Corepressor MMTR/DMAP1 is an intrinsic negative regulator of CAK kinase to regulate cell cycle progression
- Authors
- Shin, June Ho; Kane, Ho Chul; Park, Yun-Yeon; Ha, Dae Hyun; Choi, Youn Hee; Eum, Hea Young; Kang, Bong Gu; Chae, Ji Hyung; Shin, Incheol; Lee, Jae-Ho; Kim, Chul Geun
- Issue Date
- Nov-2010
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- MMTR/DMAP1; MAT1; Cell cycle progression; G1/S and G2/M transitions; CAK kinase
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.402, no.1, pp.110 - 115
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 402
- Number
- 1
- Start Page
- 110
- End Page
- 115
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/173543
- DOI
- 10.1016/j.bbrc.2010.09.126
- ISSN
- 0006-291X
- Abstract
- We have previously reported that MMTR (MAT1-mediated transcriptional repressor) is a co-repressor that inhibits TFIIH-mediated transcriptional activity via interaction with MAT1 (Kang et al., 2007). Since MAT1 is a member of the CAK kinase complex that is crucial for cell cycle progression and that regulates CDK phosphorylation as well as the general transcription factor TFIIH, we investigated MMTR function in cell cycle progression. We found that MMTR over-expression delayed G1/S and G2/M transitions, whereas co-expression of MAT1 and MMTR rescued the cell growth and proliferation rate. Moreover, MMTR was required for inhibition of CAK kinase-mediated CDK1 phosphorylation. We also showed that the expression level of MMTR was modulated during cell cycle progression. Our data support the notion that MMTR is an intrinsic negative cell cycle regulator that modulates the CAK kinase activity via interaction with MAT1.
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