Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Phosphorylation stabilizes Nanog by promoting its interaction with Pin1.

http://www.ncbi.nlm.nih.gov/pubmed/20622153

Embryonic stem cells (ESCs) can undergo unlimited self-renewal and retain the pluripotency to differentiate into all cell types in the body, thus holding great promise as a renewable source of cells for human therapy. The mechanisms that maintain self-renewal of ESCs remain unclear. Here we show that Nanog, a transcription factor crucial for the self-renewal of ESCs, is phosphorylated at multiple Ser/Thr-Pro motifs. This phosphorylation promotes the interaction between Nanog and the prolyl isomerase Pin1, leading to Nanog stabilization by suppressing its ubiquitination. Inhibition of Pin1 activity or disruption of Pin1-Nanog interaction in ESCs suppresses their capability to self-renew and to form teratomas in immunodeficient mice. Therefore, in addition to the stringent transcriptional regulation of Nanog, the expression level of Nanog is also modulated by posttranslational mechanisms.

Pubmed ID: 20622153 RIS Download

Mesh terms: Amino Acid Motifs | Amino Acid Sequence | Animals | Binding Sites | Blotting, Western | Cell Line | Cells, Cultured | Embryonic Stem Cells | Enzyme Inhibitors | Homeodomain Proteins | Humans | Mice | Mice, SCID | Molecular Sequence Data | Mutation | Peptidylprolyl Isomerase | Phenanthrolines | Phosphorylation | Protein Binding | Protein Stability | RNA Interference | Reverse Transcriptase Polymerase Chain Reaction | Sequence Homology, Amino Acid | Teratoma | Ubiquitination

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

None

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.