Phosphodiesterase-4 isoforms: intracellular targeting, regulation and potential therapeutic targets
Lead Research Organisation:
University of Glasgow
Department Name: School of Life Sciences
Abstract
Chronic Obstructive Pulmonary Disease is the fourth leading cause of death in the world. It causes lung damage through chronic inflammation. Raising the levels of a substance called cAMP inside lung cells can stop this. Potential new medicines are drugs that bind tightly to PDE4 enzymes to stop them breaking down cAMP. Unfortunately these drugs cause nausea and vomiting, preventing their use. We’ve found that there are many PDE4 subtypes but that only certain of these need to be inhibited to stop inflammation. We aim to devise novel ways to inhibit these important PDE4 subtypes, rather than all PDE4 enzymes, in order to produce effective medicines with minimal or no side-effects. To do this we will exploit our discovery that individual PDE4 subtypes have unique ‘postcodes’ built into them that allow them to be targeted to exactly the right place in cells for them to do their job properly. Our aim is to find molecules that block this correct targeting so as to stop them working properly, providing new COPD medicines. As our drugs focus on just the PDE4 subtype involved in COPD they should not have the side effects caused by current drugs that inhibit all PDE4 subtypes.
Technical Summary
cAMP is a pivotal second messenger able to exert a panoply of cell type specific effects. A multigene family of phosphodiesterases (PDEs) provide the sole means for degrading cAMP and are thus poised to play a key regulatory role in cells. Highly specialised regulatory properties, coupled with cell specific patterns of expression, provide each cell type with a sophisticated and unique means of regulating intracellular cAMP through PDE action. This diversity offers potential for developing highly specific therapeutic agents. There is great interest in developing PDE4 family selective inhibitors for treating Chronic Obstructive Pulmonary Disease (COPD), asthma and other diseases. However, the therapeutic deployment of PDE4 inhibitors has been limited by side effects, such as nausea. It is now appreciated that PDE4 activity is attributable to a large family of isoforms. This has prompted the notion that selective inhibition of particular PDE4 isoforms may maximise therapeutic benefit whilst minimising side effects. Four PDE4 genes produce around 20 isoforms that each have a unique N terminal region and either both UCR1/2 or just UCR2 regulatory domains. Individual PDE4 isoforms have unique functional roles that are attributable to defined intracellular targeting / association with protein complexes. This provides a major underpinning of compartmentalised cAMP signalling. We aim to determine the functional role and basis by which the N terminal and UCR1/2 tailor intracellular targeting, interaction with signal scaffold proteins and regulation by phosphorylation of specific PDE4 isoforms. Our studies have implications for the identification of novel means of generating inhibitors selective for specific PDE4 isoforms by preventing specific PDE4 isoforms from being targeted to their functionally relevant sites in cells. This provides a route to overcome problems in making effective isoform-selective inhibitors by traditional means, namely directed at the active site, as the PDE4 catalytic unit is identical within PDE4 sub-families & very similar between them. Identification of PDE4 interacting proteins has potential for identifying novel biomarkers for COPD. Analysis of post-translational modification of isoforms has potential for appreciating aberrant control of specific PDE4 isoforms in disease. In particular we will focus on (i) PDE4A4, which is selectively up-regulated in COPD macrophages; (ii) PDE4B2, which has been implicated as of importance in regulating macrophage functioning; (iii) PDE4D5, which is up-regulated in macrophages of smokers, regulates beta2AR functioning through beta-arrestin sequestration and is induced by hypoxia in smooth muscle cells and (iv) PDE4D3, which is the major PDE4 in monocytes.
Organisations
- University of Glasgow, United Kingdom (Lead Research Organisation)
- Washington University in St. Louis (Collaboration)
- University of Oslo, Norway (Collaboration)
- Zoology Ecology and Plant Science (Collaboration)
- Scottish Enterprise (Collaboration)
- Yeshiva University (Collaboration)
- Merck (Collaboration)
- University of Texas at San Antonio, United States (Collaboration)
- Koninklijke Philips Electronics N.V. (Collaboration)
- Basilea Pharmaceutica (Collaboration)
- Imperial Cancer Research Fund (Collaboration)
- Pfizer Ltd (Collaboration)
- University of Pennsylvania, United States (Collaboration)
- Purdue University, United States (Collaboration)
- Queen's University (Collaboration)
- F. Hoffmann-La Roche AG (Collaboration)
- University of Alabama at Birmingham, United States (Collaboration)
- deCODE Genetics (Collaboration)
- Johns Hopkins University, United States (Collaboration)
Publications

Anthony DF
(2011)
ß-Arrestin 1 inhibits the GTPase-activating protein function of ARHGAP21, promoting activation of RhoA following angiotensin II type 1A receptor stimulation.
in Molecular and cellular biology

Baeza-Raja B
(2016)
p75 Neurotrophin Receptor Regulates Energy Balance in Obesity.
in Cell reports

Baillie GS
(2009)
Compartmentalized signalling: spatial regulation of cAMP by the action of compartmentalized phosphodiesterases.
in The FEBS journal

Berthouze-Duquesnes M
(2013)
Specific interactions between Epac1, ß-arrestin2 and PDE4D5 regulate ß-adrenergic receptor subtype differential effects on cardiac hypertrophic signaling.
in Cellular signalling

Bjørgo E
(2010)
Cross talk between phosphatidylinositol 3-kinase and cyclic AMP (cAMP)-protein kinase a signaling pathways at the level of a protein kinase B/beta-arrestin/cAMP phosphodiesterase 4 complex.
in Molecular and cellular biology

Blair C
(2019)
Targeting B-Raf inhibitor resistant melanoma with novel cell penetrating peptide disrupters of PDE8A - C-Raf
in BMC Cancer

Brown KM
(2012)
Cyclic AMP-specific phosphodiesterase, PDE8A1, is activated by protein kinase A-mediated phosphorylation.
in FEBS letters

Brown KM
(2013)
Phosphodiesterase-8A binds to and regulates Raf-1 kinase.
in Proceedings of the National Academy of Sciences of the United States of America

Burton P
(2010)
Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) blocks differentiation and maintains the expression of pluripotency markers in human embryonic stem cells.
in The Biochemical journal

Christian F
(2014)
PKA phosphorylation of p62/SQSTM1 regulates PB1 domain interaction partner binding.
in Biochimica et biophysica acta
Description | FP6 (co-PI) |
Amount | £222,000 (GBP) |
Organisation | Sixth Framework Programme (FP6) |
Sector | Public |
Country | European Union (EU) |
Start | 09/2006 |
End | 09/2009 |
Description | Network of Excellence (co-PI)/Center for Translational Molecular Medicine (Netherlands) |
Amount | £208,000 (GBP) |
Organisation | Center for Translational Molecular Medicine (CTMM) |
Sector | Academic/University |
Country | Netherlands |
Start | 09/2009 |
End | 09/2012 |
Description | Project Grant (co-PI) |
Amount | £322,000 (GBP) |
Organisation | British Heart Foundation (BHF) |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 09/2010 |
End | 09/2013 |
Description | Transatlantic Network of Excellence (co-PI) |
Amount | £500,000 (GBP) |
Organisation | Transatlantic Networks of Excellence in Cardiovascular Research Program |
Sector | Charity/Non Profit |
Country | France |
Start | 09/2006 |
End | 09/2011 |
Title | DNA-PK nuclear-cytoplasmic trafficking |
Description | Use of EPAC agonists to promulgate the nuclear exit of DNA-PKc. |
Type Of Material | Model of mechanisms or symptoms - in vitro |
Provided To Others? | No |
Impact | 1. Suggests the potential therapeutic use of EPAC agonists as radio- or chemo-sensitizers by removing DNA-PKc from the nucleus and so hindering repair of double stranded breaks. 2. First identification of a mechanism where cAMP provides dual inhibitory and stimulatory inputs through different effectors. |
Title | Mapping of potential ubiquitination sites |
Description | Spot immobilized peptide arrays used for in vitro ubiquitination in order to determine potential sites of modification. |
Type Of Material | Technology assay or reagent |
Year Produced | 2008 |
Provided To Others? | Yes |
Impact | Has potential for rapid and cheap site identification that otherwise would have to be undertaken by exhaustive and expensive mutagenesis. |
Title | PDE expression profiling |
Description | We have shown that PDE expression profiling can provide a potential diagnostic indicator for different stages of prostate cancer. |
Type Of Material | Technology assay or reagent |
Provided To Others? | No |
Impact | This has led to three patents being filed. |
Title | PDE4 antisera |
Description | antisera specific for PDE4 subfamilies and various PDE4 isoforms |
Type Of Material | Antibody |
Year Produced | 2009 |
Provided To Others? | Yes |
Impact | High quality antisera developed both by ourselves and in collaboration with Millipore to aid our work and that of the academic community. |
Title | PDE4/beta-arrestin peptide disruptor |
Description | A cell permeable peptide that disrupts the association of PDE4D5 with beta-arrestin and so promulgates beta2-adrenoceptor signalling. |
Type Of Material | Technology assay or reagent |
Year Produced | 2008 |
Provided To Others? | Yes |
Impact | PDE4 inhibitors have potential utility in asthma and COPD but their deployment has been hindered due to side effects of emesis because active-site directed inhibitors act on all 25+ isoforms. This technology shows that disrupting the targeting of a specific disease-associated isoform can lead to the 'functional' inhibition of a single species. This addresses the PDE4D5 isoform, which regulates beta2-adrenoceptor signalling and causes resistance to the action of beta2 agonists used in asthma treatment as it is up-regulated with their chronic use. Our data suggests that the development of peptidomimetics or small molecules that disrupt the association of PDE4D5 with beta-arrestin will promulgate beta2-adrenoceptor signalling and so could be used in cases of beta2-agonist (eg salbutamol) resistant patients. |
Description | Cardiac IKs K+ channel |
Organisation | University of Washington |
Department | Department of Pharmacology |
Country | United States |
Sector | Academic/University |
PI Contribution | Project development Reagent provision. Mapping protein-protein interfaces with peptide arrays. Development of mutant PDE4 species. |
Collaborator Contribution | Identification of a novel system where PDE4 is involved |
Impact | Publications |
Start Year | 2008 |
Description | DISC1 partnerships |
Organisation | Johns Hopkins University |
Department | Department of Psychiatry and Behavioral Sciences |
Country | United States |
Sector | Academic/University |
PI Contribution | Project development. Protein-protein mapping reagent generation DISC1 expression |
Collaborator Contribution | novel in vivo system access novel system for analysing the PDE4 partner, DISC1 |
Impact | Publications |
Start Year | 2007 |
Description | Identification of PDE4A8, a novel cAMP phosphodiesterase |
Organisation | F. Hoffmann-La Roche AG |
Country | Global |
Sector | Private |
PI Contribution | Allowed us access to a novel PDE4A clone without having to generate it ourselves. Created useful contacts. |
Collaborator Contribution | Allowed us access to a novel PDE4A clone without having to generate it ourselves. Created useful contacts. |
Impact | Contributed experimental research work for a joint publication involved in the identification and characterisation of a novel cAMP phosphodiesterase.; Allowed us access to a novel PDE4A clone without having to generate it ourself. Given access to a company that may lead to future collaborations. Created useful contacts. |
Start Year | 2007 |
Description | Novel allosteric regulators of PDE4 |
Organisation | deCODE genetics |
Country | Iceland |
Sector | Academic/University |
PI Contribution | Analyzed the effect of a novel PDE4 selective inhibitor in one of our assays systems to determine if there was potential for collaboration. deCode has since gone into chapter 11 bankruptcy so the project could not continue. |
Collaborator Contribution | Allowed us access to novel PDE4 inhibitors, to novel structural data and to purified PDE4 proteins with possibility for joint research/publication and future funding. |
Impact | Allowed us access to novel PDE4 inhibitors, to novel structural data and to purified PDE4 proteins with possibility for joint research/publication and future funding. |
Start Year | 2008 |
Description | PDE and immunosuppression |
Organisation | Yeshiva University |
Department | Department of Molecular Pharmacology |
Country | United States |
Sector | Academic/University |
PI Contribution | Joint project management PDE4 reagents PDE4 analsyes Ubiquitin ananlsyes Peptide mapping |
Collaborator Contribution | Identification of a novel system where PDE4 is involved |
Impact | Publications Novel reagents |
Start Year | 2007 |
Description | PDE in Psychiatric disease |
Organisation | Pfizer Ltd |
Department | Psychiatry Pfizer |
Country | United Kingdom |
Sector | Private |
PI Contribution | Expertsie on PDEs Reagents Anayses of PDE actiity and expression Peptide mapping |
Collaborator Contribution | reagents access to novel in vivo systems |
Impact | Publications Imminent signing of a contract for PDE4:DISC1 research |
Start Year | 2008 |
Description | PDE4 and vascular permeability |
Organisation | Queen's University |
Department | Department of Pathology & Molecular Medicine |
Country | Canada |
Sector | Academic/University |
PI Contribution | Project management PDE4 activity and expression analyses |
Collaborator Contribution | Joint project management. Access to unique in vivo models |
Impact | Publications |
Start Year | 2007 |
Description | PDE4 antisera and cell lines |
Organisation | Merck |
Department | MilliporeSigma |
Country | United States |
Sector | Private |
PI Contribution | Jointly generating antisera to PDE4 isoforms and sub-families. We are supplying know-how and testing; they are generating the antisera and cell lines. Our lab has received 16000 GBP to offset costs plus a share in the reagents generated and Univ Glasgow will obtain a share in royalties for any sales |
Collaborator Contribution | Jointly generating antisera to PDE4 isoforms and sub-families. We are supplying know-how and testing; they are generating the antisera and cell lines. Our lab has received 16000 GBP to offset costs plus a share in the reagents generated and Univ Glasgow will obtain a share in royalties for any sales |
Impact | Jointly generating antisera to PDE4 isoforms and sub-families. We are supplying know-how and testing; they are generating the antisera and cell lines. Our lab has received 16000 GBP to offset costs plus a share in the reagents generated and Univ Glasgow will obtain a share in royalties for any sales |
Start Year | 2008 |
Description | PDE4 dimerisation |
Organisation | University of Alabama at Birmingham |
Department | Department of Radiation Oncology |
Country | United States |
Sector | Academic/University |
PI Contribution | Led study. |
Collaborator Contribution | Yeast 2-hybrid expertise; generated mutants |
Impact | Publications being written up. Impact on understanding the dynamics of PDE4 partnerships in cells. Impact on understanding selective inhibition |
Start Year | 2007 |
Description | PDE4 selective Inhibitors |
Organisation | Basilea Pharmaceutica |
Country | Switzerland |
Sector | Private |
PI Contribution | We have received funds to analyse novel PDE4 inhibitors with a view to potential further interactions with the company. |
Collaborator Contribution | Supply of novel inhibitors |
Impact | We have received funds to analyse novel PDE4 inhibitors with a view to furthering interactions should the company continue work in this new area. |
Start Year | 2007 |
Description | PDE4A and sleep |
Organisation | University of Pennsylvania |
Department | Department of Neuroscience |
Country | United States |
Sector | Academic/University |
PI Contribution | Project management Analsysis of PDE4 activity and expression Provision of reagents |
Collaborator Contribution | Publications. Access to in vivo analyses |
Impact | Publications |
Start Year | 2008 |
Description | PDE4D5 and FAK:RACK1 complexes in direction sensing complexes |
Organisation | Cancer Research UK |
Department | Edinburgh Cancer Research UK Centre |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | we describe a novel "direction-sensing" pathway that links the integrin effector focal adhesion kinase (FAK), the molecular scaffold protein RACK1, and activity of one of its client proteins, PDE4D5, a cAMP-degrading phosphodiesterase. we identified the key complexes, mapped the interaction surfaces and developed disruptors |
Collaborator Contribution | Provison of a novel system to explore the functional role of our RACK1:PDE4D5 complex |
Impact | Publication. We are developing small molecules / peptide disruptors as potential therapeutics |
Start Year | 2007 |
Description | RACK1 signalling functions |
Organisation | University College Cork |
Department | BioSciences Institute |
Country | Ireland |
Sector | Academic/University |
PI Contribution | Defining protein protein interactions with peptide arays; generating mutants; |
Collaborator Contribution | Expertise in FAK; novel cell / in vivo systems. |
Impact | Publications Peptide disruptor development. |
Start Year | 2007 |
Description | Reverse transcriptase inhibitor actions on PDE4 |
Organisation | Purdue University |
Department | Department of Medicinal Chemistry and Molecular Pharmacology |
Country | United States |
Sector | Academic/University |
PI Contribution | Analsysi of small molecules in various PDE4 assay systems |
Collaborator Contribution | Provison of small molecules for analyses in our Labs |
Impact | Publications |
Start Year | 2007 |
Description | Small molecule PDE4 subfamily inhibitors |
Organisation | University of Texas at San Antonio |
Department | Department of Biology |
Country | United States |
Sector | Academic/University |
PI Contribution | provision of pde4 sub-family specific assay systems provision of cell-based cell systems for anti-inflammatory analyses project development |
Collaborator Contribution | provision of small molecule PDE inhibitors from a novel yeast-based screen |
Impact | developing molecules for publication / IP |
Start Year | 2009 |
Description | Stem Cells |
Organisation | Scottish Enterprise |
Country | United Kingdom |
Sector | Public |
PI Contribution | PDE know how |
Collaborator Contribution | provided stem cell know how and various state of the art pieces of equipment |
Impact | PDE2 inhibitor, Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) found to block differentiation and maintains the expression of pluripotency markers in human embryonic stem cells. this has led to a patent |
Start Year | 2006 |
Description | Sub-plasmalemma cAMP compartments |
Organisation | University of Washington |
Department | Department of Pharmacology |
Country | United States |
Sector | Academic/University |
PI Contribution | Joint project development. Novel reagents: cDNA constructs, antisera Dominant neative PDE4 approach |
Collaborator Contribution | Novel system for understanding PDE4 function |
Impact | Publications |
Start Year | 2006 |
Description | T-cell receptor activation in human primary T cells |
Organisation | University of Oslo |
Department | Biotechnology Centre of Oslo |
Country | Norway |
Sector | Academic/University |
PI Contribution | Identification of a novel complex of beta-arretsin/PDE4/Akt regukated by CD28 that controls T-cell receptor activation. Mapping sites, defining function. |
Collaborator Contribution | Provided access to a novel system for analyses |
Impact | Publications |
Start Year | 2007 |
Description | cAMP signalling in prostate cancer |
Organisation | Koninklijke Philips Electronics N.V. |
Department | Philips |
Country | Global |
Sector | Private |
PI Contribution | I supervise a research student who works full-time in my laboratory. My team provide underpinning expertise of cAMP phosphodiesterases. |
Collaborator Contribution | Studentship support. Has provided new insights and indicated new directions plus access to novel technologies. |
Impact | Studentship support. Has provided new insights and indicated new directions plus access to novel technologies. Has led to three patent applications |
Start Year | 2007 |
Title | PHOSPHODIESTERASE 4D7 AS MARKER FOR MALIGNANT, HORMONE-SENSITIVE PROSTATE CANCER |
Description | The present invention relates to phosphodiesterase 4D7 (PDE4D7) for use as a marker for malignant, hormone- sensitive prostate cancer, wherein the expression of the marker is increased when comparing the expression in malignant, hormone-sensitive prostate cancer tissue, to the expression in normal tissue or benign prostate tumor tissue, and the use of PDE4D7 as a diagnostic marker for malignant, hormone-sensitive prostate cancer. The present invention also relates to a composition for diagnosing, detecting, monitoring or prognosticating malignant, hormone-sensitive prostate cancer, a corresponding detection method, a method allowing to discriminate between a benign and malignant hormone- sensitive prostate cancer and a method of data acquisition, as well as corresponding immunoassays. The present invention also relates to a method of identifying an individual for eligibility for malignant, hormone-sensitive prostate cancer as well as an immunoassay for stratifying an individual with such prostate cancer. The present invention further envisages pharmaceutical compositions and their use for the treatment of malignant, hormone-sensitive prostate cancer. |
IP Reference | WO2010131194 |
Protection | Patent application published |
Year Protection Granted | 2010 |
Licensed | No |
Impact | Expected to lead to major publications |
Title | PHOSPHODIESTERASE 4D7 AS PROSTATE CANCER MARKER |
Description | The present invention relates to phosphodiesterase 4D7 (PDE4D7) for use as a marker for prostate cancer, and the use of PDE4D7 as a marker for diagnosing, detecting, monitoring or prognosticating prostate cancer or the progression of prostate cancer. The present invention also relates to a composition for diagnosing, detecting, monitoring or prognosticating prostate cancer or the progression of prostate cancer, a corresponding method and immunoassay, a method for diagnosing, monitoring or prognosticating hormone-resistant prostate cancer vs. hormone-sensitive prostate cancer, a corresponding immunoassay, a method of data acquisition, an immunoassay for diagnosing, detecting, monitoring or prognosticating prostate cancer or the progression of prostate cancer, a method of identifying an individual for eligibility for prostate cancer therapy, an immunoassay for stratifying an individual or cohort of individuals with a prostate cancer disease, an immunoassay for stratifying an individual with prostate cancer, as well as a pharmaceutical composition comprising a compound directly stimulating or modulating the activity of PDE4D7, a compound indirectly stimulating or modulating the activity of PDE4D7, the PDE4D7 protein or a biologically active equivalent thereof, a nucleic acid encoding and expressing PDE4D7, a miRNA inhibitor specific for PDE4D7 miRNAs, a demethylation agent and/or a phosphodiesterase displacement factor. |
IP Reference | WO2010131195 |
Protection | Patent application published |
Year Protection Granted | 2010 |
Licensed | No |
Impact | Expected to lead to major publications |
Title | PHOSPHODIESTERASE 9A AS PROSTATE CANCER MARKER |
Description | The present invention relates to phosphodiesterase 9A (PDE9A) for use as a marker for prostate cancer, and the use of PDE9A as a marker for diagnosing, detecting, monitoring or prognosticating prostate cancer or the progression of prostate cancer. The present invention also relates to a composition for diagnosing, detecting, monitoring or prognosticating prostate cancer or the progression of prostate cancer, a corresponding method and immunoassay, a method for diagnosing, monitoring or prognosticating hormone-resistant prostate cancer vs. hormone-sensitive prostate cancer, a corresponding immunoassay, a method of data acquisition, an immunoassay for diagnosing, detecting, monitoring or prognosticating prostate cancer or the progression of prostate cancer, a method of identifying an individual for eligibility for prostate cancer therapy, an immunoassay for stratifying an individual or cohort of individuals with a prostate cancer disease, an immunoassay for stratifying an individual with prostate cancer. The present invention further envisages pharmaceutical compositions and their use for the treatment of prostate cancer, in particular hormone-resistant prostate cancer. |
IP Reference | WO2010131193 |
Protection | Patent application published |
Year Protection Granted | 2010 |
Licensed | No |
Impact | Exepcted to lead to major publciations |
Title | STEM CELL CULTURE METHODS |
Description | The invention provides methods for reversibly inhibiting stem cell differentiation wherein a compound of formula (I) is contacted with a stem cell. The invention further provides a method for preparing a culture medium, a culture medium supplement and a composition comprising a compound of formula (I). |
IP Reference | WO2010084300 |
Protection | Patent application published |
Year Protection Granted | 2010 |
Licensed | Yes |
Impact | generated a publication. enhanced career prospects of involved scientists |
Title | PDE4 antibody panel |
Description | A panel of antisera specifc for PDE4 sub-fmailies and specific PDE4 isoforms. Now fully developed and marketing being assessed by Milipore. |
Type | Support Tool - For Fundamental Research |
Current Stage Of Development | Market authorisation |
Year Development Stage Completed | 2010 |
Development Status | Under active development/distribution |
Impact | Will provide our group with access to first rate diagnostic reagents essential for our research. Will provide the research community with the same high quality reagents. |
URL | http://www.antibodypedia.com/gene/4321/PDE4A/antibody/555536/ABS23 |
Title | PDE4 stable cell lines |
Description | Marketing being developed by Millipore |
Type | Support Tool - For Fundamental Research |
Current Stage Of Development | Market authorisation |
Year Development Stage Completed | 2010 |
Development Status | Under active development/distribution |
Impact | Will provide a novel platform for development of PDE4 selective therapeutics to treat inflammatory disease. |
Description | Alumni letter |
Form Of Engagement Activity | A magazine, newsletter or online publication |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | described life as a biomedical scientist hopefully interested people as received feedback |
Year(s) Of Engagement Activity | 2008 |
Description | School - Renfrewshire |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Schools |
Results and Impact | Talk on research in signaling systems and biomedical impact. Hopefully increased applications to study biomedical sciences |
Year(s) Of Engagement Activity | 2008 |
Description | Science Festival Event |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Schools |
Results and Impact | Manning of a stand at a science festival event for schools. Continual flow of pupils though. Enquiries form students about courses and careers |
Year(s) Of Engagement Activity | 2010 |
Description | Sleep Radio Broadcast |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Media (as a channel to the public) |
Results and Impact | Radio broadcast interview Email contact from members of public. Contact from clinicians involved in sleep research |
Year(s) Of Engagement Activity | 2009 |
Description | Sleep press release |
Form Of Engagement Activity | A magazine, newsletter or online publication |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Media (as a channel to the public) |
Results and Impact | press release on use of PDE4 inhibitors for correcting cognitive defects upon sleep deprivation. request for information from various journalists and members of the public. |
Year(s) Of Engagement Activity | 2009 |