Towards an understanding of protein kinase B (PKB/Akt) function in mouse development
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Summary
It is found that PKBα/Akt1 was the predominant isoform in placenta and PKBγ/AKT3 is an important modulator of postnatal brain growth, and the two proteins have different roles in the maintenance of animal survival.
- Type
- dissertation
- Published
- 2004-01-01
- Cited by
- 0
- References
- 126
- Access
- Open access
- OpenAlex
- https://openalex.org/W1560315596
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:82548283
Keywords
AKT1, Protein kinase B, AKT2, PI3K/AKT/mTOR pathway, Proto-Oncogene Proteins c-akt
References
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- Targeted deletion of a branchial arch-specific enhancer reveals a role of dHAND in craniofacial development
- Biological mechanisms of environmentally induced causes of IUGR.
- Structure, expression and chromosomal mapping of c-akt: relationship to v-akt and its implications.
- Principles of Development
- Akt Activity Negatively Regulates Phosphorylation of AMP-activated Protein Kinase in the Heart*
- A motif-based profile scanning approach for genome-wide prediction of signaling pathways
- Deletion of Pten in mouse brain causes seizures, ataxia and defects in soma size resembling Lhermitte-Duclos disease
- HER-2/neu induces p53 ubiquitination via Akt-mediated MDM2 phosphorylation
- Insulin Receptor Substrate-2 Deficiency Impairs Brain Growth and Promotes Tau Phosphorylation
- Cell-autonomous regulation of cell and organ growth in Drosophila by Akt/PKB
- The Atlas of Mouse Development
- Pten regulates neuronal soma size: a mouse model of Lhermitte-Duclos disease
- Induction of the neural crest: a multigene process
- Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation
- Oncogenic kinase signalling
- Regulation of endothelium-derived nitric oxide production by the protein kinase Akt
- Mechanism of activation of protein kinase B by insulin and IGF‐1.
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