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Gene Review:

SERTAD1 - SERTA domain containing 1

Homo sapiens

Synonyms: CDK4-binding protein p34SEI1, SEI-1, SEI1, SERTA domain-containing protein 1, TRIP-Br1, ...

Tang, D.J. et al., Hayashi, R. et al., Gupta, S. et al., Li, J. et al., Tang, T.C. et al., et al.

Li, Muscarella, Joo, Knobloch, Melvin, Weghorst, Tsai,

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Disease relevance of SERTAD1

(v) The expression levels of SEI-1 and p16 were compared in 32 tumor specimens of human squamous cell carcinomas of the head and neck [1].
Here we report yeast two-hybrid screens with HPV-6 and -11 E6 proteins that identified TRIP-Br1 as a novel cellular target [2].
These data strongly suggest that SEI-1 plays an important role in the development and progression of ovarian cancer [3].

High impact information on SERTAD1

Silencing of SEI-1 gene expression by small interfering RNAs in ovarian cancer cell line SKOV3 could inhibit cell growth as well as colony formation on soft agar [3].
Chromosomal alterations including the formation of double minutes were observed in tumor cells derived from SEI-1-transformed NIH 3T3 cells [3].
Oncogenic transformation by SEI-1 is associated with chromosomal instability [3].
These data suggest that the oncogenic role of SEI-1 might be mediated at least in part via an effect on genomic instability [3].
In the present study, the oncogenic potential of SEI-1 was shown by anchorage-independent growth and tumor formation in nude mice with SEI-1-transfected NIH 3T3 mouse fibroblast cells [3].

Biological context of SERTAD1

Previous studies have shown that p34(SEI-1), also known as TRIP-Br1, is involved in cell cycle regulations by interacting with a number of important proteins including CDK4 [4].
Identification of a candidate oncogene SEI-1 within a minimal amplified region at 19q13.1 in ovarian cancer cell lines [5].
Like TRIP-Br1/p34(SEI-1) and TRIP-Br2 (SEI-2), the transactivation domain of CDCA4 was mapped within C-terminal acidic region 175-241 [6].

Other interactions of SERTAD1

The results indicate that SEI-1 was consistently overexpressed, while p16 was consistently underexpressed [1].
The TRIP-Br1/p34(SEI-1) family proteins participate in cell cycle progression by coactivating E2F1- or p53-dependent transcriptional activation [6].
1. Two candidate oncogenes, AKT2 and SEI-1, were identified in MAR2 [5].

Analytical, diagnostic and therapeutic context of SERTAD1

We observed that TRIP-Br1 interacts with low- and high-risk HPV E6 proteins in yeast, in vitro and in mammalian cell cultures [2].

References

Dissection of CDK4-binding and transactivation activities of p34(SEI-1) and comparison between functions of p34(SEI-1) and p16(INK4A). Li, J., Muscarella, P., Joo, S.H., Knobloch, T.J., Melvin, W.S., Weghorst, C.M., Tsai, M.D. Biochemistry (2005) [Pubmed]
The human papillomavirus type 11 and 16 E6 proteins modulate the cell-cycle regulator and transcription cofactor TRIP-Br1. Gupta, S., Takhar, P.P., Degenkolbe, R., Koh, C.H., Zimmermann, H., Yang, C.M., Guan Sim, K., Hsu, S.I., Bernard, H.U. Virology (2003) [Pubmed]
Oncogenic transformation by SEI-1 is associated with chromosomal instability. Tang, D.J., Hu, L., Xie, D., Wu, Q.L., Fang, Y., Zeng, Y., Sham, J.S., Guan, X.Y. Cancer Res. (2005) [Pubmed]
The nuclear protein p34SEI-1 regulates the kinase activity of cyclin-dependent kinase 4 in a concentration-dependent manner. Li, J., Melvin, W.S., Tsai, M.D., Muscarella, P. Biochemistry (2004) [Pubmed]
Identification of a candidate oncogene SEI-1 within a minimal amplified region at 19q13.1 in ovarian cancer cell lines. Tang, T.C., Sham, J.S., Xie, D., Fang, Y., Huo, K.K., Wu, Q.L., Guan, X.Y. Cancer Res. (2002) [Pubmed]
CDCA4 Is an E2F Transcription Factor Family-induced Nuclear Factor That Regulates E2F-dependent Transcriptional Activation and Cell Proliferation. Hayashi, R., Goto, Y., Ikeda, R., Yokoyama, K.K., Yoshida, K. J. Biol. Chem. (2006) [Pubmed]

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