IDENTIFICATION OF NUCLEAR PATHWAYS THAT ARE CAUSALLY INVOLVED IN NUCLEOLAR TARGETING OF NF-KAPPAB/RELA.
Lead Research Organisation:
University of Edinburgh
Department Name: College of Medicine and Veterinary Medic
Abstract
Colorectal cancer is the most common cause of cancer death amongst the non-smoking population in the UK and is a major public health issue for the British population. Unequivocal evidence indicates that aspirin and related agents can prevent colorectal cancer and cause regression of this disease. However, the potential of aspirin-like agents is limited by their toxicity. In this lab, we have been undertaking studies to understand how aspirin-like agents act against colon cancer cells, in order to develop more effective and specific alternatives. We have shown that these agents cause a molecule involved in the regulation of cell growth and death, RelA, to move from the cytoplasmic compartment of the cell to the nucleoplasmic compartment then to a nuclear compartment called the nucleolus. We have also shown that movement of RelA from the nucleoplasm to the nucleolus is important for the ability of aspirin-like agents to kill colon cancer cells. Furthermore, we have demonstrated that artificially localising RelA to the nucleolus mediates the death of this cell type
The overall objective of this study is to understand how aspirin causes RelA to move from the nucleoplasm to the nucleolus. Identifying the cellular pathways involved will allow the design of preventative/therapeutic agents that force RelA into the nucleolar compartment to kill colon cancer cells. We have already shown that a molecule called COMMD1 is important in causing RelA to go to the nucleolus in response to aspirin and that COMMD1 acts by linking a regulatory molecule called ubiquitin, to RelA.
The specific objectives of this proposal are:
1. To identify molecules that, alongside COMMD1, are important for linking ubiquitin to RelA after aspirin treatment. We will examine the role of candidate molecules that have previously been identified as playing a role in linking ubiquitin to RelA. We will also isolate COMMD1 from aspirin treated cells and use a technique called mass spectrometry to identify molecules that bind to COMMD1 in response to the agent. We will examine how aspirin effects these molecules and how aspirin upregulates COMMD1.
2. Identification of the specific parts of RelA that are linked to ubiquitin in response to aspirin and the nature of this linkage. Ubiquitin is generally linked onto proteins at specific sites called lysines. We will identify the lysines of RelA that ubiquitin is linked to in response to aspirin. Ubiquitin also links to itself on lysine molecules to form chains. We will determine which lysine on ubiquitin is critical for nucleolar translocation of RelA using, amongst other approaches, a single cell assay where ubiquitination can be visualised.
3. Identification of proteins that transport ubiquitin-linked RelA to the nucleolus. When ubiquitin is linked to a molecule, specific proteins bind to that molecule. Therefore, we suggest that when ubiquitin is linked to RelA, specific molecules bind RelA and transport the protein to the nucleolus. We will use a labelling approach and mass spectrometry to identify proteins that bind specifically to aspirin-induced, ubiquitin-linked RelA.
These complementary approaches will allow us to understand the basic science of how RelA is regulated in the nucleoplasm, how linking ubiquitin to RelA causes it to go to the nucleolus and how proteins similar to RelA locate to different compartments in the cell. More importantly, these studies may reveal a way to chemically manipulate these pathways to mimic effects of aspirin on colon cancer cells.
The overall objective of this study is to understand how aspirin causes RelA to move from the nucleoplasm to the nucleolus. Identifying the cellular pathways involved will allow the design of preventative/therapeutic agents that force RelA into the nucleolar compartment to kill colon cancer cells. We have already shown that a molecule called COMMD1 is important in causing RelA to go to the nucleolus in response to aspirin and that COMMD1 acts by linking a regulatory molecule called ubiquitin, to RelA.
The specific objectives of this proposal are:
1. To identify molecules that, alongside COMMD1, are important for linking ubiquitin to RelA after aspirin treatment. We will examine the role of candidate molecules that have previously been identified as playing a role in linking ubiquitin to RelA. We will also isolate COMMD1 from aspirin treated cells and use a technique called mass spectrometry to identify molecules that bind to COMMD1 in response to the agent. We will examine how aspirin effects these molecules and how aspirin upregulates COMMD1.
2. Identification of the specific parts of RelA that are linked to ubiquitin in response to aspirin and the nature of this linkage. Ubiquitin is generally linked onto proteins at specific sites called lysines. We will identify the lysines of RelA that ubiquitin is linked to in response to aspirin. Ubiquitin also links to itself on lysine molecules to form chains. We will determine which lysine on ubiquitin is critical for nucleolar translocation of RelA using, amongst other approaches, a single cell assay where ubiquitination can be visualised.
3. Identification of proteins that transport ubiquitin-linked RelA to the nucleolus. When ubiquitin is linked to a molecule, specific proteins bind to that molecule. Therefore, we suggest that when ubiquitin is linked to RelA, specific molecules bind RelA and transport the protein to the nucleolus. We will use a labelling approach and mass spectrometry to identify proteins that bind specifically to aspirin-induced, ubiquitin-linked RelA.
These complementary approaches will allow us to understand the basic science of how RelA is regulated in the nucleoplasm, how linking ubiquitin to RelA causes it to go to the nucleolus and how proteins similar to RelA locate to different compartments in the cell. More importantly, these studies may reveal a way to chemically manipulate these pathways to mimic effects of aspirin on colon cancer cells.
Technical Summary
Objective 1. Identification of the COMMD1 complex that ubiquitinates RelA in response to aspirin. Approaches that will be used to complete this objective include depletion of candidate proteins using siRNA followed by immunocytochemistry to detect nucleolar translocation of RelA and Ni-agarose precipitation of 6HisUb followed by anti-RelA western blot analysis to detect ubiquitination of the protein. We will also use a proteomics approach to identify novel, aspirin-induced, COMMD1 binding proteins. GST-COMMD1 will be isolated from cells +/- aspirin. COMMD1 binding proteins will be identified by SDS PAGE and mass spectrometry of excised bands. Immunocytochemistry, western blot analysis and qRTPCR will be used to analyse the effects of aspirin on components of the complex and the mechanisms by which aspirin causes increased cellular levels of COMMD1.
Objective 2. Identification of the lysine residues of RelA that are ubiquitinated in response to aspirin and the nature of this ubiquitination. Deletion and site directed mutagenesis will be used to identify domains and lysine residues of RelA important for ubiquitination. We will use ubiquitin-mediated fluorescence complementation (UbFC) assays, expression of mutated ubiquitin and linkage specific antibodies, to identify the ubiquitin linkages important for nucleolar translocation of RelA.
Objective 3. Identification of proteins that transport ubiquitinated RelA to the nucleolus. We propose a novel proteomic approach to identify proteins that specifically bind to aspirin-induced, ubiquitinated RelA which involves a combination of isolation of ubiquitinated RelA and stable isotope labelling of amino acids in culture (SILAC). Once binding proteins are identified, techniques outlined in objective 1 will be used to determine their role in aspirin-mediated nucleolar translocation of RelA.
Objective 2. Identification of the lysine residues of RelA that are ubiquitinated in response to aspirin and the nature of this ubiquitination. Deletion and site directed mutagenesis will be used to identify domains and lysine residues of RelA important for ubiquitination. We will use ubiquitin-mediated fluorescence complementation (UbFC) assays, expression of mutated ubiquitin and linkage specific antibodies, to identify the ubiquitin linkages important for nucleolar translocation of RelA.
Objective 3. Identification of proteins that transport ubiquitinated RelA to the nucleolus. We propose a novel proteomic approach to identify proteins that specifically bind to aspirin-induced, ubiquitinated RelA which involves a combination of isolation of ubiquitinated RelA and stable isotope labelling of amino acids in culture (SILAC). Once binding proteins are identified, techniques outlined in objective 1 will be used to determine their role in aspirin-mediated nucleolar translocation of RelA.
Planned Impact
The beneficiaries of this research will be:
1. Academia: As outlined in the academic beneficiaries section, this research will be of considerable and immediate interest to national and international researchers in a number of academic fields including colon cancer prevention nucleolar transport pathways, regulation of cell growth and death by NF-kB and nuclear regulation of RelA. These scientists will benefit from theoretical advancements in the fields, as well as gaining access to the biological tools that will be generated as part of the research and any methodologies developed.
2. Pharmaceutical companies: Uncontrolled NF-kB activity is a contributory factor in a number of common diseases. Therefore, pharmaceutical companies are extremely interested in developments that may lead to novel methods to inhibit this activity. Identification of pathways that cause RelA to translocate to the nucleolus has the very real potential of revealing targets for drugs that manipulate these pathways to switch off NF-kB. As the nucleolar presence of RelA causes apoptosis, the research will also be of interest to companies interested in developing novel anti-cancer agents.
3. Patients and health professionals: Identifying the mechanisms by which aspirin upregulates COMMD1 may have an immediate impact on colorectal cancer patients as it may reveal biomarkers of response in clinical trials of chemopreventative agents. In the long term, understanding the mechanisms by which NSAIDs prevent colorectal cancer may lead to the development of novel agents that could be used to prevent this disease in high risk patients.
4. General public: Media publicity of grant awards and published work will raise awareness of this preventable disease and may prompt the general public to question their risk.
1. Academia: As outlined in the academic beneficiaries section, this research will be of considerable and immediate interest to national and international researchers in a number of academic fields including colon cancer prevention nucleolar transport pathways, regulation of cell growth and death by NF-kB and nuclear regulation of RelA. These scientists will benefit from theoretical advancements in the fields, as well as gaining access to the biological tools that will be generated as part of the research and any methodologies developed.
2. Pharmaceutical companies: Uncontrolled NF-kB activity is a contributory factor in a number of common diseases. Therefore, pharmaceutical companies are extremely interested in developments that may lead to novel methods to inhibit this activity. Identification of pathways that cause RelA to translocate to the nucleolus has the very real potential of revealing targets for drugs that manipulate these pathways to switch off NF-kB. As the nucleolar presence of RelA causes apoptosis, the research will also be of interest to companies interested in developing novel anti-cancer agents.
3. Patients and health professionals: Identifying the mechanisms by which aspirin upregulates COMMD1 may have an immediate impact on colorectal cancer patients as it may reveal biomarkers of response in clinical trials of chemopreventative agents. In the long term, understanding the mechanisms by which NSAIDs prevent colorectal cancer may lead to the development of novel agents that could be used to prevent this disease in high risk patients.
4. General public: Media publicity of grant awards and published work will raise awareness of this preventable disease and may prompt the general public to question their risk.
Organisations
- University of Edinburgh (Lead Research Organisation)
- UNIVERSITY OF EDINBURGH (Collaboration)
- UNIVERSITY OF GLASGOW (Collaboration)
- UNIVERSITY OF WOLVERHAMPTON (Collaboration)
- Heriot-Watt University (Collaboration)
- Newcastle University (Collaboration)
- University of Cordoba (Collaboration)
- Pasteur Institute, Paris (Collaboration)
- Innovate Pharmaceuticals Ltd (Collaboration)
- Centre for Genetic Engineering and Biotechnology (CIGB) (Collaboration)
- UNIVERSITY OF LEEDS (Collaboration)
People |
ORCID iD |
Lesley Stark (Principal Investigator) |
Publications
O'Hara A
(2014)
p300-mediated acetylation of COMMD1 regulates its stability, and the ubiquitylation and nucleolar translocation of the RelA NF-?B subunit.
in Journal of cell science
Chen J
(2017)
Aspirin Prevention of Colorectal Cancer: Focus on NF-?B Signalling and the Nucleolus.
in Biomedicines
Tatham MH
(2017)
A Proteomic Approach to Analyze the Aspirin-mediated Lysine Acetylome.
in Molecular & cellular proteomics : MCP
Novo SM
(2017)
Ex vivo treatment of patient biopsies as a novel method to assess colorectal tumour response to the MEK1/2 inhibitor, Selumetinib.
in Scientific reports
Chen J
(2018)
Crosstalk between NF-?B and Nucleoli in the Regulation of Cellular Homeostasis.
in Cells
Chen J
(2018)
Identification of a novel TIF-IA-NF-?B nucleolar stress response pathway.
in Nucleic acids research
Chen J
(2019)
Insights into the Relationship between Nucleolar Stress and the NF-?B Pathway.
in Trends in genetics : TIG
Lobb I
(2020)
A role for autophagic receptor, P62(SQSTM1), in trafficking NF-KappaB/RelA to nucleolar aggresomes
in Submitted to cancer research
Description | Company of Biologists small meeting grant |
Amount | £1,000 (GBP) |
Organisation | Company of Biologists |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 06/2017 |
End | 06/2017 |
Description | Meeting Grant |
Amount | £1,000 (GBP) |
Organisation | Company of Biologists |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 06/2017 |
End | 06/2017 |
Description | Meeting sponsorship |
Amount | £2,000 (GBP) |
Organisation | Company of Biologists |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 09/2014 |
End | 10/2014 |
Description | Project Grant |
Amount | £15,000 (GBP) |
Organisation | Rosetrees Trust |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 06/2014 |
End | 06/2016 |
Description | Project Grants |
Amount | £13,400 (GBP) |
Organisation | Rosetrees Trust |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 07/2014 |
End | 10/2016 |
Description | Project grant |
Amount | £32,000 (GBP) |
Organisation | Bowel & Cancer Research |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 05/2017 |
End | 10/2018 |
Description | meeting sponsorship |
Amount | £1,300 (GBP) |
Organisation | European Association of Cancer Research (EACR) |
Sector | Academic/University |
Country | United Kingdom |
Start | 09/2014 |
End | 10/2014 |
Title | acute ex vivo treatment of patient biopsies |
Description | We developed an ex vivo treatment model that could be used to analyse patient sensitivity to anti-cancer treatments. We were able to maintain biopsies of fresh colonic tumours in culture and demonstrate that these responded to a number of agents in a genotype specific manner. |
Type Of Material | Model of mechanisms or symptoms - human |
Year Produced | 2017 |
Provided To Others? | Yes |
Impact | We have shared the method and are working with others to develop it for high throughput assays for drug interactions. |
Description | Analysis of TIF-IA and senescence in normal rectal mucosa |
Organisation | University of Leeds |
Department | Leeds School of Medicine |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | My research team will develop a multiplex immunohistochemistry assay to simultaneously analyse TIF-IA, active NF-kB and markers of senescence. We will then use this assay to analyse rectal mucosa samples generated in the seAFOod polyp prevention trial, headed by Mark Hull at the University of Leeds |
Collaborator Contribution | My partner will provide rectal mucosa samples from the seAFOod trial as well as clinicopathological and dietary data. They will also contribute to data analysis. |
Impact | Application to CRUK early detection primer award will be submitted imminently. |
Start Year | 2021 |
Description | Aspirin prevention of cancer in Lynch syndrome patients: Role COMMD1 and TIF-IA |
Organisation | Newcastle University |
Department | Institute of Genetic Medicine |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Initiated the collaboration. Performed immunohistochemistry on samples of normal colon from patients enrolled in CAPP2 study. Quantification and statistical analysis of immunohistochemical data. |
Collaborator Contribution | The CAPP2 project was headed by our partners - randomised trial to determine whether aspirin prevents colon tumourigenesis in Lynch syndrome patients. Partners collected and processed biopsies. They have provided sections of these biopsies for us to analyse the association between COMMD1 and aspirin response. |
Impact | Data analysis ongoing |
Start Year | 2016 |
Description | Chandra lab collaboration |
Organisation | University of Edinburgh |
Department | Institute of Genetics & Molecular Medicine |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Initiated the collaboration. provided tools to study the nucleolus in aging. |
Collaborator Contribution | Single cell RNA seq dependent on nucleolar size |
Impact | Awarded BBSRC grant |
Start Year | 2018 |
Description | Collaboration Institute pasteur Paris |
Organisation | Pasteur Institute, Paris |
Country | France |
Sector | Charity/Non Profit |
PI Contribution | Provided expertise and research tools to examine the role of nucleolar stress in chlamydia infection of cervical epithelial cells |
Collaborator Contribution | Data generation. |
Impact | No outcomes as of yet as start of collaboration. Involves a bacteriologists and a cancer cell biologist |
Start Year | 2017 |
Description | Collaboration University of Cordoba |
Organisation | University of Cordoba |
Country | Spain |
Sector | Academic/University |
PI Contribution | Staining colorectal cancer tissues microarrays (TMAs) for proteins of interest, scoring staining intensity and relating to pathophysiological markers. |
Collaborator Contribution | Staining a subset of colorectal cancers with known genotypes for COMMD1 and measuring staining intensity. |
Impact | No outputs yet. Not multi-disciplinary. |
Start Year | 2018 |
Description | Collaboration with CIGB, Havana, Cuba |
Organisation | Centre for Genetic Engineering and Biotechnology (CIGB) |
Country | Cuba |
Sector | Academic/University |
PI Contribution | i contributed significantly in the preparation of a travel fellowship to allow a PhD student from this department to work in my lab . I am now the phd students second supervisor and have input into the direction of the project. |
Collaborator Contribution | The partners have provided a PhD student to work on the joint project. They have also provided my lab with the peptide that they are developing that targets COMMD1 to use in our studies. |
Impact | On the basis of the collaboration, a PhD student from CIGB obtained a travel fellowship from the Journal of Cell Science (2013) and EMBO (2015) to undertake work in my lab. A manuscript "A novel, COMMD1 targeting peptide, CIGB-552, acts synergistically with aspirin on NF-kappaB signalling and apoptosis" has been submitted to Scientific reports. As a result of the collaboration, myself and the lab at CIGB are jointly organised the 1st Cuban NF-kappaB symposia, held at the second international convention Immunopharamacology, Varadero, 2017. This was a highly succesful conference that brought American and european scientists to Cuba. New collaborations between UK (University of Newcastle) and Cuban (CIGB) scientits have already been initiated based on this conference. |
Start Year | 2013 |
Description | Herriot Watt |
Organisation | Heriot-Watt University |
Department | Institute of Biological Chemistry, Biophysics and Bioengineering (IB3) |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Provided biological question and undertook basic molecular biology and prepared grant application |
Collaborator Contribution | Provided facilities and experience in high resolution microscopy. |
Impact | Submitted joint BBSRC grant |
Start Year | 2012 |
Description | Innovate Pharmaceuticals |
Organisation | Innovate Pharmaceuticals Ltd |
Country | United Kingdom |
Sector | Private |
PI Contribution | Innovate have provided us with a new form of liquid aspirin. We are testing this to determine efficacy against colorectal cancer and mechanism of action |
Collaborator Contribution | Innovate pharmaceutical have provided liquid aspirin. They have also provided funding for the project |
Impact | Not yet |
Start Year | 2015 |
Description | Multiplex immunohistochemistry-Sandrine prost |
Organisation | University of Edinburgh |
Department | MRC Centre for Inflammation Research |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | My research team will provide reagents and samples to develop the assay. |
Collaborator Contribution | The Prost lab will provide expertise in multiplex immunohistochemistry and image analysis |
Impact | Application for a Melville Trust PhD scholarship. Imminent application for a CRUK early detection primer award. |
Start Year | 2021 |
Description | Targeting the nucleolus for cancer prevention and therapy |
Organisation | University of Glasgow |
Department | School of Medicine Glasgow |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Analysing colorectal TMAs for altered TIF-IA and/or nucleolar function. Image quantification |
Collaborator Contribution | Provision of colorectal cancer TMAs, data analysis, correlation with additional markers. |
Impact | Invite to give Beatson Institute Seminar. Application for SCF doctoral fellowship (awaiting decision). |
Start Year | 2019 |
Description | University of wolverhampton |
Organisation | University of Wolverhampton |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Our collaborators generated aspirin analogues and we tested the anti-tumour properties and mechanisms of action of the analogues in my lab. |
Collaborator Contribution | My partners generated and refined aspirin analogues. |
Impact | Publication- Identification of aspirin analogues that repress NF-?B signalling and demonstrate anti-proliferative activity towards colorectal cancer in vitro and in vivo. Projects involved chemists and molecular biologists. Based on this publication a new collaboration was initiated with Innovate Pharmaceuticals to test a new liquid form of aspirin in my lab. |
Start Year | 2010 |
Description | CRUK fringe show |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | Fringe show organised by CRUK to allow the general public and scientists to discuss the cancer journey |
Year(s) Of Engagement Activity | 2017 |
Description | Civic reception |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Public/other audiences |
Results and Impact | Through my work on the organising committee of the 2014 NF-kb subunit meeting, I successfully obtained funding £1300 funding from Perth and Kinross Council which was matched by Visit scotland. Perth and Kinross Council hosted a drinkd reception which the lord provost of perth and kinross attended. This was covered in a press release in the local paper in which the importance of NF-kB in disease was highlighted. None that i am aware of. |
Year(s) Of Engagement Activity | 2014 |
Description | Clinical talk |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Regional |
Primary Audience | Professional Practitioners |
Results and Impact | Talk to oncologists |
Year(s) Of Engagement Activity | 2019 |
Description | International chair - 1st cuban NF-kappaB symposia |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Third sector organisations |
Results and Impact | organisation of 1st Cuban NF-kappaB symposia-purpose to bring to gether NF-kB community with medicinal chemists. this allows scientists to visit cuba and interact with Cuban scientists. |
Year(s) Of Engagement Activity | 2017 |
URL | http://www.immunovaccipharmacuba.com/index.php?module=general10 |
Description | Interview for national news |
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 | Public/other audiences |
Results and Impact | Paper published in 2018 demonstrating a link between aspirin prevention of colon cancer and the nucleolus gained extremely wide publicity. Television interview for BBC and STV, Interviews for multiple stations including BBC radio Scotland. Interviewed by a charity and video placed on YouTube. Press release covered in Newspapers worldwide including Spectator and Herald. Mentions on radio stations worldwide including spain. |
Year(s) Of Engagement Activity | 2018 |
URL | https://twitter.com/i/moments/1003956489957109760 |
Description | Public interest video |
Form Of Engagement Activity | Engagement focused website, blog or social media channel |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | Generated a video highlighting the challenges and successes of cancer research to promote cancer prevention and research funding. Posted on social media with hundreds of Views. Was encouraged to post on youtube. |
Year(s) Of Engagement Activity | 2019 |
URL | https://www.youtube.com/watch?v=hvnLpH7hRXU&t=38s |
Description | Public lecture |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Type Of Presentation | Keynote/Invited Speaker |
Geographic Reach | Regional |
Primary Audience | Public/other audiences |
Results and Impact | Public talk at Edinburgh International Science Festival. As a result. Research reported in many national papers. Awareness raised regarding Bowel cancer |
Year(s) Of Engagement Activity | 2013 |
URL | http://www.sciencefestival.co.uk/whats-on/categories/talk/healthy-lunches-aspirin-a-day |
Description | School visit (Edinburgh) |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Public/other audiences |
Results and Impact | 30 pupils engaged in a workshop. This sparked a lot of interest/questions and interest in science as a career. School increased engagement with scientists |
Year(s) Of Engagement Activity | 2013,2014 |
Description | UK Ireland NF-kappaB subunit meeting Glasgow 2015 |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | No |
Type Of Presentation | keynote/invited speaker |
Geographic Reach | National |
Primary Audience | Public/other audiences |
Results and Impact | media coverage of lord provosts visit to NF-kB workshop to promote interaction between council and visiting scientists. Council contributed money to a drinks reception and provost gave a talk. talk has yet to take place but i have noted increased interest in my research through increased email enquiries |
Year(s) Of Engagement Activity | 2015 |