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Selected Publications

Somatic Hypermutation Group

  1. Diaz, M., and Flajnik, M.F., 1998. Evolution of somatic hypermutation and gene conversion in adaptive immunity.  Immunol. Rev. 162: 13-24.[Abstract ]
  2. Diaz, M., Greenberg, A.S., and Flajnik, M.F., 1998.  Somatic hypermutation of the new antigen receptor gene (NAR) in the nurse shark does not generate the repertoire: Possible role in antigen-driven reactions in the absence of germinal centers. Proc. Natl. Acad. Sci. USA 95: 14343-14348.[Abstract ]
  3. Diaz, M., Velez, J., Singh, M., Cerny, J., and Flajnik, M.F., 1999. Mutational pattern of the nurse shark antigen receptor gene (NAR) is similar to that of mammalian Ig genes and to spontaneous mutations in evolution: the translesion synthesis model of somatic hypermutation.  Internat. Immunol. 11: 825-833.[Abstract ]
  4. Diaz, M., and Klinman, N.R., 2000. Relative roles of somatic and Darwinian evolution in shaping the antibody response. Immunol. Res. 3: 89-102.[Abstract ]
  5. Diaz M., Flajnik M.F., and Klinman, N.R., 2001.  Evolution and the molecular basis of somatic hypermutation of antigen receptor genes. Phil. Trans. Roy. Soc. Lond. B 356: 67-72.  [Abstract ]
  6. Rumfelt, L.L., Avila, D., Diaz, M.,  Bartl, S., McKinney, E.C., and Flajnik, M., 2001. A shark antibody heavy chain encoded by a non-somatically rearranged VDJ is preferentially expressed in early development and is convergent with mammalian IgG. Proc. Natl. Acad. Sci. USA 98: 1775-1780.[Abstract ]
  7. Zan, H., Komori, A., Li, Z., Cerutti, A., Schaffer, A., Flajnik, M.F., Diaz, M., and Casali, P., 2001. The translesion DNA polymerase z plays a major role in Ig and bcl-6 somatic hypermutation.  Immunity 14: 643-653.[Abstract ]
  8. Diaz, M., Verkoczy, L., Flajnik, M., and Klinman, N.F., 2001.  Decreased frequency of somatic hypermutation and impaired affinity maturation, but intact germinal center formation in mice expressing antisense RNA to DNA polymerase z.  J. Immunol. 167: 327-335.[Abstract ]
  9. Diaz, M., and Casali, P., 2002. Somatic immunoglobulin hypermutation. Curr. Opinion Immunol. 14: 235-240.[Abstract ]
  10. Diaz, M., Stanfield, R.L., Greenberg, A.S., and Flajnik, M.F., 2002. Structural analysis, selection, and ontogeny of the shark new antigen receptor (IgNAR): Identification of a new locus preferentially expressed in early development. Immunogenetics,  54:501-512.[Abstract ]
  11. Kunkel, T.A., and Diaz, M., 2002. Enzymatic cytosine deamination: friend and foe. Mol Cell. 10:962-963.[Abstract ]
  12. Bartl, S.,  Baish, M., Weissman, I.L., and Diaz, M., 2002. Did the molecules of adaptive immunity evolve from the innate immune system? Integrative and Comparative Biology 43: 338–346.
  13. Diaz, M., and Storb, U., 2003. A novel cytidine deaminase AIDs in the delivery of error-prone polymerases to immunoglobulin genes. DNA Repair, 2: 623-627.[Abstract ]
  14. Diaz, M., and Verkoczy, L., 2003.  Evolution of somatic hypermutation of antigen receptor genes.  Encyclopedia of the Human Genome. Nature Publishing Group.
  15. Diaz, M., Ray, M., Wheeler, L.J., Verkoczy, L.K., and Mathews, C.K., 2003. Mutagenesis by AID, a molecule critical to immunoglobulin hypermutation, is not caused by an alteration of the precursor nucleotide pool. Mol Immunol. 40:261-268.[Abstract ]
  16. Diaz, M., Watson, N.B., Turkington, G., Verkoczy, L.K., Klinman, N.R., and McGregor, W., 2003. Decreased frequency and highly aberrant spectrum of ultraviolet-induced mutations in the hprt gene of mouse fibroblasts expressing antisense RNA to DNA polymerase zeta.  Mol Cancer Res.  1:836-847.[Abstract ]
  17. Rogozin, I.B., and Diaz, M., 2004. Cutting edge: DGYW/WRCH is a better predictor of mutability at G:C bases in Ig hypermutation than the widely accepted RGYW/WRCY motif and probably reflects a two-step activation-induced cytidine deaminase-triggered process. J Immunol. 172:3382-3384.[Abstract ]
  18. Rumfelt, L.L., Diaz, M., Lohr, R.L., Mochon, E., and Flajnik, M.F., 2004. Unprecedented multiplicity of Ig transmembrane and secretory mRNA forms in the cartilaginous fish. J Immunol. 173:1129-1139.[Abstract ]
  19. Brar, S.S., Watson, M., and Diaz, M., 2004. Activation-induced cytosine deaminase, AID, is actively exported out of the nucleus but retained by the induction of DNA breaks. J Biol Chem. 279:26395-26401.[Abstract ]
  20. Diaz, M., and Lawrence, C., 2005. An update on the role of translesion synthesis DNA polymerases in Ig hypermutation. Trends Immunol. 26:215-220.[Abstract ]
  21. Xiao, Z., and Diaz, M., 2005.  In Trends in Immunology Research, Chapter 7: Somatic Immunoglobulin Hypermutation in the Memory B Cell Response, editor: Veskler, B. A. (Nova Science, Hauppauge NY) pp 135-146.
  22. Xiao, Z., Ray, M., Jiang, C., Clark, A.B., Rogozin, I.B., and Diaz, M., 2007. Known components of the immunoglobulin A:T mutational machinery are intact in Burkitt lymphoma cell lines with G:C bias. Mol Immunol. 44:2659-2666.[Abstract ]
  23. Brar, S.S., Sacho, E., Tessmer, I., Croteau, D.L., Erie, D.A., and Diaz, M., 2007. Activation-induced deaminase, AID, is catalytically active as a monomer on single-stranded DNA. DNA Repair (Amst). 2008 Jan 1;7(1):77-87.[Abstract ]
  24. Jiang, C., Foley, J., Clayton, N., Joniken, M., Herbert, R., and Diaz, M., 2007. Abrogation of lupus nephritis in activation-induced deaminase (AID)-deficient MRL/lpr Mice. J Immunol 178:7422-7431.[Abstract ]
  25. Brar, S.S., Sacho, E.J., Tessmer, I., Croteau, D.L., Erie, D.A., and Diaz, M., 2008. Activation-induced deaminase AID, is catalytically active as a monomer on single-stranded DNA. 7(1):77-87.[Abstract ]
  26. Jiang, C., Zhao, M.L., and Diaz, M., 2009. Activation-induced deaminase heterozygous MRL/lpr mice are delayed in the production of high-affinity pathogenic antibodies and in the development of lupus nephritis. Immunology. 126(1):102-113.[Abstract ]
  27. Verkoczy L, Chen Y, Bouton-Verbille H, Zhang J, Diaz M, Hutchinson J, Ouyang YB, Alam SM, Holl TM, Hwang KK, Kelsoe G, Haynes BF.  Rescue of HIV-1 Broad Neutralizing Antibody-Expressing B cells in 2F5 VH/VL Knock-in Mice Reveals Multiple Tolerance Controls. Journal of Immunology 2011 187(7):3785-97. [Abstract ]
  28. Jiang, C., Zhao, M.L., Scearce, R.M., and Diaz, M., 2011. Activation-induced deaminase-deficient MRL/lpr mice secrete high levels of protective antibodies against lupus nephritis. Arthritis and rheumatism. 63(4):1086-1095.[Abstract ]
  29. Daly J, Bebenek K, Watt DL, Richter K, Jiang C, Zhao ML, Ray M, McGregor WG, Kunkel TA, Diaz M, 2012. Altered Ig Hypermutation Pattern and Frequency in Complementary Mouse Models of DNA Polymerase ζ Activity.  J Immunol. ;188(11):5528-37.[Abstract ]
  30. Jiang C, Zhao ML, Waters KM, Diaz M, 2012. Activation-induced deaminase contributes to the antibody-independent role of B cells in the development of autoimmunity. Autoimmunity 2012 45(6):440-8.[Abstract ]
  31. Richter K, Burch L, Chao F, Henke D, Jiang C, Daly J, Zhao ML, Kissling G, Diaz M. 2012. Altered pattern of immunoglobulin hypermutation in mice deficient in Slip-GC protein. J Biol Chem 287(38):31856-31865.[Abstract ]
  32. Diaz M. 2013. The role of activation-induced deaminase in lupus nephritis. Autoimmunity 46(2):115-120.[Abstract ]

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