Interaction of restin with transcription factors.

Abstract

Restin, a member of melanoma-associated antigen superfamily gene, was first cloned from differentiated leukemia cell induced by all trans-retinoic acid, and was able to inhibit cell proliferation, but the molecular mechanism was not clear. Since Restin was localized in cell nucleus, and its homolog member, Necdin (neuronal growth suppressor factor), could interact with transcription factors p53 and E2F1, we proposed that Restin might also function as Necdin through interacting with some transcription factors. In this study, transcription factors p53, AP1, ATFs and E2Fs were cloned and used in the mammalian two-hybrid system to identify their interaction with Restin. The results showed that only ATF3 had a strong interaction with Restin. It is interesting to know that ATF3 was an important transcription factor for G1 cell cycle initiation in physiological stress response. It was possible that the inhibition of cell proliferation by Restin might be related with the inhibition of ATF3 activity.

• Authors: Yousheng Wu, Fan Lu, Yinxin Qi, Ruihua Wang, Jian Zhang, Zifan Lu, Zhongliang Zhao
• Journal: Science in China. Series C, Life sciences (Sci China C Life Sci) Vol. 48 Issue 3 Pg. 256-62 (Jun 2005) ISSN: 1006-9305 [Print] China
• PMID: 16092758 (Publication Type: Comparative Study, Journal Article)

Chemical References

• Cell Cycle Proteins
• DNA-Binding Proteins
• E2F Transcription Factors
• E2F1 Transcription Factor
• Microtubule-Associated Proteins
• Neoplasm Proteins
• Transcription Factor AP-1
• Transcription Factors
• Tumor Suppressor Protein p53
• cytoplasmic linker protein 170

Topics

• Animals
• Cell Cycle Proteins (genetics, metabolism)
• Cell Line, Tumor
• DNA-Binding Proteins (genetics, metabolism)
• E2F Transcription Factors
• E2F1 Transcription Factor
• Microtubule-Associated Proteins (genetics, metabolism)
• Neoplasm Proteins (genetics, metabolism)
• Plasmids (genetics)
• Protein Binding
• Transcription Factor AP-1 (genetics, metabolism)
• Transcription Factors (genetics, metabolism)
• Tumor Suppressor Protein p53 (genetics, metabolism)
• Two-Hybrid System Techniques