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2 additional projects are components of the KMT2D loss disrupts cell cycle and hypoxic responses in neurodevelopmental models of Kabuki syndrome.
We conducted genome-wide analysis of KMT2D binding sites in a hippocampal cell line to define KMT2D-dependent functions in neuronal context
Overall design: ChIP-seq in wild-type HT22 cells and HT22 cells with CRISPR-Cas9 mediated deletion of the KMT2D enzymatic SET methyltransferase domain, comparing KMT2D-pulldown and input controls
| Accession | PRJNA521221; GEO: GSE126166 |
| Data Type | Epigenomics |
| Scope | Multiisolate |
| Organism | Mus musculus[Taxonomy ID: 10090] Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus; Mus musculus |
| Submission | Registration date: 6-Feb-2019
Johns Hopkins School of Medicine |
| Relevance | Model Organism |
Project Data:
| Resource Name | Number
of Links |
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| Sequence data |
| SRA Experiments | 2 |
| Other datasets |
| BioSample | 2 |
| GEO DataSets | 1 |