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Mark R Crompton

Researcher at Royal Holloway, University of London

Publications -  7
Citations -  414

Mark R Crompton is an academic researcher from Royal Holloway, University of London. The author has contributed to research in topics: PTK6 & Signal transduction. The author has an hindex of 7, co-authored 7 publications receiving 403 citations.

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Expression of the BRK tyrosine kinase in mammary epithelial cells enhances the coupling of EGF signalling to PI 3-kinase and Akt, via erbB3 phosphorylation.

TL;DR: It is reported that BRK expression in mammary epithelial cells, at pathologically relevant levels, results in an enhanced phosphorylation of the epidermal growth factor receptor-related receptor erbB3 in response to epider mal growth factor.
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Use of RNA interference to validate Brk as a novel therapeutic target in breast cancer: Brk promotes breast carcinoma cell proliferation

TL;DR: RNA interference is used to efficiently and specifically downregulate Brk protein levels in breast carcinoma cells, and this results in a significant suppression of their proliferation, identifying Brk as a novel target for antiproliferative therapy in the majority of breast cancers.
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The cell adhesion molecule neuroplastin-65 inhibits hippocampal long-term potentiation via a mitogen-activated protein kinase p38-dependent reduction in surface expression of GluR1-containing glutamate receptors

TL;DR: The results indicate that neuroplastin‐65 binding and associated stimulation of p38MAPK activity are upstream of a mechanism to control surface glutamate receptor expression and thereby influence plasticity at excitatory hippocampal synapses.
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Expression and Oncogenic Role of Brk (PTK6/Sik) Protein Tyrosine Kinase in Lymphocytes

TL;DR: Constutive expression of the protein tyrosine kinase Brk in a large proportion of cutaneous T-cell lymphomas and other transformed T- and B-cell populations indicates that Brk may play a key role in lymphomagenesis, hence identifying the kinase as a potential therapeutic target in lymphomas.
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Targeting primary human leukaemia cells with RNA interference: Bcr-Abl targeting inhibits myeloid progenitor self-renewal in chronic myeloid leukaemia cells.

TL;DR: Through the functional targeting of an oncogene in primary human tumour cells, it is demonstrated that Bcr‐Abl enhances CML progenitor cell amplification, and that RNAi may be suitable for development as a specific anti‐leukaemia treatment.