Table 3 |
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Major physiological roles of cullins revealed by deletion studies with model organisms |
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Protein |
Mouse |
C. elegans |
Drosophila |
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CUL1 |
Cell cycle and embryogenesis [66,67], with KO phenotypes, including: embryonic lethality E5.5 to E6.5; accumulation of cyclin E; increased apoptosis in the ectoderm; large trophoblast giant cells in blastocytes |
Cell cycle [1]; germline apoptosis [68]; sex determination [69] |
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CUL2 |
No mouse model |
G1-to-S transition [74]; mitosis [74,75]; germline lineage [76]; meiosis [77-79]; polarity [77-79]; oogenesis [80]; MPK1 activation [80]; hypoxic response, aging [81,82] |
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CUL3 |
Cell cycle and embryogenesis [83], with KO phenotypes including embryonic lethality <E7.5; accumulation of cyclin E; impaired S-phase entry; failure to endocycle in trophoblasts |
Eye development [72]; sensory organ [87]; neurons [88]; hedgehog signaling [89,90]; actin cytoskeleton and cell movement [91,92] |
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CUL4 |
Deletion of Cul4a alone yields no major defects in development as mice lacking Cul4a exons 17 to 19 are viable and normal [93], and mice lacking Cul4a exons 4 to 8 are viable, showing mild decrease in mouse embryonic fibroblast proliferation [33]; a role in DNA repair as skin-specific CUL4A KO show increased resistance to UV-induced skin carcinogenesis [93] |
DNA replication [22] |
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CUL5 |
No mouse model |
Cell fate specification [96]; synapse formation [96]; oogenesis [97] |
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CUL7 |
Embryonic development, as KO showed neonatal death [98]; required for growth in embryo and placenta [98]; formation of vascular structure [98] |
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PARC |
Not essential for development, as KO is viable and normal [99] |
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E, embryonic day; KO, knockout. |
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Sarikas et al. Genome Biology 2011 12:220 doi:10.1186/gb-2011-12-4-220 |
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