DrAna Costa-Pereira
Director of Centre for Languages, Culture & Communication
Centre for Languages, Culture and Communication - Central Faculty
Orcid identifier0000-0001-8265-8065 (opens in a new tab)
- Director of Centre for Languages, Culture & CommunicationCentre for Languages, Culture and Communication - Central Faculty
- 020 7594 9352 (Work)
- S302, Sherfield Building, South Kensington Campus, United Kingdom
RESEARCH
MAIN RESEARCH OBJECTIVES
As a scientist, my most significant contribution to science has been the discovery that cytokine signalling specificity is not determined by the specific interaction of the ligand (postcard) and the receptor (postbox). That is to say that, within reason, the postcard and post box are irrelevant to fully deciphering the message written on the postcard, for it is the cellular environment with all its ‘molecular machines’ in place that effectively ‘seals the deal’. This is crucial for the output of many biological processes since our cells are never subjected to a single molecular signal and are in a state of permanent flux. Perhaps more importantly, or certainly more tangible to everyday life, is the fact that many molecular therapies using chemical inhibitors can fall foul of this.
My lab continues to utilise JAK/STAT signalling as a paradigm to unravel the molecular details of how signal transduction specificity is achieved and to translate this information into more effectively targeted cancer therapies. More specifically, we wish to:
unravel novel layers of regulation of signalling in response to IFNs (type I and II) and IL-6-type cytokines, with particular emphasis on the definition of the mechanism(s) of the mutational switch of an IL-6 response to an IFN-γ-like response in the absence of STAT3 - likely important in cancers where inflammation plays a major role;
establish the contribution of STATs, JAKs and other kinases (such as DAPKs, ERKs and AKTs) to molecular mechanisms that enable cancer cells to survive apoptosis triggered by diverse stimuli and/or evade the immune system;
utilise this information to devise alternative modalities of defeating drug resistance in the clinic.
To this end, we use/will use CRISPRs and RNAi technology as a starting point and classical molecular and cellular technics, combined with our expertise on high-throughput screening (HTS) using flow cytometry-based assays, as well as, good old fashioned antiviral assays.
REVIEWER
FUNDING
MRC | BBSRC | Pancreatic Cancer Research Fund (PCRF) | British Heart Foundation (BHF) | Chief Scientist Office Experimental and Translational Medicine Research Committee (Scotland) | Research Foundation Flanders (FWO) (Belgium)
EDITORIAL
J Cell Sci | J Molec Endocrinol | Gene Exp Pat | Molec and Cel Endocrinol | J Biol Chem | Gene Ther | PLoS One | J Eur Immunol | Cytokine | Eur J Cell Biol | FEBS J | FASEB | J Immunol Meth | JAK-STAT | Oncogene | Mol Cel Biol
As a scientist, my most significant contribution to science has been the discovery that cytokine signalling specificity is not determined by the specific interaction of the ligand (postcard) and the receptor (postbox). That is to say that, within reason, the postcard and post box are irrelevant to fully deciphering the message written on the postcard, for it is the cellular environment with all its ‘molecular machines’ in place that effectively ‘seals the deal’. This is crucial for the output of many biological processes since our cells are never subjected to a single molecular signal and are in a state of permanent flux. Perhaps more importantly, or certainly more tangible to everyday life, is the fact that many molecular therapies using chemical inhibitors can fall foul of this.
My lab continues to utilise JAK/STAT signalling as a paradigm to unravel the molecular details of how signal transduction specificity is achieved and to translate this information into more effectively targeted cancer therapies. More specifically, we wish to:
unravel novel layers of regulation of signalling in response to IFNs (type I and II) and IL-6-type cytokines, with particular emphasis on the definition of the mechanism(s) of the mutational switch of an IL-6 response to an IFN-γ-like response in the absence of STAT3 - likely important in cancers where inflammation plays a major role;
establish the contribution of STATs, JAKs and other kinases (such as DAPKs, ERKs and AKTs) to molecular mechanisms that enable cancer cells to survive apoptosis triggered by diverse stimuli and/or evade the immune system;
utilise this information to devise alternative modalities of defeating drug resistance in the clinic.
To this end, we use/will use CRISPRs and RNAi technology as a starting point and classical molecular and cellular technics, combined with our expertise on high-throughput screening (HTS) using flow cytometry-based assays, as well as, good old fashioned antiviral assays.
REVIEWER
FUNDING
MRC | BBSRC | Pancreatic Cancer Research Fund (PCRF) | British Heart Foundation (BHF) | Chief Scientist Office Experimental and Translational Medicine Research Committee (Scotland) | Research Foundation Flanders (FWO) (Belgium)
EDITORIAL
J Cell Sci | J Molec Endocrinol | Gene Exp Pat | Molec and Cel Endocrinol | J Biol Chem | Gene Ther | PLoS One | J Eur Immunol | Cytokine | Eur J Cell Biol | FEBS J | FASEB | J Immunol Meth | JAK-STAT | Oncogene | Mol Cel Biol