Non long terminal receptor

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L1 retrotransposons are the most prominent cause of [[cancer|cancer]]. L1 retrotransposons are associated with two [[open reading frames|open reading frames]]; ORF1 and ORF2<ref>Ioannis Papasotiriou, Katerina Pantopikou, Panagiotis Apostolou. L1 retrotransposon expression in circulating tumor cells. 2017. [cited 8/11/2018] Available from:[https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0171466 journals.plos.org/plosone/article]</ref>. ORF2 affects the [[enzymes|enzymes]] [[endonuclease|endonuclease]] and [[reverse transcriptase|reverse transcriptase]] which both have genetic implications in carcinogenesis though their activity, ORF2 is associated with [[chaperon|chaperon]] activity<ref>Ioannis Papasotiriou, Katerina Pantopikou, Panagiotis Apostolou. L1 retrotransposon expression in circulating tumor cells. 2017. [cited 8/11/2018] Available from:[https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0171466 journals.plos.org/plosone/article]</ref>. When the full length L1 source element is transcribed we obtain a bicistronic [[mRNA|mRNA]] that is subsequently converted into a [[ribonucleoprotein complex|ribonucleoprotein complex]]<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>. This complex moves from the [[cytoplasm|cytoplasm]] into the [[nucleus|nucleus]] of cells where it is inserted in [[genomic DNA|genomic DNA]] using a specific primer motif leading to the addition of the L1 sequence into another location in the [[DNA|DNA]] [[genome|genome]]<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>. This is known as the mobilization of L1 retrotransposons<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>. 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<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>. 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<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>.  
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L1 retrotransposons are the most prominent cause of [[Cancer|cancer]]. L1 retrotransposons are associated with two [[Open reading frames|open reading frames]]; ORF1 and ORF2<ref>Ioannis Papasotiriou, Katerina Pantopikou, Panagiotis Apostolou. L1 retrotransposon expression in circulating tumor cells. 2017. [cited 8/11/2018] Available from:[https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0171466 journals.plos.org/plosone/article]</ref>. ORF1 affects the [[Enzymes|enzymes]] [[Endonuclease|endonuclease]] and [[Reverse transcriptase|reverse transcriptase]] which both have genetic implications in carcinogenesis though their activity, ORF2 is associated with [[Chaperon|chaperon]] activity<ref>Ioannis Papasotiriou, Katerina Pantopikou, Panagiotis Apostolou. L1 retrotransposon expression in circulating tumor cells. 2017. [cited 8/11/2018] Available from:[https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0171466 journals.plos.org/plosone/article]</ref>. When the full length L1 source element is transcribed we obtain a bicistronic [[MRNA|mRNA]] that is subsequently converted into a [[Ribonucleoprotein complex|ribonucleoprotein complex]]<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>. This complex moves from the [[Cytoplasm|cytoplasm]] into the [[Nucleus|nucleus]] of cells where it is inserted in [[Genomic DNA|genomic DNA]] using a specific primer motif leading to the addition of the L1 sequence into another location in the [[DNA|DNA]] [[Genome|genome]]<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>. This is known as the mobilization of L1 retrotransposons<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>. 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<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>. 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<ref>MDPI/David J.Garfinkel . The Role of somatic L1 Retrotransposition in Human Cancers. 2017. [cited 8/11/2018]; Available from:[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/ www.ncbi.nlm.nih.gov/pmc/articles/PMC5490808/]</ref>.  
  
 
=== References  ===
 
=== References  ===
  
 
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Revision as of 10:45, 8 December 2018

L1 retrotransposons are the most prominent cause of cancer. L1 retrotransposons are associated with two open reading frames; ORF1 and ORF2[1]. ORF1 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[3]. 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[4]. This is known as the mobilization of L1 retrotransposons[5]. 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[6]. 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[7].

References

  1. 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
  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
  3. 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/
  4. 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/
  5. 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/
  6. 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/
  7. 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/

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