Personal data
Name:
Nationality :
Email:
Current Position
2005- present
2008-present
July 2012
Previous Positions
1994-1998
1999- 2005
1999-2004
2000-2007
2005-2008
2007-2010
2006-present
Katja Simon
German katja.simon@ndm.ox.ac.uk
Independent grant funding
Head of the Translational Immunology Laboratory, Biomedical Research
Centre, NIHR
Awarded open-end contract by Oxford University, Associate Professor
Postdoc 1 Centre d'Immunologie Marseille Luminy, France, Signalling and cell death in the thymus , A-M. Schmitt-Verhulst
Postdoc 2 Weatherall Institute of Molecular Medicine (WIMM), Oxford,
Death receptors in immunity, Gavin Screaton
Organiser and Lecturer of " Methods and Techniques" course for first year DPhil students, WIMM
Tutor in Immunology and Cell Death to Undergraduate students
Lecturer for the Final Honour School of Medicine and MsC Integrated
Immunology, University of Oxford
Examiner of the MsC course Integrated Immunology
Supervision of 7 PhD students, 3 have completed, one was Departmental
Graduate Prize winner in 2010, and won WIMM prize for best student presentation in 2013

Research Achievements
In my PhD with Avrion Mitchison at the Deutsche RheumaforschungszentrumBerlin, I was first to describe that Th1 cytokines mediate rheumatoid arthritis (PNAS 1994), an observation for which I was awarded the European Award for Young Investigators in Rheumatology
Research. From my postdoc onwards I became interested in cell fate decisions in the immune system namely cell death and autophagy. Deficiency in either can lead to inflammation and/or autoimmunity. As a postdoctoral fellow with Anne-Marie Schmitt-Verhulst at the CIML in Marseille, my key achievements included the identification of signalling molecules in thymic cell death (Int Immunol 1996, Immunology 1997, Cell Death and Diff
2000).
In a second postdoc with Gavin Screaton (WIMM Oxford), I investigated the role of TRAIL, a cell death receptor, in thymic tolerance using human and murine thymic organ cultures and in vivo models (PNAS 2001). I demonstrated that Fas ligand breaks tolerance and induces inflammation leading to tumour rejection mediated by tumour antibodies (Cancer Cell 2002, patent 1096). I generated anti-melanoma tumour-rejecting monoclonal antibodies (Int
Immunol 2008), which cross-react with human melanoma (Cancer Research 2009). With this system we elucidated how the initial innate anti-tumour response, including NK cells and neutrophils, is inhibited by regulatory T cells (Eur J Immunol 2007, review in Oncogene
2008). I also initiated the idea that lowering the threshold of thymic tolerance results in tumour immunity (PlosOne 2012).
I have had autonomous funding since 2005 (AICR, BBSRC, Wellcome Trust). In 2006 I obtained the title of Honorary Research Lecturer by the University of Oxford, in 2014 that of
Associate Professor. I am a member of common room at Wolfson College. My lab at the
WIMM has pioneered the analysis of autophagy in the immuno-hematopoietic system. By conditionally deleting the core autophagy gene Atg7, we were among the first to show how autophagy shapes the differentiation of hematopoietic cells. Red blood cells, T and B lymphocytes undergo early cell death with mice developing severe anemia and lymphopenia.
Immature red blood cells are prone to death due to ROS production caused by an inability to remove mitochondria during development through autophagy (mitophagy) (PNAS 2010, reviews in Autophagy 2010, Cell Cycle 2010). Moreover, we first demonstrated that stem cells require mitophagy for their maintenance, thus preventing DNA damage and malignancy
(J.Exp Med 2011, reviews Autophagy 2011 & Cell Cycle 2011). Due to these important contributions to the emerging autophagy field, I am regularly invited to speak at international
Autophagy, Hematology and Immunology meetings.
In 2008 I was appointed as the head of the TIL (Oxford Biomedical Research Center, NIHR) at the John Radcliffe Hospital. This laboratory is an "Immunology hub" for the Oxford clinical research community. It gives advice and trains clinicians and establishes novel state-of-theart immunological assays, mostly flow cytometry based (LSR2 and Image stream). The remit of the TIL is to adopt assays developed to make progress in one disease rapidly to work in other areas. We set up a novel single cell assay for autophagy and mitochondrial damage detection in primary cells using imaging flow cytometry (Autophagy 2012, Cold Spring
Harbour Protocols, in press), that is being used by many research groups and has led to several publications (Nature Nanotechnology 2011, J Neurochem 2011, Am J Hum Gen
2012, Guidelines for Autophagy techniques, Autophagy 2012, Biochem J 2012, Mol Biol Rep
2012) and several successful grant co-applications (Wellcome Trust 2011-2014, MRC 2012-
2015, Waterloo foundation 2012-2013, Kidney Research UK 2012-2015, Lady Tata 2013)

What are the Future Aims of Your Current Group?
The interplay between autophagy, cell cycle control and, senescence and malignancy is emerging as a key feature in tumour development, which we will be investigating over the next five years in the haematopoietic system. Our tools, conditional Atg7 and Atg5 mouse models, autophagy detection techniques in human primary cells, as well as state-of-the-art immunological and haematological techniques, make us highly competitive in this field.
The pathways that lead to division and growth in multicellular organisms have been conserved from single to multi-cellular organisms. One such conserved pathway is autophagy. Autophagy is the major lysosomal mechanism to degrade macromolecules in the cell. Cell growth in response to environmental conditions is regulated by two antagonistic processes: protein synthesis (anabolism) and autophagy (catabolism), integrating signals from growth factors, amino acids and energy status through the TOR complex. mTOR signaling inhibits autophagy while it positively regulates protein synthesis. Autophagy can also respond directly independently of mTOR to the cellular milieu.
Under certain environmental or developmental conditions, cells leave the cell cycle to enter one of three types of cell cycle arrest (G0) namely quiescence, senescence or terminal differentiation . While mTOR activation has been shown to activate cell growth and cycling in hematopoietic cells, our results indicate that autophagy directly inhibits proliferation and exit of the cell cycle. Understanding the control of TOR signaling and autophagy in this process is relevant to disease, in particular malignancy. Our previous work shows that autophagy is required in the maintenance of quiescence in hematopoietic stem cells (HSC) and terminal differentiation of neutrophils, both critical events in myeloid malignancy.
The hematopoietic system provides an ideal physiological system to study the interplay between cell cycle and autophagy and a typical quiescent cell is the HSC. The hematopoietic system develops in a hierarchical fashion; a small number of long-term stem cells that are quiescent divide to become progenitors that proliferate and differentiate into mature blood cell lineages produced in large numbers.
A second more mature hematopoietic stem-like cell type is the memory T cell. Like HSCs memory T cells have to exit cell cycle to enter quiescence . Immunological memory is a hallmark feature of the adaptive immune system to fight recurring pathogens. After an infection has been resolved, a few of the specific T lymphocytes are retained in a resting pre-terminally differentiated state known as memory cells. It is thought that immunological memory depends on a stem-cell-like, self-renewing population of lymphocytes with the multipotent ability to derive central memory, effector memory and effector T cells.
Thirdly our data shows that the terminal differentiation of neutrophils is controlled by autophagy. After their terminal differentiation, neutrophils have a finite lifespan of a few days.
Neutrophils are well characterised by surface markers, functional features and morphologically by granules and nuclear shape. Only differentiated neutrophils undergo cell death, immature neutrophils accumulate and cause disease, in particular myeloid malignancy (ref).
Over the next five years, we are setting out to understand the role of autophagy in cell cycle exit and maintenance of quiescence and terminal differentiation in hematopoietic cells, in both physiological and pathological settings.
We will be addressing the following 3 main questions. This work is being funded by the

Wellcome Trust new investigator award from August 2014 onwards for 5 years.
Can immune senescence be reversed by modulation of autophagy?
Some infectious diseases such as seasonal influenza mostly affect the aged, while only 1 in 3 elderly respond to the annual flu vaccination. We will correlate vaccination efficiency with autophagy levels and modulate autophagy while vaccinating mice. We will attempt to improve memory T cell responses by increasing autophagy genetically and pharmacologically
How does autophagy contribute to myeloid proliferation and malignancy?
Preliminary data in the myeloid lineage suggests that (1) autophagy deficiency leads to a change in metabolism by proteomics (Warburg effect), (2) neutrophils remain undifferentiated and immature, a hallmark of myeloid mailgnancy, and (3) inflammasome activity is increased.
Are these findings linked and do they contribute to enhanced proliferation and transformation of this lineage? Does autophagy induction lead to differentiation and death of transformed myeloid cells?
How does autophagy regulate stem cell differentiation and quiescence?
From our data that autophagy is highly active in hematopoietic stem cells (HSCs) and other data, we postulate that autophagy contributes to the longevity of HSCs while avoiding ageing and differentiation. Telomere length and damage will be monitored in HSCs and autophagy will be increased genetically. Is autophagy needed for remodelling during differentiation, and remaining in a state of quiescence? Describing a role for autophagy in hematopoietic stem cellness is an entirely novel concept applicable to other stem cells and cancer.
How do these Aims Contribute to the Understanding and/or Management of Human
Disease?
Aged individuals are less efficient at fighting off infections, with the consequence that some infectious diseases such as seasonal influenza mostly affect the aged. As we are facing new emerging infectious diseases and some vaccinations are likely to be administered at a more advanced age, this has become a substantial health and socio-economic problem that needs addressing urgently. Myeloid malignancies and proliferation are another contributing factor to morbidity in the aged. We are planning to undertake a small molecule library screen for autophagy modulators. Our work will address how to enhance healthy life span, while contributing to the elucidation of basic concepts in autophagy, senescence and cancer biology.
As autophagy is impinging on many areas of biomedical research, interdisciplinary research is necessarily part of my programme. We have a network of collaborators across the medical division (P Klenerman NDM, M Tarsounas Gray Institute, D Ferguson NDCLS, E Soilleux
NDCLS) and in the WIMM (SE Jacobsen, P Vyas, A Townsend) making this programme successful. Other national and international collaborators will also help us to elucidate basic as well translational aspects in this field.
In 2008, we founded the Translational Immunology Lab (JRH, Oxford BRC, NIHR) as part of the
Immunity theme, an "Immunology hub" where we give advice, train scientists and perform stateof-the-art flow cytometry-based immunological assays for translational studies. In addition, we set up a high throughput and objective statistically rigorous quantification of autophagic flux

using the Image stream, with concomitant surface marker detection, essential for the study of autophagy in clinical samples. Over 30 groups across the Medical Science Division are using this assay, which has led to 3 publications with 4 more in revision, and 4 grants awarded so far.
We are currently setting up a FlowFish protocol on telomere length for the ImageStream.
Lay Summary of Research
Due to medical progress and improved hygiene, the population of the developed world is ageing, with the number of people aged over 65 in the UK expected to rise dramatically, from 600 million to nearly 2 billion in 2050. The elderly population is facing increased morbidity and mortality.
One of the contributing factors is the ageing of the immune system termed immune senescence.
Aged individuals are less efficient at fighting off infections, with the consequence that some infectious diseases such as seasonal influenza mostly affect the aged. Crucially the elderly also take longer to recover from infections and do not respond to vaccinations, such as the annual flu vaccination, thus reducing the impact of preventive medicine. As we are facing new emerging infectious diseases and some vaccinations are likely to be administered at a more advanced age, this has become a substantial health and socio-economic problem that needs addressing urgently.
Autophagy is a major cellular pathway responsible for the degradation of cellular toxic waste and recycling. It is known that calorie restriction, exercise and certain drugs turn autophagy on, maintaining a healthy status in aged cells, preventing the onset of age-related diseases like
Parkinson’s, Alzheimer’s, muscle wasting and osteoporosis.
We have shown that autophagy is declining with age in human immune cells, contributing to failure to fight off infections, and responding to vaccinations. With our research we are aiming to reverse this decline, at least temporarily, for example during flu vaccination of the elderly.
Furthermore our previous research also shows that certain blood cancer types (myeloid dysplasia and myeloid malignancies), prevalent in the aged, develop when autophagy is deficient. Understanding the process of autophagy and how it contributes to ageing and agerelated diseases will help to design therapies and life style changes that will prevent these diseases.

All Publications Over the Past 5 Years
1) Simon AK *, Jones E*, Richards H*, Wright K, Godkin A, Screaton G and Gallimore A.
(2007) Regulatory T cell inhibit Fas ligand induced innate and adaptive immunity. Eur J
Immunol 37, 758-767.
2) Simon AK , NewsomDavis T*, Frayne MEF*, Ch’en PF-T*, McMichael AJ and Screaton
GRS (2008) Generation of tumour-rejecting anti-carbohydrate monoclonal antibodies using melanoma modified with Fas Ligand, Int Immunol 20: 525-34
3) Arsov I, Li X, Matthews G, Coradin J, Hartmann B, Simon AK , Sealfon SC and Yue Z.
(2008) BAC-mediated transgenic expression of fluorescent autophagic protein Beclin 1 reveals a role for Beclin 1 in lymphocyte development, Cell Death Diff 15 : 1385-95
4) Gallimore AM and Simon AK (2008) Positive and Negative influences of regulatory T cells on tumour immunity, Oncogene 27: 5886-93
5) Newsom-Davis TE, Wang D, Steinman L, Chen PF, Wang LX, Simon AK and
Screaton.GR (2009) Enhanced immune recognition of cryptic glycan markers in human tumours, Cancer Research , 69, 2018-25
6) Hong H, Gu Y, Zhang, H, Simon AK , Chen X, Wu C, Xu X-N, and Jiang S, (2009)
Depletion of CD4 + CD25 + regulatory T cells enhances natural killer T cell-mediated antitumour immunity in a murine mammary breast cancer model, Clin Exp Immunol ,
159:93-9
7) Mortensen M, Ferguson DJP, Edelmann M, Kessler B, Morten KJ, Komatsu M and
Simon AK (2009) Loss of autophagy in erythroid cells leads to defective removal of mitochondria and lethal anaemia in vivo. Proc Natl Acad Sci 107 :832-837
8) Mortensen M and Simon AK (2010) Nonredundant role of Atg7 in mitochondrial clearance during erythroid development. Autophagy , 6 : 423-5.
9) Krashias G, Simon AK , Wegmann F, Kok WL, Ho LP, Stevens D, Skehel J, Heeney JL,
Moghaddam AE, Sattentau QJ. (2010) Potent adaptive immune responses induced against HIV-1 gp140 and influenza virus HA by a polyanionic carbomer. Vaccine
28:2482-9
10) Mortensen M, Ferguson, D and Simon AK (2010) Mitochondrial clearance by autophagy in developing erythrocytes: clearly important, but just how much so? Cell Cycle , 9:1901-
6
11) Richards H, Williams A, Jones J, Hindley J, Godkin A, Simon AK and Gallimore, A
(2010) Novel role of regulatory T cells in limiting early neutrophil responses in skin,
Immunology , 131: 583-592
12) Mortensen, M, Soilleux EJ, Tripp R, Stranks AJ, Djordjevic G, Kranc KR* and Simon AK*
(2011) The autophagy protein Atg7 is essential for hematopoietic stem cell maintenance and leukemia prevention. J Exp Med 208:455 –67
13) Mortensen M*, Watson AS* and Simon AK (2011) Lack of autophagy in the hematopoietic system leads to loss of hematopoietic stem cell function and dysregulated myeloid proliferation Autophagy 7: 9:1-2
14) Watson AS*, Mortensen M* and Simon AK (2011) Autophagy in the pathogenesis of myelodysplastic syndrome and acute myeloid leukemia, Cell Cycle 10:11, 1-7
15) Sood A, Salih S, Roh D, Lacharme-Lora L, Parry M, Hardiman B, Keehan R, Grummer
R, Winterhager F, Gokhame P, Andrews P, Abbott C, Forbes K, Westwood M, Aplin J,
Ingham E, Papageorgiou I, Berry M, Liu J, Dick A, Garland RJ, Williams N, Singh R,
Simon AK , Lewis M, Ham J, Roger L, Baird DM, Crompton LA, Caldwell MA ,Swallwell
H, Machlin MB, Lopez-Castejon G, Randall A, Lin H, Suleiman M-S, Evans H, Newson
R, Case CP (2011) Signalling of DNA damage and cytokines across cellular barriers exposed to nanoparticles depends on barrier thickness. Nature Nanotechnology , 6
(12), 824-833.

16) Kwok AS, Phadwal K, Turner 1 BJ, Oliver PL, Raw A, Simon AK , Talbot K and Agashe VR
(2011) HspB8 Mutation Causing Hereditary Distal Motor Neuropathy Impairs Lysosomal
Delivery of Autophagosomes, Journal of Neurochemistry , 187 (10) 5268-76.
17) Phadwal K, Alegre Abarrategui J, Watson A, Pike L, Anbalagan S, Hammond EM,
Wade-Martins R, McMichael A, Klenerman P and Simon AK (2012) Autophagic flux
18) measurement in primary cells: Impaired levels of macroautophagy in immunosenescent
T cells Autophagy , 8 (4).
+
Medullary Epithelium (2012) Roberts A, White AJ, Jenkinson, WE, Turchinovich G,
Nakmura K, Withers DR, McConnnell FM, Desanti GE, Benezech C, Pamell SM,
Cunningham AF, Paolino M, Penninger J, Simon AK , Nitta T, Ohigashi I, Takaham Y,
Casamano JH, Hayday H, Lane PJL, Jenkinson EJ, Anderson G, Immunity 36 (4) 427-
437
19)
Träger U, Sierro S, Djordjevic G, Bouzo B, Khandwala S, Meloni A, Mortensen M and
Simon AK (2012) The immune response to melanoma is limited by thymic selection of self-antigens . PlosOne, 7 (4): e35005
20) Lopez-Herrera G, Tampella G, Pan-
Hammarström Q, Herholz P, Trujillo-Vargas CM,
Phadwal K, Simon AK, Moutschen M, Etzioni A, Mory A, Srugo I, Melamed D, Hultenby
K, Liu C, Baronio M, Vitali M, Philippet P, Dideberg V, Aghamohammadi A, Rezaei N,
Enright V, Du L, Salzer U, Eibel H, Pfeifer D, Veelken H, Stauss H, Lougaris V, Plebani
A, Gertz EM, Schäffer AA, Hammarström
L and Bodo Grimbacher (2012) Deleterious
LRBA mutations in a novel syndrome of immune deficiency and autoimmunity, Am J
Hum Gen , Jun 8;90(6):986-1001. Epub May 17
21) Klionsky DJ et al (1400 authors)(2012) Guidelines for the Use and Interpretation of
Assays for Monitoring Autophagy in Higher Eukaryotes, Autophagy Apr;8(4):445-544
22) Phadwal K, Watson AS and Simon AK (2012) Tightrope Act : Autophagy in stem cell renewal, differentiation, proliferation and aging, Cell and Mol Life Sciences , June 5
23) Pike LR, Singleton DC, Buffa F, Abramczyk O, Phadwal K, Li JL, Simon AK , Murray JT,
Harris AL (2012) Transcriptional upregulation of Ulk1 by ATF4 contributes to cancer cell survival. Biochem J . Oct 18
24) Pike LR, Phadwal K, Simon AK , Harris AL (2012) ATF4 orchestrates a program a BH3only protein expression in severe hypoxia (2012) Mol Biol Rep . 2012 Dec;39
(12):10811-22
25) Guan , JL, Simon AK , Prescott M, Menendez JA, Liu F, Fen Wang F, Wang C, Wolvetang
A, Vazquez-Martin A and Zhang J (2013) Autophagy in Stem Cells Autophagy , 13, 9 (6)
26) Simon AK and Ballabio A (2013) T.rex attacks the lysosome, Nature Immunology 14
(1)
27) Puleston D and Simon AK (2013) Autophagy in the Immune system, Immunology , Aug
31
28) Pienaar IS, Harrison IF, Elson JL, Bury A, Woll P, Simon AK , Dexter DT (2013) An animal model mimicking pedunculopontine nucleus cholinergic degeneration in
Parkinson's disease, Brain Struc Funct , in press
29) Puleston D, Phadwal K, Watson AS, Soilleux EJ, Chittaranjan, S, Bortnik SB, Ktistakis
TK, Gorski SM*, Simon AK * (2013) Autophagy detection techniques in primary mammalian cells, Cold Spring Harbor Protocols , in press
30) Clarke AJ, Ellinghaus U, Cortini A, Stranks A, Simon AK , Botto M, Vyse TJ. (2013)
Autophagy is activated in systemic lupus erythematosus and required for plasmablast development ,.
Ann Rheum Dis . doi: 10.1136/annrheumdis-2013-204343. [Epub ahead of print]
31) Henson SM, Lanna A, Riddell NE, Franzese O, Macaulay R, Griffiths SJ, Puleston DJ,
Watson AS, Simon AK , Tooze SA, Akbar AN (2014) p38 signaling inhibits mTORC1independent autophagy in senescent human CD8+ T cells, J Clin Invest

doi:1172/JCI75051
32) Jabir MS, Ritchie ND, Li D, Bayes HK, Tourlomousis P, Puleston D, Lupton A, Hopkins
L, Simon AK , Bryant C, Evans TJ. (2014) Caspase-1 cleavage of the TLR adaptor TRIF inhibits autophagy and β-interferon production during Pseudomonas aeruginosa infection. Cell Host Microbe 15(2):214-27. doi: 10.1016/j.chom.2014.01.010
33) MS Jabir, L Hopkins, N Ritchie, I Ullah, H Bayes, P Tourlomousis, A Lupton, D Puleston,
AK Simon , C Bryant and TJ Evans (2014) NLRC4 Activation by Pseudomonas aeruginosa is Dependent on Mitochondrial Damage and is Down-regulated by
Autophagy, Autophagy , in press
34) DJ Curtis, A Sood, TJ Phillips, VH Leinster, A Nishiguchi, C Coyle, L Lacharme-Lora, O
Beaumont, H Kemp, R Goodall, L Cornes, M Giugliano,RA Barone, M Matsusaki, M
Akashi, HY Tanaka, M Kano, J McGarvey, ND Halemani, K Simon , R Keehan, W Ind, T
Masters, S Grant, S Athwal,G Collett, D Tannetta, IL Sargent, E Scull-Brown, X Liu, K
Aquilina, N Cohen, JD Lane, M Thoresen, J Hanley, A Randall, CP Case. Secretions from placenta, after hypoxia/reoxygenation, can damage developing neurones of brain under experimental conditions. Exp Neurol . 2014 May 10;261C:386-395.
Publications submitted/ under review
1) D Puleston, H Zhang*, T Powell*, E Lipina, S Sims, M Sitbon, V Cerundolo, P
Klenerman*, A Townsend*, AK Simon, Autophagy as a critical regulator of CD8 + T cell memory and a route to improved vaccination in the elderly, revised manuscript in preparation, e-life
2) AS Watson, A Stranks, S Khandwala, M Lutterop, P Woll, K Phadwal, M Mortensen, D
Puleston, G Djordjevic, D Ferguson, E Soilleux, SE Jacobsen, AK Simon.
Deficient autophagy ties hematopoietic stem cell dysfunction to myeloid dysplasia and acute myeloid leukemia, submitted, Cell Reports
3) AJ Stranks, M Mortensen, DJP Ferguson, DJ Puleston, K Shenderov, AS Watson, K
Phadwal, J McGouran, B Kessler, V Cerundolo, AK Simon. Reduced maturation and antigen presentation in autophagy-deficient macrophages is consistent with inflammaging, J Innate Immunity, revised version in preparation, Journal of Innate Immunity
Ten Key Publications Throughout your Career
1) Simon AK , Seipelt E, Sieper J (1994). Divergent T cell cytokine patterns in inflammatory arthritis. Proc Natl Acad Sci 91, 8562-8566
2) Simon AK , Auphan N, Schmitt-Verhulst AM (1996). Developmental control of antigeninduced thymic transcription factors. Int Immunol 9, 1421-1428
3) Simon AK , Auphan N, Pophillat M, Boyer C, Ghosh S, Rincon M, Flavell RA, Schmitt-
Verhulst AM. (2000) The lack of NF-kappaB transactivation and PKCepsilon expression in CD4+CD8+ thymocytes correlates with negative selection. Cell Death Differ 12, 253-
62
4) Simon AK , Williams O, Mongkolsapaya, J, Boquan J, Xu X, Walczak H, Screaton GR.
(2001) TRAIL in T cell development: sensitivity of human thymocytes. Proc Natl Acad
Sci 98, 5150-5163
5) Simon AK *, Gallimore A*, Jones E, Cerundolo V, Screaton GR (2002). Fas ligand breaks tolerance to self-antigens and induces tumour immunity mediated by antibodies.
Cancer Cell 2 , 315-322.

6) Simon AK *, Jones E*, Richards H*, Wright K, Godkin A, Screaton G and Gallimore A.
(2007) Regulatory T cell inhibit Fas ligand induced innate and adaptive immunity. Eur J
Immunol 37, 758-767.
7) Simon AK , Newsom-
Davis T*, Frayne MEF*, Ch’en PF-T*, McMichael AJ and Screaton
GRS (2008) Generation of tumour-rejecting anti-carbohydrate monoclonal antibodies using melanoma modified with Fas Ligand, Int Immunol 20: 525-34
8) Mortensen M, Ferguson DJP, Edelmann M, Kessler B, Morten KJ, Komatsu M and
Simon AK (2009) Loss of autophagy in erythroid cells leads to defective removal of mitochondria and lethal anaemia in vivo. Proc Natl Acad Sci 107 :832-837
9) Mortensen, M, Soilleux EJ, Tripp R, Stranks AJ, Djordjevic G, Kranc KR* and Simon
AK* (2011) The autophagy protein Atg7 is essential for hematopoietic stem cell maintenance and leukemia prevention. J Exp Med 208:455
–67
10) Phadwal K, Alegre Abarrategui J, Watson A, Pike L, Anbalagan S, Hammond EM,
Wade-Martins R, McMichael A, Klenerman P and Simon AK (2012) Autophagic flux measurement in primary cells: Impaired levels of macroautophagy in immunosenescent
T cells Autophagy , 8 (4).
Markers of Esteem
1994
2013/2014
2014
European award for young investigators in Rheumatology research
Member of Deutsche Forschungsgemeinschaft committee for SFB evaluation of consortium of 17 projects on autophagy, Frankfurt University
Member of AERES evaluation committee of Institute of Molecular
Genetics, Montpellier
Current Grant Support
2008-2017 Biomedical Research Centre , my salary funded by NIHR
(consumables £50,000/year for 1 postdoc + 1 RA)
2012-2015
2012-2015
Immunity Theme leader: Paul Klenerman
MRC project grant, Developing Induced pluripotent stem cells as a model to investigate tissue specific mitochondrial disease, appprox £250, 000,
Co-applicant with J Poulton, F Brook, K Morten, N Ashley, R Wade-
Martins, S Cowley
Kidney Research UK , Mechanism of interstitial nephritis, fibrosis and renal failure due to Uromodulin mutations, £235,920, Co-applicant with Raj
Thakker
2014-2019 New Investigator Award, Role of autophagy in quiescence of healthy hematopoietic cells, £962,500