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    Polm polymerase (DNA directed), mu [ Mus musculus (house mouse) ]

    Gene ID: 54125, updated on 12-May-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    The atomic structure of an NHEJ junction with a Pol x construct that mimics Pol mu in a reconstituted system explained the distinctive properties of Pol mu compared with TdT. The structure suggested a mechanism of base selection relying on Loop1 and taking instructions via the in trans templating base independently of the primer strand.

    Structural evidence for an in trans base selection mechanism involving Loop1 in polymerase μ at an NHEJ double-strand break junction.
    Loc'h J, Gerodimos CA, Rosario S, Tekpinar M, Lieber MR, Delarue M., Free PMC Article

    03/14/2020
    Findings demonstrate that Polmu is necessary for proper retinal development, and support that the generation of DNA double-strand breaks and their repair via the non-homologous end-joining pathway are genuine processes involved in neural development.

    Increased neuronal death and disturbed axonal growth in the Polμ-deficient mouse embryonic retina.
    Baleriola J, Álvarez-Lindo N, de la Villa P, Bernad A, Blanco L, Suárez T, de la Rosa EJ., Free PMC Article

    04/14/2018
    A role for PolMU in the prevention of sarcomagenesis on a murine P53-deficient background was identified.

    Polμ deficiency induces moderate shortening of P53(-/-) mouse lifespan and modifies tumor spectrum.
    Escudero B, Herrero D, Torres Y, Cañón S, Molina A, Carmona RM, Suela J, Blanco L, Samper E, Bernad A.

    08/19/2017
    Pol mu and Pol lambda play a key role in conferring on NHEJ the flexibility required for accurate and efficient repair

    Essential role for polymerase specialization in cellular nonhomologous end joining.
    Pryor JM, Waters CA, Aza A, Asagoshi K, Strom C, Mieczkowski PA, Blanco L, Ramsden DA., Free PMC Article

    04/30/2016
    Polmu deficiency activates transcriptional networks that reduce constitutive apoptosis, leading to enhanced liver repair at old age.

    Polμ deficiency increases resistance to oxidative damage and delays liver aging.
    Escudero B, Lucas D, Albo C, Dhup S, Bacher JW, Sánchez-Muñoz A, Fernández M, Rivera-Torres J, Carmona RM, Fuster E, Carreiro C, Bernad R, González MA, Andrés V, Blanco L, Roche E, Fabregat I, Samper E, Bernad A., Free PMC Article

    12/19/2015
    DNA polymerase mu has a role in decreased learning and brain long-term potentiation in aged mice

    Increased learning and brain long-term potentiation in aged mice lacking DNA polymerase μ.
    Lucas D, Delgado-García JM, Escudero B, Albo C, Aza A, Acín-Pérez R, Torres Y, Moreno P, Enríquez JA, Samper E, Blanco L, Fairén A, Bernad A, Gruart A., Free PMC Article

    08/31/2013
    These data point to a critical role for pol mu as a global repair player that increases the efficiency and the fidelity of non-homologous end-joining.

    DNA polymerase μ is a global player in the repair of non-homologous end-joining substrates.
    Chayot R, Montagne B, Ricchetti M.

    08/11/2012
    pronounced senescence in pololymerase mu deficient cells

    Lack of DNA polymerase μ affects the kinetics of DNA double-strand break repair and impacts on cellular senescence.
    Chayot R, Danckaert A, Montagne B, Ricchetti M.

    03/19/2011
    A series of molecular-dynamics simulations with and without the incoming nucleotide in various forms, including mutant systems, based on pol mu's crystal ternary structure, were analyzed.

    Modeling DNA polymerase μ motions: subtle transitions before chemistry.
    Li Y, Schlick T., Free PMC Article

    03/5/2011
    Polm is required for hematopoietic development with an role in maintaining genetic stability in hematopoietic and non-hematopoietic tissues.

    Altered hematopoiesis in mice lacking DNA polymerase mu is due to inefficient double-strand break repair.
    Lucas D, Escudero B, Ligos JM, Segovia JC, Estrada JC, Terrados G, Blanco L, Samper E, Bernad A., Free PMC Article

    01/21/2010
    Polmu participates in the repair of early-embryo, RAG-induced double-strand breaks and subsequently may contribute to preserve the genomic stability and cellular homeostasis of lymphohematopoietic precursors during development

    A role for DNA polymerase mu in the emerging DJH rearrangements of the postgastrulation mouse embryo.
    Gozalbo-López B, Andrade P, Terrados G, de Andrés B, Serrano N, Cortegano I, Palacios B, Bernad A, Blanco L, Marcos MA, Gaspar ML., Free PMC Article

    01/21/2010
    Pol mu promotes accuracy during Ig kappa recombination.

    A gradient of template dependence defines distinct biological roles for family X polymerases in nonhomologous end joining.
    Nick McElhinny SA, Havener JM, Garcia-Diaz M, Juárez R, Bebenek K, Kee BL, Blanco L, Kunkel TA, Ramsden DA.

    01/21/2010
    Pol mu is not required for normal Ig gene hypermutation.

    Cutting edge: DNA polymerases mu and lambda are dispensable for Ig gene hypermutation.
    Bertocci B, De Smet A, Flatter E, Dahan A, Bories JC, Landreau C, Weill JC, Reynaud CA.

    01/21/2010
    The crystal structure of the polymerase domain of murine Pol mu bound to gapped DNA with a correct dNTP at the active site reveals substrate interactions with side chains in Pol mu that differ from other family X members.

    Structural insight into the substrate specificity of DNA Polymerase mu.
    Moon AF, Garcia-Diaz M, Bebenek K, Davis BJ, Zhong X, Ramsden DA, Kunkel TA, Pedersen LC.

    01/21/2010
    third hypervariable region assumes for each immunoglobulin chain, with pol lambda maintaining a large heavy chain junctional heterogeneity and pol mu ensuring a restricted light chain junctional variability

    Nonoverlapping functions of DNA polymerases mu, lambda, and terminal deoxynucleotidyltransferase during immunoglobulin V(D)J recombination in vivo.
    Bertocci B, De Smet A, Weill JC, Reynaud CA.

    01/21/2010
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