Selected Publications

  • Beermann, M.L., Homma, S., and Miller, J.B. (2022) Proximity ligation assay to detect DUX4 protein in FSHD1 muscle: A pilot study. BMC Research Notes 15:163. online access
  • Masteika, I. F., Sathya, A., Homma, S., Miller, B.M., Boyce, F.M., and Miller, J.B. (2022) Downstream events initiated by expression of FSHD-associated DUX4: Studies of nucleocytoplasmic transport, γH2AX accumulation, and Bax/Bak-dependence. Biology Open vol. 11, bio059145 online access
  • Mitsuhashi, H., Homma, S., Beermann, M.L., Ishimaru, S., Takeda, H., Yu, B.K., Liu, K., Duraiswamy, S., Boyce, F.M., and Miller, J.B. (2019) Efficient system for upstream mRNA trans-splicing to generate covalent, head-to-tail, protein multimers. Scientific Reports 9:2274 pp. 1-15. online access 
  •  Mitsuhashi, H., Ishimaru, S., Homma, S., Yu, B., Honma, Y., Beermann, J.L., and Miller, J.B. (2018) Functional domains of the FSHD-associated DUX4 protein. Biology Open Apr 4. pii: bio.033977. doi: 10.1242/bio.033977. online access 
  • Yoon, S., Beermann, M.L., Yu, B., Shao, D., Bachschmid, M., and Miller, J.B. (2018) Aberrant caspase activation in laminin-α2-deficient human myogenic cells is mediated by p53 and sirtuin activity. Journal of Neuromuscular Diseases. 5:59-73. online publication Dec 20, 2017 doi: 10.3233/JND-170262. PubMed PMID: 29278895. online access
  • Homma, S., Beermann, M.L., Yu, B., Boyce, F.M., and Miller, J.B. (2016) Nuclear bodies reorganize during myogenesis and are differentially disrupted by expression of FSHD-associated DUX4. Skeletal Muscle vol. 6, paper 42, pp 1-16.  online access
  • Jones. T.I., King, O.D., Himeda, C.L., Homma, S., Chen, J.C.J., Beermann, M.L., Yan, C., Emerson, C.P., Miller, J.B., Wagner, K.R., Jones, P.L. (2015) Individual epigenetic status of the pathogenic D4Z4 macrosatellite correlates with disease in facioscapulohumeral muscular dystrophy. Clinical Epigenetics Vol. 7, paper 37, pp 1-22online access
  • Homma, S., Beermann, M.L., Boyce, F., and Miller, J.B. (2015) Expression of FSHD-associated DUX4-FL alters proteostasis and induces TDP-43 aggregation. Ann. Clin. Transl. Neurol. 2:151-166 online access This paper was profiled in FSH Watch (Winter 2015, p.5)
  • Himeda, C., Debarnot, C., Homma, S., Beermann, M.L., Miller, J.B., Jones, P.L., and Jones, T.I. (2014) Myogenic enhancers regulate expression of the facioscapulohumeral muscular dystrophy associated DUX4 gene. Mol. Cell. Biol. 34:1942-1955  This paper was profiled in FSH Watch (Spring 2014, p.15)
  • Yoon, S., Stadler, G., Beermann, M.L., Schmidt, E.V., Windelborn, J.A., Wright, W.E., and Miller, J.B. (2013) Immortalized myogenic cells from Congenital Muscular Dystrophy Type1A patients recapitulate aberrant caspase activation in pathogenesis: A new tool for MDC1A research. Skeletal Muscle 3:28 (6 December 2013)(Read the article)
  • Jones, T.I., Chen, J.C.J., Rahimov, F., Homma, S., Arashiro, P., Beermann, M.L., King, O.D., Miller, J.B., Kunkel, L.M., Emerson, C.P., Wagner, K.R., and Jones, P.L. (2012) Facioscapulohumeral muscular dystrophy family studies of DUX4 expression: Evidence for disease modifiers and a quantitative model of pathogenesis. Hum. Mol. Genet. 21:4419-4430. (Abstract from PubMed). This paper was profiled in MDA Quest magazine.
  • Homma, S., Chen, J.C.J., Rahimov, F., Beermann, M.L., Hanger, K., Bibat, G.M., Wagner, K.R., Kunkel, L.M., Emerson, C.P., and Miller, J.B. (2012) A unique library of myogenic cells from facioscapulohumeral muscular dystrophy subjects and unaffected relatives: Family, disease, and cell function. Eur. J. Hum. Genet. 20:404-410 (Abstract from PubMed)
  • Homma, S., Beermann, M.L., and Miller, J.B. (2011) Peripheral nerve pathology, including aberrant Schwann cell differentiation, is ameliorated by doxycycline in a laminin-alpha2-deficient mouse model of congenital muscular dystrophy. Hum. Mol. Genet. 20:2662-2672 (Abstract from PubMed)
  • Beermann, M.L., Ardelt, M.A., Girgenrath, M., and Miller, J.B. (2010) Prdm1 (Blimp-1) and the expression of fast and slow myosin heavy chain isoforms during avian myogenesis. PLoS One 5(4): e9951.
  • Vishnudas, V.K. and Miller, J. B. (2009) Interaction of Ku70 with Bax regulates pathogenesis in laminin-alpha2-deficient human muscle cell and mouse models of congenital muscular dystrophy. Hum. Mol. Genet. 18:4467-4477. (Full text from PubMed Central)
  • Girgenrath, M., Beermann, M. L., Vishnudas, V. K., Homma, S., and Miller, J. B. (2008) Pathology is alleviated by doxycycline in a laminin-alpha2-deficient mouse model of congenital muscular dystrophy. Ann. Neurol. 65:47-56 (Published Online: Dec 11, 2008 DOI: 10.1002/ana.21523) (Full text from PubMed Central) *This paper was selected as a research highlight by Nature Reviews Neurology and was profiled in MDA Quest magazine.
  • Girgenrath, M., Weng, S., Kostek, C. A., Browning, B., Wang, M., Brown, S.A., Winkles, J. A., Michaelson, J. S., Allaire, N; Schneider, P., Scott, M., Hsu, Y-M., Yagita, H., Flavell, R. A., Miller, J. B., Burkly, L. C., and Zheng, T. S. (2006) TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration. EMBO J. 25:5826–5839.
  • Miller, J. B. and Girgenrath, M. (2006) Role of apoptosis in neuromuscular diseases and potential usefulness of anti-apoptosis therapy. Trends Mol. Med. 12:279-286.
  • Dominov, J. A., Kravetz, A. J., Ardelt, M., Kostek, C. A., Beermann, M. L., Miller, J. B. (2005) Muscle-specific BCL2 expression ameliorates muscle disease in laminin-alpha2-deficient, but not dystrophin-deficient, mice. Hum Mol Genet. 14(8):1029-40.
  • Girgenrath, M., Kostek, C. A., and Miller, J. B. (2005) Diseased muscles that lack dystrophin or laminin-alpha2 have altered compositions and proliferation of resident stem cells. BMC Neurol. Vol. 5, paper 7 (pp1-10)
  • Girgenrath, M., Dominov, J. A., Kostek, C. A., Miller, J. B. (2004) Inhibition of apoptosis improves outcome in a model of congenital muscular dystrophy. J Clin Invest. 114(11):1635-1639. This paper was profiled in MDA Quest magazine (vol. 12, no. 1. Jan. 2005)
  • Nowak, J. A., Malowitz, J., Girgenrath, M., Kostek, C. A., Kravetz, A. J., Dominov, J. A., Miller, J. B. (2004) Immortalization of mouse myogenic cells can occur without loss of p16INK4a, p19ARF, or p53 and is accelerated by inactivation of Bax. BMC Cell Biol. 5(1):1-14.
  • Lykke-Andersen, K, Schaefer, L., Menon, S., Deng, X.-W., Miller, J. B. and Wei, N. (2003). Disruption of COP9 subunit Csn2 in mouse causes deficient cell proliferation, accumulation of p53 and cyclin E, and early embryonic death. Mol. Cell. Biol. 23:6790-6797.
  • Pavlath, G. K., Dominov, J. A., Kegley, K. M., and Miller, J. B. (2003) Regeneration of skeletal muscles with altered timing of expression of the myogenic bHLH factor MRF4. Am. J. Pathol. 162:1685-1691.
  • Kostek, C., Dominov, J.A., and Miller, J.B. (2002) Upregulation of MHC class I accompanies, but is not required for, spontaneous myopathy in dysferlin-deficient SJL/J mice. Am. J. Pathol. 160:833-839.
  • Miller, J. B. (2001) Developmental biology of skeletal muscle. In: Disorders of Voluntary Muscle, 7th edition (Camb. U. Press) Eds. G. Karpati, R.C. Griggs & D. Hilton-Jones pp 26-41.
  • Dominov, J.A., Houlihan-Kawamoto C. A., Swap C. J., and Miller, J.B. (2001). Pro- and anti-apototic members of the Bcl-2 family in skeletal muscle: A distinct role for Bcl-2 in later stages of myogenesis. Dev. Dynam. 220:18-26.
  • Schaefer, L., Engman, H., and Miller, J. B. (2000). Coding sequence, chromosomal localization, and expression pattern of Nrf1: the mouse homolog of Drosophila erect-wing. Mammalian Genome 11:104-110.
  • Schaefer, L., Beermann, M. L., and Miller, J. B. (1999). Coding sequence, genomic organization, chromosomal localization, and expression pattern of the signalosome component Cops2: The mouse homologue of Drosophila alien. Genomics 56:310-316.
  • Miller, J. B., Schaefer, L., and Dominov, J. A. (1999) Seeking muscle stem cells. Curr. Top. Dev. Biol. 43, 191-219.
  • Dominov, J.A., Dunn, J.J., and Miller, J.B. (1998) Bcl-2 expression identifies an early stage of myogenesis and promotes clonal expansion of muscle cells. J. Cell Biol. 142:537-544.
  • Zhu, Z. and Miller, J.B. (1997) MRF4 can substitute for myogenin during early stages of myogenesis. Dev. Dynam. 209:233-241.
  • Mei, L., Kachinsky, A. M., Seiden, J. E., Kuncl, R.W., Miller, J. B. and Huganir, R. L. (1996) Differential expression of PTP1D, a protein tyrosine phosphatase with two SH2 domains, in a slow and fast skeletal muscle fibers. Exp. Cell Res. 224:379-390.
  • Nikovits, W., Wang, G., Feldman, J. L., Miller, J. B., Wade, R., Nelson, L., and Stockdale, F. E. (1996) Isolation and characterization of an avian slow myosin heavy chain gene expressed during embryonic skeletal muscle fiber formation. J. Biol. Chem. 271:17047-53.
  • Dominov, J.A. and Miller, J.B. (1996) POU homeodomain genes and myogenesis. Dev. Genet. 19:108-118.
  • Block, N.E., Zhu, Z., Kachinsky, A.M., Dominov, J.A., and Miller, J.B. (1996) Acceleration of somitic myogenesis in embryos of myogenin promoter-MRF4 transgenic mice. Dev. Dynam. 207:382-394.
  • Miller, J.B. (1995) Making one cell from two. Nature 377:575-576.
  • Miller, J.B. and Boyce, F.M. (1995) Gene therapy by and for muscles. Trends Genet. 11:163-165.
  • Smith, T.H. and Miller, J.B. (1994) Somite subdomains, muscle cell origins, and the four muscle regulatory factor proteins. J. Cell Biol. 127, 95-105.
  • Smith, T.H., Block, N.E., Rhodes, S.J., Konieczny, S.F. and Miller, J.B. (1993) A unique pattern of expression of the four muscle regulatory factors distinguishes somitic from embryonic, fetal, and newborn mouse myogenic cells. Development 117:1125-1133.
  • Miner, J.H., Miller, J.B., and Wold, B.J. (1992) Skeletal muscle phenotypes initiated by ectopic MyoD in transgenic mouse hearts. Development 114:853-860.
  • Miller, J.B. (1992) Myoblast diversity in skeletal myogenesis: How much and to what end? Cell 69:1-3.
  • Block, N.E. and Miller, J.B. (1992) MRF4, a myogenic helix-loop-helix protein, produces multiple changes in the myogenic program of BC3H-1 cells. Mol. Cell. Biol. 12:2484-2492.