Enhancer type: | Enhancer | |
Disease: | -- | |
DO: | -- | |
Mesh: | -- | |
Distance from TSS: | >2KB | |
Pubmed ID: | 29967281 |
Enhancer experiment: | Luciferase Reporter Assay,ChIP-seq | |
Enhancer experiment description: | We found an SP9 ChIP-Seq peak at the Six3 promoter region (−5 to +411 of the TSS) (Fig. 9C), and several additional peaks upstream of the Six3 gene (regions 1, 2 and 3) (Fig. 9C);Thus, these noncoding domains are strong candidates for the Six3 promoter and three Six3 enhancers. |
Target gene : | Six3(E130112M24Rika,Six3alpha,Six3b,Six3beta,Six3) | |
Strong evidence: | -- | |
Less strong evidence: | ChIP-seq,Luciferase Reporter Assay | |
Target gene experiment description: | Together,the results of ChIP-seq and Dual-Luciferase assay provide evidence that SP9 promotes Six3 expression in the LGE SVZ through its direct binding to the promoter and possibly through binding to regulatory elements within the Six3 locus. |
TF name : | Six3(E130112M24Rika��Six3alpha,Six3b,Six3beta,Six3) | |
TF experiment: | RNA-seq,ChIP-seq | |
TF experiment description: | SP8 and SP9 together drive expression of the transcription factor Six3 in a spatially restricted domain of the LGE subventricular zone. Conditional deletion of Six3 also prevents the formation of most D2 MSNs, phenocopying the Sp8/9 mutants.This implies that there are additional mechanisms that regulate the generation of D2 MSNs in Sp9-KO mice, one of which was suggested by the LGE RNA-Seq analysis. We identified that expression of the TF Six3 was decreased ∼5-fold in E16.5 Sp8/9-DCKO mice compared with control mice. |
Enhancer function : | -- |
Enhancer function experiment: | -- |
Enhancer function experiment description: |
-- |
SNP ID: | -- | |
SNP position: | -- |
SNP experiment: | -- |
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