Difference between revisions of "Basson"

From OpenWetWare
Jump to: navigation, search
(FGF signalling in development and disease)
(Replacing page with '{{deleteme}}')
(4 intermediate revisions by the same user not shown)
Line 1: Line 1:
<!--Possible lab page template. To use simply copy the following text into you lab page and then replace each instance of LabName with your own lab's name-->
<div style="padding: 10px; width: 720px; border: 5px solid #000000;">
== Welcome to the Basson lab at King's College London ==
'''Our research is aimed at uncovering the epigenetic mechanisms that control brain development and underlie neurodevelopmental disorders'''
The Basson laboratory is located on the 27th floor of Guy's Hospital in the Department of Craniofacial and Stem Cell Biology and affiliated with the MRC Centre for Developmental Neurobiology on Guy's Campus [http://www.kcl.ac.uk/depsta/biomedical/mrc/index.php?page=http://www.kcl.ac.uk/depsta/biomedical/mrc/ResearchGroup.php?GroupID=18]'''
== FGF signalling in development and disease ==
All organs in the body originate from relatively simple structures in the embryo. For example a simple epithelial tube, the neural tube, develops into the highly complex brain.  The many forces and growth factors that act upon embryonic tissues are precisely coordinated to shape the morphogenesis of more complex structures. We are interested in understanding how signalling centres are established in the embryo and how signalling pathways are regulated during development. Current research projects in the lab primarily focus on the fibroblast growth factor (FGF) signalling pathway and our aim is to understand how deregulated FGF signalling results in birth defects and cellular malfunction. Our most recent research identified haploinsufficiency of Chd7, a chromatin remodelling factor mutated in CHARGE syndrome, as a potential cause for cerebellar vermis hypoplasia and identified deregulated FGF signalling as the underlying mechanism.
== Chromatin remodelling in neural development and autism ==
Haploinsufficiency of the chromatin remodelling factors, CHD7 and CHD8, have been associated with the development of autism spectrum disorders (ASDs). We are using a range of in vivo models and in vitro approaches to understand the function of these factors in brain development and to elucidate the mechanisms whereby insufficiency of these factors might cause autism.
== In the press ==
Our work on the cerebellum and autism features in a new article in International Innovation:
== Manuscripts in press ==
*Chakkalakal, J., Jones, K., Basson, M.A. & Brack, A.S. (2012) The aged niche disrupts muscle stem cell quiescence. '''Nature''' (in press).
*Magnani, D., Amaniti, E-M., Benadiba, C., Hasenpusch-Theil, K., Yu, T., Basson, M.A., Price, D.J., Lebrand, C. & Theil, T. (2012) Gli3 controls corpus callosum formation by positioning midline guideposts during telencephalic patterning. '''Cerebral Cortex''' (in press).
*Pitera, J.E., Woolf, A.S., Basson, M.A. & Scambler, P.J. (2012) Sprouty1 haploinsufficiency permits kidney maturation in Fraser syndrome renal agenesis mice. '''J. Am. Soc. Nephrol.''' (in press).
== Publications in press ==

Latest revision as of 08:50, 13 February 2016

Crop.png It has been requested that this page be removed with restriction endonucleases.
Other articles for deletion are listed here.