Abstract
Regulation of GSK3β-FBXW7-JUNB Axis
Highlights
In the last decade the involvement of the activator protein 1 (AP-1) in human cancer has been demonstrated
We have found that GSK3β-mediated phosphorylation of JUNB on a critical consensus phosphodegron induces FBXW7 E3-ligase recruitment and its degradation in late G2
We reported that abnormal conditions that stabilize JUNB, including mutations in the consensus phosphodegron or deletion of the FBXW7, lead to transcriptional activation of cyclin A2 and repression of DDX11, a DNA helicase essential for sister chromatid cohesion
Summary
In the last decade the involvement of the activator protein 1 (AP-1) in human cancer has been demonstrated. Low JUNB levels in mitosis allow c-Jun to induce cyclin D1 transcription and progression into G1. Member-specific Jun modifications seem to be important for the regulation of their protein expression during cell cycle progression. In our published article [2] we provide evidence of the molecular mechanism involved in JUNB degradation in G2.
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