76 research outputs found
MRI is a DNA Damage Response Adaptor during Classical Non-Homologous End Joining. Hung et al.
These are the original data files for the Molecular Cell manuscript titled "MRI is a DNA Damage Response Adaptor during Classical Non-Homologous End Joining" by Hung et al. The paper characterizes the role of a small disordered peptide MRI (modulator of retrovirus infection, also known as CYREN) in promoting non-homologous end joining (NHEJ). Specifically, MRI associates with diverse DNA damage response factors at its termini and increases their avidity for chromatin at DNA double-strand breaks (DSBs). Moreover, MRI functions redundantly with XLF in DSB repair, and the loss of both proteins severely impairs V(D)J recombination in lymphocytes and leads to embryonic lethality in mice. We thus purpose that MRI acts as an adaptor that helps to enhance the efficiency of NHEJ
T cell receptor (TCR) ι/δ locus enhancer identity and position are critical for the assembly of TCR δ and ι variable region genes
T cell receptor (TCR) δ and ι variable region genes are assembled from germ-line gene segments located in a single chromosomal locus in which TCRδ segments are situated between TCRι segments. The TCRι enhancer (Eι) located at the 3Ⲡend of the TCRι/δ locus functions over a long chromosomal distance to promote TCRι rearrangement and maximal TCRδ expression; whereas the TCRδ enhancer (Eδ) is located among the TCRδ segments and functions with additional element(s) to mediate TCRδ rearrangement. We used gene-targeted mutation to evaluate whether the identity of Eι and the position of Eδ are critical for the developmental stage-specific assembly of TCR δ and ι variable region genes. Specific replacement of Eι with Eδ, the core Eι element (EιC), or the Ig heavy chain intronic enhancer (iEΟ), all of which promote accessibility in the context of transgenic V(D)J recombination substrates, did not promote a significant level of TCRι rearrangement beyond that observed in the absence of Eι. Therefore, the identity and full complement of Eι-binding sites are critical for promoting accessibility within the TCRι locus. In the absence of the endogenous Eδ element, specific replacement of Eι with Eδ also did not promote TCRδ rearrangement. However, deletion of intervening TCRι/δ locus sequences to restore the inserted Eδ to its normal chromosomal position relative to 5Ⲡsequences rescued TCRδ rearrangement. Therefore, unlike Eι, Eδ lacks ability to function over the large intervening TCRι locus and/or Eδ function requires proximity to additional upstream element(s) to promote TCRδ accessibility
Cutting Edge: Cell-Autonomous Control of IL-7 Response Revealed in a Novel Stage of Precursor B Cells
Exposure to childhood infections and risk of EpsteinâBarr virusâdefined Hodgkin's lymphoma in women
Dasatinib (D) in previously treated metastatic colorectal cancer (mCRC) patients: A phase II trial of the University of Chicago phase II consortium.
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