Strange India All Strange Things About India and world


  • 1.

    Muramatsu, M. et al. Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme. Cell 102, 553–563 (2000).

    CAS 
    Article 

    Google Scholar 

  • 2.

    Feng, Y., Seija, N., JM, D. I. N. & Martin, A. AID in antibody diversification: there and back again. Trends Immunol. 41, 586–600 (2020).

    CAS 
    Article 

    Google Scholar 

  • 3.

    Cascalho, M., Wong, J., Steinberg, C. & Wabl, M. Mismatch repair co-opted by hypermutation. Science 279, 1207–1210 (1998).

    ADS 
    CAS 
    Article 

    Google Scholar 

  • 4.

    Di Noia, J. & Neuberger, M. S. Altering the pathway of immunoglobulin hypermutation by inhibiting uracil-DNA glycosylase. Nature 419, 43–48 (2002).

    ADS 
    Article 

    Google Scholar 

  • 5.

    Wiesendanger, M., Kneitz, B., Edelmann, W. & Scharff, M. D. Somatic hypermutation in MutS homologue (MSH)3-, MSH6-, and MSH3/MSH6-deficient mice reveals a role for the MSH2-MSH6 heterodimer in modulating the base substitution pattern. J. Exp. Med. 191, 579–584 (2000).

    CAS 
    Article 

    Google Scholar 

  • 6.

    Rada, C., Di Noia, J. M. & Neuberger, M. S. Mismatch recognition and uracil excision provide complementary paths to both Ig switching and the A/T-focused phase of somatic mutation. Mol. Cell 16, 163–171 (2004).

    CAS 
    Article 

    Google Scholar 

  • 7.

    Rada, C. et al. Immunoglobulin isotype switching is inhibited and somatic hypermutation perturbed in UNG-deficient mice. Curr. Biol. 12, 1748–1755 (2002).

    CAS 
    Article 

    Google Scholar 

  • 8.

    Guo, C. et al. Ugene, a newly identified protein that is commonly overexpressed in cancer and binds uracil DNA glycosylase. Cancer Res. 68, 6118–6126 (2008).

    CAS 
    Article 

    Google Scholar 

  • 9.

    Muramatsu, M. et al. Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells. J. Biol. Chem. 274, 18470–18476 (1999).

    CAS 
    Article 

    Google Scholar 

  • 10.

    Lawson, K. A. et al. Functional genomic landscape of cancer-intrinsic evasion of killing by T cells. Nature 586, 120–126 (2020).

    ADS 
    CAS 
    Article 

    Google Scholar 

  • 11.

    Pan-Hammarstrom, Q. et al. Impact of DNA ligase IV on nonhomologous end joining pathways during class switch recombination in human cells. J. Exp. Med. 201, 189–194 (2005).

    Article 

    Google Scholar 

  • 12.

    Ward, I. M. et al. 53BP1 is required for class switch recombination. J. Cell Biol. 165, 459–464 (2004).

    CAS 
    Article 

    Google Scholar 

  • 13.

    Yan, C. T. et al. IgH class switching and translocations use a robust non-classical end-joining pathway. Nature 449, 478–482 (2007).

    ADS 
    CAS 
    Article 

    Google Scholar 

  • 14.

    Perez-Duran, P. et al. UNG shapes the specificity of AID-induced somatic hypermutation. J. Exp. Med. 209, 1379–1389 (2012).

    CAS 
    Article 

    Google Scholar 

  • 15.

    Frieder, D., Larijani, M., Collins, C., Shulman, M. & Martin, A. The concerted action of Msh2 and UNG stimulates somatic hypermutation at A.T base pairs. Mol. Cell. Biol. 29, 5148–5157 (2009).

    CAS 
    Article 

    Google Scholar 

  • 16.

    Thientosapol, E. S. et al. Proximity to AGCT sequences dictates MMR-independent versus MMR-dependent mechanisms for AID-induced mutation via UNG2. Nucleic Acids Res. 45, 3146–3157 (2017).

    CAS 
    PubMed 

    Google Scholar 

  • 17.

    Martin, A. et al. Msh2 ATPase activity is essential for somatic hypermutation at a-T basepairs and for efficient class switch recombination. J. Exp. Med. 198, 1171–1178 (2003).

    CAS 
    Article 

    Google Scholar 

  • 18.

    Phung, Q. H. et al. Increased hypermutation at G and C nucleotides in immunoglobulin variable genes from mice deficient in the MSH2 mismatch repair protein. J. Exp. Med. 187, 1745–1751 (1998).

    CAS 
    Article 

    Google Scholar 

  • 19.

    Delbos, F., Aoufouchi, S., Faili, A., Weill, J. C. & Reynaud, C. A. DNA polymerase eta is the sole contributor of A/T modifications during immunoglobulin gene hypermutation in the mouse. J. Exp. Med. 204, 17–23 (2007).

    CAS 
    Article 

    Google Scholar 

  • 20.

    Arakawa, H., Saribasak, H. & Buerstedde, J. M. Activation-induced cytidine deaminase initiates immunoglobulin gene conversion and hypermutation by a common intermediate. PLoS Biol. 2, E179 (2004).

    Article 

    Google Scholar 

  • 21.

    Di Noia, J. M. & Neuberger, M. S. Immunoglobulin gene conversion in chicken DT40 cells largely proceeds through an abasic site intermediate generated by excision of the uracil produced by AID-mediated deoxycytidine deamination. Eur. J. Immunol. 34, 504–508 (2004).

    Article 

    Google Scholar 

  • 22.

    Campo, V. A. et al. MSH6- or PMS2-deficiency causes re-replication in DT40 B cells, but it has little effect on immunoglobulin gene conversion or on repair of AID-generated uracils. Nucleic Acids Res. 41, 3032–3046 (2013).

    CAS 
    Article 

    Google Scholar 

  • 23.

    Di Noia, J. M., Rada, C. & Neuberger, M. S. SMUG1 is able to excise uracil from immunoglobulin genes: insight into mutation versus repair. EMBO J. 25, 585–595 (2006).

    Article 

    Google Scholar 

  • 24.

    Wang, Q. et al. The cell cycle restricts activation-induced cytidine deaminase activity to early G1. J. Exp. Med. 214, 49–58 (2017).

    CAS 
    Article 

    Google Scholar 

  • 25.

    Cappelli, E. et al. Rates of base excision repair are not solely dependent on levels of initiating enzymes. Carcinogenesis 22, 387–393 (2001).

    CAS 
    Article 

    Google Scholar 

  • 26.

    Krusong, K., Carpenter, E. P., Bellamy, S. R., Savva, R. & Baldwin, G. S. A comparative study of uracil-DNA glycosylases from human and herpes simplex virus type 1. J. Biol. Chem. 281, 4983–4992 (2006).

    CAS 
    Article 

    Google Scholar 

  • 27.

    Krokan, H. E. et al. Error-free versus mutagenic processing of genomic uracil–relevance to cancer. DNA Repair 19, 38–47 (2014).

    CAS 
    Article 

    Google Scholar 

  • 28.

    Zeng, X. et al. DNA polymerase eta is an A–T mutator in somatic hypermutation of immunoglobulin variable genes. Nat. Immunol. 2, 537–541 (2001).

    CAS 
    Article 

    Google Scholar 

  • 29.

    Belcheva, A. et al. Gut microbial metabolism drives transformation of MSH2-deficient colon epithelial cells. Cell 158, 288–299 (2014).

    CAS 
    Article 

    Google Scholar 

  • 30.

    Ramachandran, S. et al. The SAGA deubiquitination module promotes DNA repair and class switch recombination through ATM and DNAPK-mediated γH2AX formation. Cell Rep. 15, 1554–1565 (2016).

    CAS 
    Article 

    Google Scholar 

  • 31.

    Aregger, M., Chandrashekhar, M., Tong, A. H. Y., Chan, K. & Moffat, J. Pooled lentiviral CRISPR–Cas9 screens for functional genomics in mammalian cells. Methods Mol. Biol. 1869, 169–188 (2019).

    CAS 
    Article 

    Google Scholar 

  • 32.

    Sarno, A. et al. Uracil–DNA glycosylase UNG1 isoform variant supports class switch recombination and repairs nuclear genomic uracil. Nucleic Acids Res. 47, 4569–4585 (2019).

    CAS 
    Article 

    Google Scholar 

  • 33.

    Li, C. et al. The H2B deubiquitinase Usp22 promotes antibody class switch recombination by facilitating non-homologous end joining. Nat. Commun. 9, 1006 (2018).

    ADS 
    Article 

    Google Scholar 

  • 34.

    Li, C. et al. Early-life programming of mesenteric lymph node stromal cell identity by the lymphotoxin pathway regulates adult mucosal immunity. Sci. Immunol. 4, aax1027 (2019).

    Article 

    Google Scholar 

  • 35.

    Liu, M. et al. Two levels of protection for the B cell genome during somatic hypermutation. Nature 451, 841–845 (2008).

    ADS 
    CAS 
    Article 

    Google Scholar 

  • 36.

    Siriwardena, S. U., Perera, M. L. W., Senevirathne, V., Stewart, J. & Bhagwat, A. S. A tumor-promoting phorbol ester causes a large increase in APOBEC3A expression and a moderate increase in APOBEC3B expression in a normal human keratinocyte cell line without increasing genomic uracils. Mol. Cell. Biol. 39, e00238-18 (2019).

    CAS 
    Article 

    Google Scholar 

  • 37.

    So, C. C., Ramachandran, S. & Martin, A. E3 ubiquitin ligases RNF20 and RNF40 are required for double-stranded break (DSB) repair: evidence for monoubiquitination of histone H2B lysine 120 as a novel axis of DSB signaling and repair. Mol. Cell. Biol. 39, e00488-18 (2019).

    CAS 
    Article 

    Google Scholar 

  • 38.

    Boulianne, B. et al. AID-expressing germinal center B cells cluster normally within lymph node follicles in the absence of FDCM1+ CD35+ follicular dendritic cells but dissipate prematurely. J. Immunol. 191, 4521–4530 (2013).

    CAS 
    Article 

    Google Scholar 



  • Source link

    Leave a Reply

    Your email address will not be published. Required fields are marked *