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| Title / Description | Genome-wide analysis of E157D PPARγ transcriptional activity in NIH-3T3 fibroblasts |
| Accession | GSE37990 |
| Summary | The E157D PPARγ mutation presents as an atypical case of familial partial lipodystrophy and diabetes in a human cohort and has a novel molecular mechanism. The mutation is located in the DNA-binding domain, has no dominant negative activity but disrupts transcription activation after the protein has bound the DNA. The mutation causes a transcriptional activation defect on many PPARγ target genes, while some genes are induced normally. A small number of non-PPARγ target genes are induced by the E157D mutant, possibly leading to the atypical features in this cohort. |
| Organism | Mus musculus |
| Platform | GPL6887 |
| Normalized | False |
| Parsed SOFT file |
| Differential expression method | Characteristic Direction |
| Cutoff | 500 |
| Cell | NIH3T3 (PPARγ2 E157D) |
| Perturbation | Rosiglitazone |
| Disease | 20uM - 24 hrs |
| Principal Component Analysis | |
| Hierarchical clustering |
| Gene lists | Enrichr | L1000CDS2 | PAEA | |
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