The physiology of Cymbidium plantlets cultured in vitro under conditions of high carbon dioxide and low photosynthetic photon flux density

Journal of Horticultural Science and Biotechnology745632-638JHSB

Stat3 promotes directional cell migration by regulating Rac1 activity via its activator βPIX

10.1242/jcs.057109Journal of Cell Science122224150-4159JNCS

Drug-induced liver injury associated with Complementary and Alternative Medicine: A review of adverse event reports in an Asian community from 2009 to 2014

10.1186/s12906-016-1168-zBMC Complementary and Alternative Medicine16119

Relationships between cholesterol efflux and high-density lipoprotein particles in patients with type 2 diabetes mellitus

10.1016/j.jacl.2011.06.016Journal of Clinical Lipidology56467-47

Cep55 regulation of PI3K/Akt signaling is required for neocortical development and ciliogenesis

Homozygous nonsense mutations in CEP55 are associated with several congenital malformations that lead to perinatal lethality suggesting that it plays a critical role in regulation of embryonic development. CEP55 has previously been studied as a crucial regulator of cytokinesis, predominantly in transformed cells, and its dysregulation is linked to carcinogenesis. However, its molecular functions during embryonic development in mammals require further investigation. We have generated a Cep55 knockout (Cep55(-/-) mouse model which demonstrated preweaning lethality associated with a wide range of neural defects. Focusing our analysis on the neocortex, we show that Cep55(-/-) embryos exhibited depleted neural stem/progenitor cells in the ventricular zone as a result of significantly increased cellular apoptosis. Mechanistically, we demonstrated that Cep55-loss downregulates the pGsk3β/β-Catenin/Myc axis in an Akt-dependent manner. The elevated apoptosis of neural stem/progenitors was recapitulated using Cep55-deficient human cerebral organoids and we could rescue the phenotype by inhibiting active Gsk3β. Additionally, we show that Cep55-loss leads to a significant reduction of ciliated cells, highlighting a novel role in regulating ciliogenesis. Collectively, our findings demonstrate a critical role of Cep55 during brain development and provide mechanistic insights that may have important implications for genetic syndromes associated with Cep55-loss.Behnam Rashidieh, Belal Shohayeb, Amanda Louise Bain, Patrick R.J. Fortuna, Debottam Sinha, Andrew Burgess, Richard Mills, Rachael C. Adams, J. Alejandro Lopez, Peter Blumbergs, John Finnie, Murugan Kalimutho, Michael Piper, James Edward Hudson, Dominic C.H. Ng, Kum Kum Khanna