We are analyzing https://link.springer.com/article/10.1186/gm97.

Title:
LINE dancing in the human genome: transposable elements and disease | Genome Medicine
Description:
Transposable elements (TEs) have been consistently underestimated in their contribution to genetic instability and human disease. TEs can cause human disease by creating insertional mutations in genes, and also contributing to genetic instability through non-allelic homologous recombination and introduction of sequences that evolve into various cis-acting signals that alter gene expression. Other outcomes of TE activity, such as their potential to cause DNA double-strand breaks or to modulate the epigenetic state of chromosomes, are less fully characterized. The currently active human transposable elements are members of the non-LTR retroelement families, LINE-1, Alu (SINE), and SVA. The impact of germline insertional mutagenesis by TEs is well established, whereas the rate of post-insertional TE-mediated germline mutations and all forms of somatic mutations remain less well quantified. The number of human diseases discovered to be associated with non-allelic homologous recombination between TEs, and particularly between Alu elements, is growing at an unprecedented rate. Improvement in the technology for detection of such events, as well as the mounting interest in the research and medical communities in resolving the underlying causes of the human diseases with unknown etiology, explain this increase. Here, we focus on the most recent advances in understanding of the impact of the active human TEs on the stability of the human genome and its relevance to human disease.
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Keywords {🔍}

pubmed, article, scholar, google, human, cas, elements, alu, central, gene, genome, dna, activity, retrotransposition, recombination, expression, line, genetic, element, deininger, tes, diseases, disease, genomic, res, mutations, figure, events, cancer, sva, orf, region, cellular, transposable, sequences, insertion, repair, deletions, transcription, cell, genet, kazazian, genes, active, insertions, rna, batzer, mol, royengel, instability,

Topics {✒️}

adenomatous polyposis coli acute myelogenous leukemia l1-induced double-strand breaks long-distance pcr-based screening dna double-strand breaks tissue-specific transcription factors acute myeloid leukemia variable length a-tail x-chromosome-linked diseases caused dna deamination-independent mechanism l1-endonuclease-mediated events te-mediated insertional mutagenesis current retrotrans-positional activity x-linked genetic defects endonuclease-independent line-1 retrotransposition alu element-mediated nahr wild-type genetic background double-strand breaks high-copy-number elements single-copy l1 transgene alu-mediated homologous recombination hominid-specific retroposon family nhej-negative hamster cells genome-wide hypomethy lation functional cis-acting sequence alu-alu recombination underlies alu-alu recombination events von hippel-lindau syndrome te-induced dna damage line-1 insertion-mediated deletion extensive alu-alu recombination full-length l1 enters quantitative real-time pcr nih/nia grant 5k01ag030074 cell type-specific expression genome-wide expression profiles open reading frames small insertion/deletion events ldl receptor gene nahr-mediated events article number 97 reverse transcriptase activities article belancio partial tandem duplication rna-mediated transposition process human mobile elements specific genetic background partial tandem duplications dna-methyl-transferase-3 privacy choices/manage cookies

Questions {❓}

Comeaux MS, Roy-Engel AM, Hedges DJ, Deininger PL: Diverse cis factors controlling Alu retrotransposition: what causes Alu elements to die?

Schema {🗺️}

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         headline:LINE dancing in the human genome: transposable elements and disease
         description:Transposable elements (TEs) have been consistently underestimated in their contribution to genetic instability and human disease. TEs can cause human disease by creating insertional mutations in genes, and also contributing to genetic instability through non-allelic homologous recombination and introduction of sequences that evolve into various cis-acting signals that alter gene expression. Other outcomes of TE activity, such as their potential to cause DNA double-strand breaks or to modulate the epigenetic state of chromosomes, are less fully characterized. The currently active human transposable elements are members of the non-LTR retroelement families, LINE-1, Alu (SINE), and SVA. The impact of germline insertional mutagenesis by TEs is well established, whereas the rate of post-insertional TE-mediated germline mutations and all forms of somatic mutations remain less well quantified. The number of human diseases discovered to be associated with non-allelic homologous recombination between TEs, and particularly between Alu elements, is growing at an unprecedented rate. Improvement in the technology for detection of such events, as well as the mounting interest in the research and medical communities in resolving the underlying causes of the human diseases with unknown etiology, explain this increase. Here, we focus on the most recent advances in understanding of the impact of the active human TEs on the stability of the human genome and its relevance to human disease.
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      headline:LINE dancing in the human genome: transposable elements and disease
      description:Transposable elements (TEs) have been consistently underestimated in their contribution to genetic instability and human disease. TEs can cause human disease by creating insertional mutations in genes, and also contributing to genetic instability through non-allelic homologous recombination and introduction of sequences that evolve into various cis-acting signals that alter gene expression. Other outcomes of TE activity, such as their potential to cause DNA double-strand breaks or to modulate the epigenetic state of chromosomes, are less fully characterized. The currently active human transposable elements are members of the non-LTR retroelement families, LINE-1, Alu (SINE), and SVA. The impact of germline insertional mutagenesis by TEs is well established, whereas the rate of post-insertional TE-mediated germline mutations and all forms of somatic mutations remain less well quantified. The number of human diseases discovered to be associated with non-allelic homologous recombination between TEs, and particularly between Alu elements, is growing at an unprecedented rate. Improvement in the technology for detection of such events, as well as the mounting interest in the research and medical communities in resolving the underlying causes of the human diseases with unknown etiology, explain this increase. Here, we focus on the most recent advances in understanding of the impact of the active human TEs on the stability of the human genome and its relevance to human disease.
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      dateModified:2009-10-27T00:00:00Z
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      keywords:
         Adenomatous Polyposis Coli
         Acute Myelogenous Leukemia
         Variable Number Tandem Repeat
         Lysinuric Protein Intolerance
         Choroideremia
         Human Genetics
         Metabolomics
         Bioinformatics
         Medicine/Public Health
         general
         Cancer Research
         Systems Biology
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      name:Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane Cancer Center, Tulane University, New Orleans, USA
      name:Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane Cancer Center, Tulane University, New Orleans, USA

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