Journal Articles
Blum, Stefan, Ji, Ying, Pennisi, David, Li, Zhixiu, Leo, Paul, McCombe, Pamela and Brown, Matthew A. (2018). Genome-wide association study in Guillain-Barré syndrome. Journal of Neuroimmunology, 323, 109-114. doi: 10.1016/j.jneuroim.2018.07.016
Tam, Oliver H., Pennisi, David, Wilkinson, Lorine, Little, Melissa H., Wazin, Fatima, Wan, Victor L. and Lovicu, Frank J. (2018). Crim1 is required for maintenance of the ocular lens epithelium. Experimental Eye Research, 170, 58-66. doi: 10.1016/j.exer.2018.02.012
Li, Z., Haynes, K., Pennisi, D. J., Anderson, L. K., Song, X., Thomas, G. P., Kenna, T., Leo, P. and Brown, M. A. (2017). Epigenetic and gene expression analysis of ankylosing spondylitis-associated loci implicate immune cells and the gut in the disease pathogenesis. Genes and Immunity, 18 (3), 135-143. doi: 10.1038/gene.2017.11
Iyer, Swati, Chhabra, Yash, Harvey, Tracey J., Wang, Richard, Chiu, Han Sheng, Smith, A. G., Thomas, Walter G., Pennisi, David J. and Piper, Michael (2017). CRIM1 is necessary for coronary vascular endothelial cell development and homeostasis. Journal of Molecular Histology, 48 (1), 53-61. doi: 10.1007/s10735-016-9702-3
Pennisi, David J. (2016). Towards consensus on coronary vessel development: coronary arterial endothelial cells derive primarily from the sinus venosus during embryogenesis. Circulation Research, 118 (12), 1861-1862. doi: 10.1161/CIRCRESAHA.116.308934
Iyer, Swati, Chou, Fang Yu, Wang, Richard, Chiu, Han Sheng, Raju, Vinay K. Sundar, Little, Melissa H., Thomas, Walter G., Piper, Michael and Pennisi, David J. (2016). Crim1 has cell-autonomous and paracrine roles during embryonic heart development. Scientific Reports, 6 (1) 19832, 19832 .1-19832 .15. doi: 10.1038/srep19832
Iyer, Swati, Pennisi, David J. and Piper, Michael (2016). Crim1 – a regulator of developmental organogenesis. Histology And Histopathology, 31 (10), 1049-1057. doi: 10.14670/HH-11-766
Phua, Yu Leng, Martel, Nick, Pennisi, David J., Little, Melissa H. and Wilkinson, Lorine J. (2013). Distinct sites of renal fibrosis in the Crim1 mutant mice arise from multiple cellular origins. Journal of Pathology, 229 (5), 685-696. doi: 10.1002/path.4155
Chiu, Han Sheng, York, Philippe J., Wilkinson, Lorine, Zhang, Pumin, Little, Melissa H. and Pennisi, David J. (2012). Production of a mouse line with a conditional Crim1 mutant allele. Genesis, 50 (9), 711-716. doi: 10.1002/dvg.22032
Pennisi, D. J., Kinna, G., Chiu, H. S., Simmons, D. G., Wilkinson, L. and Little, M. H. (2012). Crim1 has an essential role in glycogen trophoblast cell and sinusoidal-trophoblast giant cell development in the placenta. Placenta, 33 (3), 175-182. doi: 10.1016/j.placenta.2011.12.014
Little, Melissa, Georgas, Kylie, Pennisi, David and Wilkinson, Lorine (2010). Kidney development: Two tales of tubulogenesis. Current Topics in Developmental Biology, 90 (C), 193-229. doi: 10.1016/S0070-2153(10)90005-7
Wilkinson, L, Gilbert, T, Sipos, A, Toma, I, Pennisi, D. J., Peti-Peterdi, J and Little, M. H. (2009). Loss of renal microvascular integrity in postnatal Crim1 hypomorphic transgenic mice. Kidney International, 76 (11), 1161-1171. doi: 10.1038/ki.2009.345
Pennisi, D. J. and Mikawa, T (2009). FGFR-1 is required by epicardium-derived cells for myocardial invasion and correct coronary vascular lineage differentiation. Developmental Biology, 328 (1), 148-159. doi: 10.1016/j.ydbio.2009.01.023
Pennisi, David J., Wilkinson, Lorine, Kolle, Gabriel, Sohaskey, Michael L., Gillinder, Kevin, Piper, Michael J., McAvoy, John W., Lovicu, Frank J. and Little, Melissa H. (2007). Crim1(KST264/KST264) mice display a disruption of the Crim1 gene resulting in perinatal lethality with defects in multiple organ systems. Developmental Dynamics, 236 (2), 502-511. doi: 10.1002/dvdy.21015
Wilkinson, Lorine, Gilbert, Thierry, Kinna, Genevieve, Ruta, Leah-Anne, Pennisi, David, Kett, Michelle and Little, Melissa H. (2007). Crim1(KST264/KST264) mice implicate Crim1 in the regulation of vascular endothelial growth factor-A activity during glomerular vascular development. Journal of The American Society of Nephrology, 18 (6), 1697-1708. doi: 10.1681/ASN.2006091012
Pennisi, David J. and Mikawa, Takashi (2005). Normal patterning of the coronary capillary plexus is dependent on the correct transmural gradient of FGF expression in the myocardium. Developmental Biology, 279 (2), 378-390. doi: 10.1016/j.ydbio.2004.12.028
Hatcher, Cathy J., Diman, Nata Y.S.-G., Kim, Min-Su, Pennisi, David, Song, Yan, Goldstein, Marsha M., Mikawa, Takashi and Basson, Craig T. (2004). A role for Tbx5 in proepicardial cell migration during cardiogenesis. Physiological Genomics, 18 (2), 129-140. doi: 10.1152/physiolgenomics.00060.2004
Hall, Christopher E., Hurtado, Romulo, Hewett, Kenneth W., Shulimovich, Maxim, Poma, Clifton P., Reckova, Maria, Justus, Chip, Pennisi, David J., Tobita, Kimimasa, Sedmera, David, Gourdie, Robert G. and Mikawa, Takashi (2004). Hemodynamic-dependent patterning of endothelin converting enzyme 1 expression and differentiation of impulse-conducting Purkinje fibers in the embryonic heart. Development, 131 (3), 581-592. doi: 10.1242/dev.00947
Pennisi, David J., Ballard, Victoria L. T. and Mikawa, Takashi (2003). Epicardium is required for the full rate of myocyte proliferation and levels of expression of myocyte mitogenic factors FGF2 and its receptor, FGFR-1, but not for transmural myocardial patterning in the embryonic chick heart. Developmental Dynamics, 228 (2), 162-172. doi: 10.1002/dvdy.10360
Hosking, B. M., Wyeth, J. R., Pennisi, D. J., Wang, S. C. M., Koopman, P. and Muscat, G. E. O. (2001). Cloning and functional analysis of the Sry-related HMG box gene, Sox18. Gene, 262 (1-2), 239-247. doi: 10.1016/S0378-1119(00)00525-4
Pennisi, D. J., James, K. M., Hosking, B., Muscat, G. E. and Koopman, P. A. (2000). Structure, Mapping, and Expression of Human SOX18. Mammalian Genome, 11 (12), 1147-1149. doi: 10.1007/s003350010216
Pennisi, D, Gardner, J, Chambers, D, Hosking, B, Peters, J, Muscat, G, Abbott, C and Koopman, P (2000). Mutations in Sox18 underlie cardiovascular and hair follicle defects in ragged mice. Nature Genetics, 24 (4), 434-437. doi: 10.1038/74301
Pennisi, D., Bowles, J, Nagy, A., Muscat, G. and Koopman, P. (2000). Mice null for Sox18 are viable and display a mild coat defect. Molecular and Cell Biology, 20 (24), 9331-9336. doi: 10.1128/MCB.20.24.9331-9336.2000
Greenfield, Andy, Carrel, Laura, Pennisi, David, Philippe, Christophe, Quaderi, Nandita, Siggers, Pamela, Steiner, Kirsten, Tam, Patrick P. L., Monaco, Anthony P., Willard, Huntington F. and Koopman, Peter (1998). The UTX gene escapes X inactivation in mice and humans. Human Molecular Genetics, 7 (4), 737-742. doi: 10.1093/hmg/7.4.737
Greenfield, Andy, Scott, Diane, Pennisi, David, Ehrmann, Ingrid, Ellis, Pamela, Cooper, Leanne, Simpson, Elizabeth and Koopman, Peter (1996). An H-YDb epitope is encoded by a novel mouse Y chromosome gene. Nature Genetics, 14 (4), 474-478. doi: 10.1038/ng1296-474
Conference Papers
Wilkinson, L. J., Neal, C., Aroney, S., Pennisi, D. J. and Little, M. H. (2012). Podocyte Specific Deletion of Crim1 Leads to Glomerular Filtration Barrier Defects. 48th Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology, Auckland, New Zealand, 27-29 August 2012. Richmond, VIC Australia: Wiley-Blackwell Publishing Asia. doi: 10.1111/j.1440-1797.2012.01631.x
Pennisi, David J., Chiu, Han S., Vinay, K. S., Wilkinson, Lorine, Zhang, Pumin and Little, Melissa H. (2010). Mice null for Crim1 display altered BMP/TGF beta signaling, defects in multiple organ systems and die in utero with severe cardiovascular defects. 69th Annual Meeting of the Society-for-Developmental-Biology/Japanese-Society-of-Developmental-Biologists, Albuquerque NM, AUG 05-09, 2010. SAN DIEGO: ACADEMIC PRESS INC ELSEVIER SCIENCE. doi: 10.1016/j.ydbio.2010.05.270
Wilkinson, L., Kinna, G., Gilbert, T., Pennisi, D. and Little, M. (2007). Normal Renal Vascular Development Is Dependant On Crim1 and its Regulation of Vegfa. HOBOKEN: WILEY-BLACKWELL.
Pennisi, D., Wilkinson, L., Kolle, G., Gillinder, K. and Little, M. (2005). A hypomorphic mutant of Crim1 reveals a requirement on Crim1 for proper development. AMSTERDAM: ELSEVIER SCIENCE BV.