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María L. García-Rubio

Researcher at Spanish National Research Council

Publications -  45
Citations -  3392

María L. García-Rubio is an academic researcher from Spanish National Research Council. The author has contributed to research in topics: Transcription (biology) & Genome instability. The author has an hindex of 27, co-authored 40 publications receiving 2929 citations. Previous affiliations of María L. García-Rubio include Pablo de Olavide University & University of Seville.

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Transcription-Coupled Nucleotide Excision Repair Factors Promote R-Loop-Induced Genome Instability

TL;DR: Surprisingly, DSB formation requires the transcription-coupled nucleotide excision repair (TC-NER) factor Cockayne syndrome group B (CSB), but not the global genome repair protein XPC, which reveals an unexpected and potentially deleterious role for TC-NER factors in driving R-loop-induced DNA damage and genome instability.
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BRCA2 prevents R-loop accumulation and associates with TREX-2 mRNA export factor PCID2

TL;DR: It is shown that the human TREX-2 complex, which is involved in mRNP biogenesis and export, prevents genome instability as determined by the accumulation of γ-H2AX (Ser-139 phosphorylated histone H2AX) and 53BP1 foci and single-cell electrophoresis in cells depleted of the TREX -2 subunits PCID2, GANP and DSS1.
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The Fanconi Anemia Pathway Protects Genome Integrity from R-loops

TL;DR: It is concluded that co-transcriptional R loops and R loop-mediated DNA damage greatly contribute to genome instability and that one major function of the FA pathway is to protect cells from R loops.
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Genome-wide function of THO/TREX in active genes prevents R-loop-dependent replication obstacles.

TL;DR: A genome‐wide function for THO–Sub2 in transcription elongation and mRNP biogenesis that function to prevent the accumulation of transcription‐mediated replication obstacles, including R‐loops is established.
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The yeast and human FACT chromatin-reorganizing complexes solve R-loop-mediated transcription–replication conflicts

TL;DR: It is shown that recombination factors are required for the survival of yeast FACT mutants, consistent with an accumulation of DNA breaks that is detected by Rad52 foci and transcription-dependent hyperrecombination.