Non long terminal receptor

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 L1 retrotransposons are the most prominent cause of cancer . L1 retrotransposons are associated with two open reading frames; ORF1 and ORF2 (2). ORF2 affects the enzymes endonuclease and reverse transcriptase which both have genetic implications in carcinogenesis though their activity, ORF2 is associated with chaperon activity (2). When the full length L1 source element is transcribed we obtain a bicistronic mRNA that is subsequently converted into a ribonucleoprotein complex (1). This complex moves from the cytoplasm into the nucleus of cells where it is inserted in genomic DNA using a specific primer motif leading to the addition of the L1 sequence into another location in the DNA genome (1). This is known as the mobilization of L1 retrotransposons (1). Furthermore, like the action of a catalyst the L1 source element can be used again as a template for further mobilization, this leads to uncontrolled replication in cancer cells (1). The human body however is equipped against L1 mobilization through processes such as DNA methylation that involve rapping of the
DNA sequence around histone proteins preventing its transcription through promoter inactivation (1). However, L1 retrotransposons are not the only transposon sub-family that may lead to cancer initiation.


References:

1. MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:
www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/

2.Ioannis Papasotiriou, Katerina Pantopikou, Panagiotis Apostolou. L1 retrotransposon expression in circulating tumor cells. 2017. [cited 8/11/2018] Available from:
journals.plos.org/plosone/article

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