Liabakk NB - Search Results

1

RPA guides UNG to uracil in ssDNA to facilitate antibody class switching and repair of mutagenic uracil at the replication fork.

Hayran AB, Liabakk NB, Aas PA, Kusnierczyk A, Vågbø CB, Sarno A, Iveland TS, Chawla K, Zahn A, Di Noia JM, Slupphaug G, Kavli B. Hayran AB, et al. Among authors: liabakk nb. Nucleic Acids Res. 2024 Jan 25;52(2):784-800. doi: 10.1093/nar/gkad1115. Nucleic Acids Res. 2024. PMID: 38000394 Free PMC article.

2

Repair of U/G and U/A in DNA by UNG2-associated repair complexes takes place predominantly by short-patch repair both in proliferating and growth-arrested cells.

Akbari M, Otterlei M, Peña-Diaz J, Aas PA, Kavli B, Liabakk NB, Hagen L, Imai K, Durandy A, Slupphaug G, Krokan HE. Akbari M, et al. Among authors: liabakk nb. Nucleic Acids Res. 2004 Oct 12;32(18):5486-98. doi: 10.1093/nar/gkh872. Print 2004. Nucleic Acids Res. 2004. PMID: 15479784 Free PMC article.

3

RPA2 winged-helix domain facilitates UNG-mediated removal of uracil from ssDNA; implications for repair of mutagenic uracil at the replication fork.

Kavli B, Iveland TS, Buchinger E, Hagen L, Liabakk NB, Aas PA, Obermann TS, Aachmann FL, Slupphaug G. Kavli B, et al. Among authors: liabakk nb. Nucleic Acids Res. 2021 Apr 19;49(7):3948-3966. doi: 10.1093/nar/gkab195. Nucleic Acids Res. 2021. PMID: 33784377 Free PMC article.

4

B cells from hyper-IgM patients carrying UNG mutations lack ability to remove uracil from ssDNA and have elevated genomic uracil.

Kavli B, Andersen S, Otterlei M, Liabakk NB, Imai K, Fischer A, Durandy A, Krokan HE, Slupphaug G. Kavli B, et al. Among authors: liabakk nb. J Exp Med. 2005 Jun 20;201(12):2011-21. doi: 10.1084/jem.20050042. J Exp Med. 2005. PMID: 15967827 Free PMC article.

5

A combined nuclear and nucleolar localization motif in activation-induced cytidine deaminase (AID) controls immunoglobulin class switching.

Hu Y, Ericsson I, Torseth K, Methot SP, Sundheim O, Liabakk NB, Slupphaug G, Di Noia JM, Krokan HE, Kavli B. Hu Y, et al. Among authors: liabakk nb. J Mol Biol. 2013 Jan 23;425(2):424-43. doi: 10.1016/j.jmb.2012.11.026. Epub 2012 Nov 23. J Mol Biol. 2013. PMID: 23183374

6

Identification of a novel, widespread, and functionally important PCNA-binding motif.

Gilljam KM, Feyzi E, Aas PA, Sousa MM, Müller R, Vågbø CB, Catterall TC, Liabakk NB, Slupphaug G, Drabløs F, Krokan HE, Otterlei M. Gilljam KM, et al. Among authors: liabakk nb. J Cell Biol. 2009 Sep 7;186(5):645-54. doi: 10.1083/jcb.200903138. J Cell Biol. 2009. PMID: 19736315 Free PMC article.

7

An inverse switch in DNA base excision and strand break repair contributes to melphalan resistance in multiple myeloma cells.

Sousa MM, Zub KA, Aas PA, Hanssen-Bauer A, Demirovic A, Sarno A, Tian E, Liabakk NB, Slupphaug G. Sousa MM, et al. Among authors: liabakk nb. PLoS One. 2013;8(2):e55493. doi: 10.1371/journal.pone.0055493. Epub 2013 Feb 6. PLoS One. 2013. PMID: 23405159 Free PMC article.

8

Cell cycle-specific UNG2 phosphorylations regulate protein turnover, activity and association with RPA.

Hagen L, Kavli B, Sousa MM, Torseth K, Liabakk NB, Sundheim O, Pena-Diaz J, Otterlei M, Hørning O, Jensen ON, Krokan HE, Slupphaug G. Hagen L, et al. Among authors: liabakk nb. EMBO J. 2008 Jan 9;27(1):51-61. doi: 10.1038/sj.emboj.7601958. Epub 2007 Dec 13. EMBO J. 2008. PMID: 18079698 Free PMC article.

9

Activation-induced cytidine deaminase (AID) is localized to subnuclear domains enriched in splicing factors.

Hu Y, Ericsson I, Doseth B, Liabakk NB, Krokan HE, Kavli B. Hu Y, et al. Among authors: liabakk nb. Exp Cell Res. 2014 Mar 10;322(1):178-92. doi: 10.1016/j.yexcr.2014.01.004. Epub 2014 Jan 13. Exp Cell Res. 2014. PMID: 24434356 Free article.

10

Nucleotide excision repair is associated with the replisome and its efficiency depends on a direct interaction between XPA and PCNA.

Gilljam KM, Müller R, Liabakk NB, Otterlei M. Gilljam KM, et al. Among authors: liabakk nb. PLoS One. 2012;7(11):e49199. doi: 10.1371/journal.pone.0049199. Epub 2012 Nov 13. PLoS One. 2012. PMID: 23152873 Free PMC article.

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