Boldin, M.P., and Baltimore, D. (2011) miRNAs, new effectors and regulators of NF-kB. Immunol Rev, In press.

Boldin, M.P.*, Taganov, K.D.* [equal contribution], Rao, D. S., Yang, L., Zhao, J. L., Kalwani, M., Garcia-Flores, Y., Luong, M, Devrekanli, A., Xu, J., Sun, G., Tay, J., Linsley, P.S., and Baltimore, D. (2011) miR-146a is a significant molecular brake on autoimmunity, myeloproliferation, and cancer in mice. J Exp Med, 208:1189-201.

Zhao J.L., Rao D.S., Boldin M.P., Taganov K.D., O'Connell, R.M., Baltimore, D. (2011) NF-kB dysregulation in miR-146a-deficient mice drives the development of myeloid malignancies. Proc Natl Acad Sci U S A, 108:9184-9.

Lu, L-F., Boldin, M.P., Chaudhry, A., Lin, L-L., Taganov, K.D., Yoshimura, A., Baltimore, D., and Rudensky, A. Y. (2010). Function of miR-146a in controlling Treg cell-mediated regulation of Th1 responses. Cell, 142:914-29.

Baltimore, D., Boldin, M.P., O'Connell, R.M., Rao, D.S., and Taganov, K.D. (2008).  MicroRNAs: novel regulators of immune cell development and function. Nature Immunology 9:839-45.

O'Connell, R.M., Rao, D.S., Chaudhuri, A. A., Boldin, M.P., Taganov, K.D., Nicoll, J., Paquette, R.N., and Baltimore D. (2008). Sustained expression of microRNA-155 in hematopoietic stem cells causes a myeloproliferative disorder. J Exp Med, 205: 585-594.

Taganov*, K.D., Boldin*, M.P. [equal contribution], and Baltimore D. (2007). MicroRNAs and immunity: tiny players in a big field. Immunity, 26:133-137

O'Connell, R.M., Taganov, K.D., Boldin, M.P., Cheng, G., and Baltimore D. (2007). MicroRNA-155 is induced during the macrophage inflammatory response. Proc Natl Acad Sci U S A, 104:1604-1609.

Taganov*, K.D., Boldin*, M.P. [equal contribution], Chang, K.J., and Baltimore, D. (2006). NF-kappaB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. Proc Natl Acad Sci U S A, 103:12481-12486.

Wallach, D., Varfolomeev, E.E., Malinin, N.L., Goltsev, Y.V., Kovalenko, A.V., and Boldin, M.P. (1999). Tumor necrosis factor receptor and Fas signaling mechanisms. Annu Rev Immunol. 17:331-367.

Malinin, N.L., Boldin, M.P., Kovalenko, A. V., and Wallach, D. (1997). MAP3K-related kinase involved in NF-kB induction by TNF, CD95 and IL-1. Nature, 385:540-544.

Boldin, M.P., Goncharov, T.M., Goltsev, Y.V., and Wallach, D. (1996). Involvement of MACH, a novel MORT1/FADD-interacting protease in Fas/APO-1- and TNF receptor-induced cell death. Cell, 85:803-815.

Varfolomeev*, E. E., Boldin*, M. P. [equal contribution], Goncharov, T. M., Wallach, D. (1996). A potential mechanism of "cross-talk" between the p55 tumor necrosis factor (TNF) receptor and Fas/APO-1: Proteins binding to the death domains of the two receptors bind also to each other. J Exp Med, 183:1271-1275.

Boldin*, M. P., Varfolomeev*, E.E. [equal contribution], Pancer, Z., Mett, I.L., Camonis, J.H., and Wallach D. (1995). A novel protein that interacts with the death domain of Fas/APO1 contains a sequence motif related to the death domain. J Biol Chem, 270:7795-7798.

Boldin*, M. P., Mett*, I. L. [equal contribution], Varfolomeev, E. E., Chumakov, I., Shemer-Avni, Y., Camonis, J. H., and Wallach, D. (1995). Self-association of the 'death domains' of the p55 tumor necrosis factor (TNF) receptor and Fas/APO1 prompts signaling for TNF and Fas/APO1 effects. J Biol Chem, 270:387-391.