Abstract

c-Jun activation domain-binding protein 1 (JAB1) was originally identified as a c-Jun co-activator and subsequently discovered to be a component of the COP9 signalosome (CSN) complex. JAB1, which is also known as CSN5, affects many partner proteins through protein-protein interaction, which leads to protein degradation and transcriptional activation. Thereby, JAB1/CSN5 functions as a multifunctional protein involved in the regulation of cell cycle, signal transduction, and DNA repair. In particular, JAB1/CSN5 plays an essential role in tumorigenesis by degrading tumor suppressor proteins and activating oncogenic transcription factors. JAB1/CSN5 overexpression has been observed in various types of cancer, and it has been multifunctionally involved in cancer progression. In this review, we provide an overview of the roles of JAB1/CSN5 in tumorigenesis and summarize recent findings that highlight the novel roles of JAB1/CSN5 in this process

Highlights

  • Inactivation of oncogenic proteins and induction of tumor suppressor proteins have provided an effective avenue for treating cancer cells

  • We provide succinct information on the roles of Jun activation domain-binding protein 1 (JAB1)/CSN5 in tumorigenesis

  • JAB1/CSN5 interacts with multiple proteins and affects many aspects of tumorigenesis in both the nucleus and the cytoplasm

Read more

Summary

Introduction

Inactivation of oncogenic proteins and induction of tumor suppressor proteins have provided an effective avenue for treating cancer cells. JAB1 interacts with multiple proteins and affects many aspects of tumorigenesis, such as protein degradation of tumor suppressors and activation of oncogenic transcription factors. JAB1/ CSN5 has many binding partners and affects their protein stability and transcriptional activity. JAB1/CSN5 translocates these proteins from the nucleus to the cytoplasm and subsequently degrades them in the proteasome.

Results
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.