Bio

Michael March, Research Scientist

Michael March is a Research Scientist who joined CAG in July of 2010. He currently plays two roles for the Center - he designs and performs molecular and cell biology experiments in order to expand the results of our genetics analyses with functional biological data. He has also worked to implement the computer code used to perform phenome-wide association studies (PheWAS) and apply the PheWAS approach to the CAG patient database.

His focus at CAG has been primarily the study of asthma. He has contributed functional data to a collaboration that identified the CDHR3 gene as a susceptibility locus for asthma exacerbations (Bønnelykke et al., 2014), as well as analysis to a second collaboration examining the effects of stress on the response to asthma medications (Brehm et al., 2015). He has also authored several review articles about the genetics of asthma.

He earned a Bachelor of Science degree from Ursinus College in 1996 with a major in Biology. He earned a Ph.D. in 2003 from the Department of Microbiology at the University of Virginia, where he studied the inhibition of B cell signaling cascades by the inositol phosphatase SHIP in the laboratory of Dr. Kodimangalam Ravichandran.

After earning his doctorate, and before joining CAG, he was a post-doctoral fellow at the National Institutes of Health, in the laboratory of Dr. Eric Long. While at NIH, his research focused on the role of the integrin LFA-1 in the activation of human natural killer cells. He designed an experimental system that allowed the unbiased identification of signaling molecules activated by LFA-1, alone and in combination with other NK cell receptors. His group identified a pathway dependent on paxillin that controls lytic granule movement in NK cells, and described the unexpected dependence of this pathway on ITAM-dependent signaling (March et al, 2010). This work has continued in Dr. Long’s laboratory, and the system has led to further publications (Zhang et al. 2014).

Publications

CAG Publications**

**An updated list of publications is available at My NCBI Collections.

Roles of Lck, Syk and ZAP-70 tyrosine kinases in TCR-mediated phosphorylation of the adapter protein Shc.
Walk SF, March ME, Ravichandran KS.
Eur J Immunol. 1998 Aug;28(8):2265-75.



The genetics of asthma and allergic disorders.
March ME, Sleiman PM, Hakonarson H.
Discov Med. 2011 Jan;11(56):35-45. Review.



Use of transfected Drosophila S2 cells to study NK cell activation.
March ME, Gross CC, Long EO.
Methods Mol Biol. 2010;612:67-88. doi: 10.1007/978-1-60761-362-6_6.



Recruitment of activation receptors at inhibitory NK cell immune synapses.
Schleinitz N, March ME, Long EO.
PLoS One. 2008 Sep 26;3(9):e3278. doi: 10.1371/journal.pone.0003278.



Activation, coactivation, and costimulation of resting human natural killer cells.
Bryceson YT, March ME, Ljunggren HG, Long EO.
Immunol Rev. 2006 Dec;214:73-91. Review.



Synergy among receptors on resting NK cells for the activation of natural cytotoxicity and cytokine secretion.
Bryceson YT, March ME, Ljunggren HG, Long EO.
Blood. 2006 Jan 1;107(1):159-66. Epub 2005 Sep 8.



Cytolytic granule polarization and degranulation controlled by different receptors in resting NK cells.
Bryceson YT, March ME, Barber DF, Ljunggren HG, Long EO.
J Exp Med. 2005 Oct 3;202(7):1001-12.



Regulation of the immune response by SHIP.
March ME, Ravichandran K.
Semin Immunol. 2002 Feb;14(1):37-47. Review.



p135 src homology 2 domain-containing inositol 5'-phosphatase (SHIPbeta ) isoform can substitute for p145 SHIP in fcgamma RIIB1-mediated inhibitory signaling in B cells.
March ME, Lucas DM, Aman MJ, Ravichandran KS.
J Biol Chem. 2000 Sep 29;275(39):29960-7.



Essential role for the C-terminal noncatalytic region of SHIP in FcgammaRIIB1-mediated inhibitory signaling.
Aman MJ, Walk SF, March ME, Su HP, Carver DJ, Ravichandran KS.
Mol Cell Biol. 2000 May;20(10):3576-89.



Stress and Bronchodilator Response in Children with Asthma.
Brehm JM, Ramratnam SK, Tse SM, Croteau-Chonka DC, Pino-Yanes M, Rosas-Salazar C, Litonjua AA, Raby BA, Boutaoui N, Han YY, Chen W, Forno E, Marsland AL, Nugent NR, Eng C, Colón-Semidey A, Alvarez M, Acosta-Pérez E, Spear ML, Martinez FD, Avila L, Weiss ST, et al.
Am J Respir Crit Care Med. 2015 Jul 1;192(1):47-56. doi: 10.1164/rccm.201501-0037OC.



A signaling network stimulated by β2 integrin promotes the polarization of lytic granules in cytotoxic cells.
Zhang M, March ME, Lane WS, Long EO.
Sci Signal. 2014 Oct 7;7(346):ra96. doi: 10.1126/scisignal.2005629.



A genome-wide association study identifies CDHR3 as a susceptibility locus for early childhood asthma with severe exacerbations.
Bønnelykke K, Sleiman P, Nielsen K, Kreiner-Møller E, Mercader JM, Belgrave D, den Dekker HT, Husby A, Sevelsted A, Faura-Tellez G, Mortensen LJ, Paternoster L, Flaaten R, Mølgaard A, Smart DE, Thomsen PF, Rasmussen MA, Bonàs-Guarch S, Holst C, Nohr EA, Yadav R, March ME, et al.
Nat Genet. 2014 Jan;46(1):51-5. doi: 10.1038/ng.2830. Epub 2013 Nov 17.



Genetic polymorphisms and associated susceptibility to asthma.
March ME, Sleiman PM, Hakonarson H.
Int J Gen Med. 2013 Apr 17;6:253-65. doi: 10.2147/IJGM.S28156. Print 2013.



Meta-analysis of genome-wide association studies identifies three new risk loci for atopic dermatitis.
Paternoster L, Standl M, Chen CM, Ramasamy A, Bønnelykke K, Duijts L, Ferreira MA, Alves AC, Thyssen JP, Albrecht E, Baurecht H, Feenstra B, Sleiman PM, Hysi P, Warrington NM, Curjuric I, Myhre R, Curtin JA, Groen-Blokhuis MM, Kerkhof M, Sääf A, Franke A, et al.
Nat Genet. 2011 Dec 25;44(2):187-92. doi: 10.1038/ng.1017.



β2 integrin induces TCRζ-Syk-phospholipase C-γ phosphorylation and paxillin-dependent granule polarization in human NK cells.
March ME, Long EO.
J Immunol. 2011 Mar 1;186(5):2998-3005. doi: 10.4049/jimmunol.1002438. Epub 2011 Jan 26.