Dr Richard Jenner's Laboratory
Keywords: Transcription; chromatin; T-cell; HIV; non-coding RNA.
Dr Richard Jenner: SLMS Profile, Publications
Email r.jenner@ucl.ac.uk /Telephone +44-20-7679-6815
Research Group
Dr Manuel Beltran-Nebot
Dr Keijo Viiri
Ms Catherine Evans
Ms Carla Araujo
Location
UCL Cancer Institute (Bloomsbury),
Paul O'Gorman Building, 72 Huntley Street,
London WC1E 6BT
Brief Description
The overall aim of our lab is to understand how the genome specifies the different identities of specialised cell types. We are currently focused on understanding how non-coding RNAs function with transcriptional and chromatin regulators to direct gene expression. We have three main research programmes:
1. Role of non-coding RNAs in polycomb-mediated repression.
Polycomb proteins maintain cell identity by repressing the expression of developmental regulators specific for other cell types. We have identified a class of 50-200nt short RNAs transcribed from the 5’ end of polycomb target genes (Kanhere et al., 2010). The short RNAs interact with PRC2 through a stem-loop structure, cause gene repression and are depleted from polycomb target genes activated during cell differentiation. These results support a role for short RNAs in the association of PRC2 with its target genes.
2. Transcriptional regulation of CD4+ T-cell differentiation. CD4+ T helper (Th) cells can differentiate into a number of effector types that tailor the immune response to different pathogens. We have mapped the binding sites of the Th1 and Th2 master regulators T-bet and GATA-3 in primary human T cells and found that these factors act through a shared set of target genes (Jenner et al., 2009). We are currently exploring the mechanisms through which T-bet and GATA-3 regulate transcription.
3. Regulation of gene expression in virus infected cells.
We use viral mechanisms of transcriptional regulation as models for how cellular gene expression is controlled. We are currently investigating the molecular mechanisms by which HIV latency is maintained and through which HIV Tat alters host gene expression.
Page last modified on 26 nov 12 14:22 by Karen Rumsey
