Alternative Splicing Generates Different 5' UTRs in OCT4B Variants.

Autor: Poursani EM; Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran., Mehravar M; Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran., Shahryari A; Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran., Mowla SJ; Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran., Mohammad Soltani B; Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Jazyk: angličtina
Zdroj: Avicenna journal of medical biotechnology [Avicenna J Med Biotechnol] 2017 Oct-Dec; Vol. 9 (4), pp. 201-204.
Abstrakt: Background: The human OCT4 gene, responsible for pluripotency and self-renewal of Embryonic Stem (ES) and Embryonic Carcinoma (EC) cells, can generate several transcripts (OCT4A, OCT4B-variant 2, OCT4B-variant 3, OCT4B-variant 5, OCT4B1, OCT4 B2 and OCT4B3) by alternative splicing and alternative promoters. OCT4A that is responsible for ES and EC cell stemness properties is transcribed from a promoter upstream of Exon1a in those cells. The OCT4B group variants (OCT4B-variant2, OCT4B-variant3, OCT4B-variant5, OCT4B1, OCT4B2 and OCT4B3) are transcribed from a different promoter located in intron 1 and some of them respond to the cell stresses, but cannot sustain the ES/EC cell self-renewal. However, the exact function of OCT4B group variants is still unclear.
Methods: In the present study, we employed RT-PCR and sequencing approaches to explore different forms of OCT4 transcripts.
Results: Our data revealed that the OCT4B group variants (OCT4B-variant2, OCT4 B-variant3, OCT4B1, OCT4B2 and OCT4B3) have longer 5' UTR in the human bladder carcinoma cell line of 5637.
Conclusion: These OCT4 variants undergo alternative splicing in their 5' UTR which might exert regulatory roles in transcription and translation mechanisms.
Databáze: MEDLINE
Externí odkaz: