myt1l, Pou3f4, Olig2) the conversion of mouse fibroblasts to neurons. |
The preparation time of this page was 0.0 [sec].
