For the Mouse gene set with the same name, see VANLOO_SP3_TARGETS_DN

Systematic name M2354
Brief description Genes down-regulated in E12.5 hearts from mice with SP3 [GeneID=6670] knockout compared to the wild type organ.
Full description or abstract Mice lacking the zinc finger transcription factor specificity protein 3 (Sp3) die prenatally in the C57BL/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at embryonic day 10.5 (E10.5), and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analyzed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. Chromatin immunoprecipitation analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small-molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development and suggest that it has a crucial role in myocardial differentiation.
Collection C2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 17923686   Authors: van Loo PF,Mahtab EA,Wisse LJ,Hou J,Grosveld F,Suske G,Philipsen S,Gittenberger-de Groot AC
Exact source Fig. 7B: FC < 1
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Source species Mus musculus
Contributed by Arthur Liberzon (MSigDB Team)
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Version history 3.1: First introduced

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