BCAS3
Breast carcinoma amplified sequence 3, also known as BCAS3, is a protein which in humans is encoded by the BCAS3 gene.[5][6] BCAS3 is a gene that is amplified and overexpressed in breast cancer cells.[6]
Function
The BCAS3 gene is regulated by estrogen receptor alpha (ER-α).[7] The PELP1 protein acts as a transcriptional coactivator of estrogen receptor induced BCAS3 gene expression. In addition BCAS3 possesses histone acetyltransferase activity and itself appears to act as a coactivator of ER-α.[8][better source needed] Furthermore, BCAS3 requires PELP1 to function as a coactivator in ER-α. Hence BCAS3 apparently is involved in a positive feedback loop leading to ER-α mediated signal amplification.[8][better source needed]
References
- ^ a b c GRCh38: Ensembl release 89: ENSG00000141376 – Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000059439 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Entrez Gene: BCAS3 breast carcinoma amplified sequence 3".
- ^ a b Bärlund M, Monni O, Weaver JD, Kauraniemi P, Sauter G, Heiskanen M, Kallioniemi OP, Kallioniemi A (December 2002). "Cloning of BCAS3 (17q23) and BCAS4 (20q13) genes that undergo amplification, overexpression, and fusion in breast cancer". Genes Chromosomes Cancer. 35 (4): 311–7. doi:10.1002/gcc.10121. PMID 12378525. S2CID 9759638.
- ^ Gururaj AE, Singh RR, Rayala SK, Holm C, den Hollander P, Zhang H, Balasenthil S, Talukder AH, Landberg G, Kumar R (April 2006). "MTA1, a transcriptional activator of breast cancer amplified sequence 3". Proc. Natl. Acad. Sci. U.S.A. 103 (17): 6670–5. Bibcode:2006PNAS..103.6670G. doi:10.1073/pnas.0601989103. PMC 1458939. PMID 16617102.
- ^ a b Gururaj AE, Peng S, Vadlamudi RK, Kumar R (August 2007). "Estrogen induces expression of BCAS3, a novel estrogen receptor-alpha coactivator, through proline-, glutamic acid-, and leucine-rich protein-1 (PELP1)". Mol. Endocrinol. 21 (8): 1847–60. doi:10.1210/me.2006-0514. PMID 17505058. (Retracted, see doi:10.1210/me.2014-1149, Retraction Watch)
External links
- Human BCAS3 genome location and BCAS3 gene details page in the UCSC Genome Browser.
Further reading
- Maruyama K, Sugano S (1994). "Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides". Gene. 138 (1–2): 171–4. doi:10.1016/0378-1119(94)90802-8. PMID 8125298.
- Suzuki Y, Yoshitomo-Nakagawa K, Maruyama K, et al. (1997). "Construction and characterization of a full length-enriched and a 5'-end-enriched cDNA library". Gene. 200 (1–2): 149–56. doi:10.1016/S0378-1119(97)00411-3. PMID 9373149.
- Bärlund M, Monni O, Weaver JD, et al. (2003). "Cloning of BCAS3 (17q23) and BCAS4 (20q13) genes that undergo amplification, overexpression, and fusion in breast cancer". Genes Chromosomes Cancer. 35 (4): 311–7. doi:10.1002/gcc.10121. PMID 12378525. S2CID 9759638.
- Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. Bibcode:2002PNAS...9916899M. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
- Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs". Nat. Genet. 36 (1): 40–5. doi:10.1038/ng1285. PMID 14702039.
- Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC)". Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMC 528928. PMID 15489334.
- Kimura K, Wakamatsu A, Suzuki Y, et al. (2006). "Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes". Genome Res. 16 (1): 55–65. doi:10.1101/gr.4039406. PMC 1356129. PMID 16344560.
- Gururaj AE, Singh RR, Rayala SK, et al. (2006). "MTA1, a transcriptional activator of breast cancer amplified sequence 3". Proc. Natl. Acad. Sci. U.S.A. 103 (17): 6670–5. Bibcode:2006PNAS..103.6670G. doi:10.1073/pnas.0601989103. PMC 1458939. PMID 16617102.
- Gururaj AE, Holm C, Landberg G, Kumar R (2006). "Breast cancer-amplified sequence 3, a target of metastasis-associated protein 1, contributes to tamoxifen resistance in premenopausal patients with breast cancer". Cell Cycle. 5 (13): 1407–10. doi:10.4161/cc.5.13.2924. PMID 16855396.
- Gururaj AE, Peng S, Vadlamudi RK, Kumar R (2007). "Estrogen induces expression of BCAS3, a novel estrogen receptor-alpha coactivator, through proline-, glutamic acid-, and leucine-rich protein-1 (PELP1)". Mol. Endocrinol. 21 (8): 1847–60. doi:10.1210/me.2006-0514. PMID 17505058. (Retracted, see doi:10.1210/me.2014-1149, Retraction Watch)
 | This article on a gene on human chromosome 17 is a stub. You can help Wikipedia by adding missing information. |
Content Disclaimer
Informasi ini disarikan dari Wikipedia dan disajikan kembali untuk tujuan edukasi. Konten tersedia di bawah lisensi CC BY-SA 3.0. Kami tidak bertanggung jawab atas ketidakakuratan data yang bersumber dari kontribusi publik tersebut.
- The information displayed on this website is sourced in part or in whole from Wikipedia and has been adapted for the purpose of restating it. We strive to provide accurate and relevant information, however:
- There is no guarantee of absolute accuracy. Wikipedia is an open, collaborative project that can be edited by anyone, so information is subject to change.
- It is not intended to constitute professional advice. The content displayed is for informational and educational purposes only. For important decisions (e.g., medical, legal, or financial), please consult a professional.
- Content copyright. Wikipedia is licensed under the Creative Commons Attribution-ShareAlike License (CC BY-SA). This means that content may be reused with appropriate attribution and shared under a similar license.
- Responsible use. Any risk arising from the use of information from this website is entirely the responsibility of the user.