The document is a curriculum vitae for Dr. Abdallah K. Al-Hakim, who has extensive training and research experience in biochemistry, including postdoctoral research studying the DNA damage response pathway and centrosome regulation, PhD research characterizing protein kinases, and MSc research on adenylyl cyclase isoforms; he has published numerous papers in high-impact journals and received several awards and fellowships for his work.

1. CURRICULUM VITAE
Abdallah K. AL-HAKIM, PhD
Samuel Lunenfeld Research Institute, 600 University Avenue, Toronto, Canada, M5G 1X5
abdallah.alhakim@gmail.com; Tel: +1 647 866 6192
TRAINING AND EDUCATION
2007–2011 Post doctorate, Durocher laboratory
Samuel Lunenfeld Research Institute, Mount Sinai Hospital,
Toronto, Canada
2004-2007 PhD, Alessi laboratory
MRC Protein Phosphorylation Unit, University of Dundee, UK
2000-2002 MSc, Schimmer laboratory
Banting & Best Research Institute, University of Toronto,
Canada
1996-2000 Bachelor of Science (Honors) with high distinction
Overall GPA: 3.7/4.0 (A-) Final year GPA: 3.9/4.0 (A+)
University of Toronto, Canada
RESEARCH EXPERIENCE
2007-2011 Postdoctoral researcher, Samuel Lunenfeld Research
Institute, Toronto, Canada
Supervisor: Dr. Dan Durocher
DNA Damage
To move toward new cancer treatments, it is critical that we understand the mechanisms
that underpin the body’s defences against mutation or DNA strand breaks. A key project
that I led was the characterization of a newly discovered, critical component of signalling
downstream of DNA double strand breaks, RNF168 E3 ligase. To understand how this
protein mediates these important downstream events, I developed a comprehensive plan to
characterize and elucidate its role in the DNA damage response. Together with my
colleagues we dissected the DNA damage response pathway and established RNF168 as a
key regulators of this important pathway. Furthermore, we provided clinical evidence that
mutations in this enzyme are the likely cause of the cellular and developmental phenotypes
associated with RIDDLE syndrome, an immunodeficiency disease. I was also involved in
follow-up work to determine the identity of the deubiquitylating enzyme that opposes the
activity of RNF168. Together with Shinichiro Nakada, a postdoctoral fellow in our laboratory,
I identified OTUB1 as the deubiquitylating enzyme in this process. We identified a non-
canonical function of OTUB1, which rather than acting as a deubiquitylating enzyme,
antagonises RNF168-dependent ubiquitylation by binding to and inhibiting the E2 enzyme
(UBC13) that cooperates with RNF168. My discovery of these new players of the DNA
damage response was an integral part of publications in the journals Cell and Nature.
Importantly, my work has led to identification of two druggable enzyme targets that can be
exploited to kill cancer cells that have elevated DNA damage response.
Centrosome regulation
Working in the Samuel Lunenfeld Research Institute allowed me to explore further
collaborations with many of the world-class scientists in different fields of study. To this end,
I setup a collaborative project with Pelletier group, a centrosome-focused laboratory, to

2. study the involvement of UPS (ubiquitin proteasome system) at the centrosome. Together
with Laurence Pelletier, I devised a project to characterize the interactome of CP110, a key
regulator of centrosome duplication and its regulation through ubiquitylation is important for
maintaining genomic integrity which left unchecked leads to cancer. I employed AP/MS
techniques and identified a number of interesting partners that include the E3 ligases
HERC2 and neuralized-like protein NEURL4. Further biological characterization of these
proteins showed them to be localized to the centrosome and their depletion led to formation
of abnormal centrosomal structures. I carried out further mass spectrometry analysis of
NEURL4, HERC2 and CEP97 (reported partner for CP110) and determined that two protein
complexes exist in cells. One complex includes CEP97-CP110-NEURL4 and the other is
composed of NEURL4-HERC2. My work also demonstrated that HERC2 is the E3 ligase
that ubiquitylates NEURL4, suggesting that this activity is important for regulating
centrosome architecture. My manuscript for this work was recently accepted for publication
in the journal of molecular and cellular proteomics.
Drug development
My extensive networking within the institute coupled to my expertise in the area of
ubiquitylation made me a sought after target for more collaboration. One such example was
my involvement with Sicheri group in characterizing CC0651, the small molecule inhibitor of
CDC34. This exciting work, which was recently published in CELL, indicates that it is
possible to develop a highly selective inhibitor of an E2 enzyme and raises the possibility of
targeting other E2s in similar manner. I provided significant contributions to discussion of the
project and to the experimental designs that demonstrated the remarkable specificity of this
inhibitor. I have supplemented my academic research experience with further training in the
business development through participation in entrepreneurship courses and venture capital
investment courses. Also, I became involved in the local biotechnology community by
volunteering for the Toronto Biotechnology Initiative group.
2004-2007 PhD, MRC Protein Phosphorylation Unit, University of
Dundee, UK
Supervisor: Professor Dario Alessi
Project: Characterization of the AMPK-subfamily of protein kinases
I chose to pursue my PhD at the world-renowned MRC protein phosphorylation Unit (PPU).
This decision was made with two goals in mind, the first was to gain a better global scientific
perspective and be exposed to different management strategies. This international element
has always been important to me and is reflected in my bilingualism and ability to
communicate and work with teams around the world. This was also reflected in my extensive
participation in team rowing competitions where I represented Canada at the university level
in Europe, Asia and United States. The second was to be exposed to the industry links that
the PPU had established with a consortium of big pharmaceutical companies (AstraZeneca,
Boehringer Ingelheim, GlaxoSmithKline, Merck-Serono and Pfizer). My PhD desertion
focused on studying a novel family of protein kinases that was activated by LKB1 kinase.
This was an important project because mutations in LKB1 have linked it to Peutz Jeghers
syndrome and it was critical to understand whether these downstream kinases were also
involved in this disease. This was a critical first step to validate these kinase as potential
drug targets for the treatments of cancer and diabetes.
To study this novel family, I was the first in the institute to successfully develop a modified
version of the tandem affinity purification strategy. I employed this technique to study the

3. interacting partners of the twelve AMPK-related kinases. Using mass spectrometry, I
identified, I identified a number of novel binding partners that interacted with one or more of
the AMPK subfamily enzymes, including ubiquitin specific protease-9 (USP9) and isoforms
of the phospho-protein binding adaptor 14-3-3. I carried out further studies characterized the
interaction between 14-3-3 and the kinases QSK and SIK. I found that the 14-3-3 bound
directly to the T-loop Thr residue of QSK and SIK, after these were phosphorylated by LKB1
This study provided the first example of 14-3-3 binding directly to the T-loop of a protein
kinase and influencing its catalytic activity and cellular localization.
The success of my TAP purification strategy made me the go-to-person in the institute
regarding this biochemical technique and I was in a position to offer advice to many
colleagues. Also, my pool of stable cell lines was highly requested by collaborators and I
sent these cell lines to many laboratories around the world. I had the opportunity to present
my findings to the quarterly meetings of the pharmaceutical consortium at the institute. This
afforded me the opportunity to talk with pharmaceutical representatives and gain a
perspective regarding their research targets.
During the second half of my PhD, I was interested in studying the crosstalk between
ubiquitylation and phosphorylation mechanisms. This was a novel area at the time but one
that I could foresee becoming an important one for future drug development. I decided to
further characterize the interaction between USP9 and the AMPK-related kinases NUAK1
and MARK4. This was a departure from the focus research area of my institute and
therefore I sought to build a scientific network with the ubiquitylation experts in the
University. This was an important step in ensuring rapid progress through this project. My
work demonstrated that both of these kinases were ubiquitylated in vivo. I showed that
USP9 catalyses the removal of polyubiquitin chains from wild-type NUAK1. Topological
analysis revealed that ubiquitin monomers attached to NUAK1 and MARK4 were linked by
Lys(29) and/or Lys(33) rather than the more common Lys(48)/Lys(63) linkage chains. I also
provided evidence suggesting that polyubiquitylation may inhibit activity of these enzymes.
The success of my work in this field allowed me further opportunities to network with the
pharmaceutical companies during their visits to the institute and solidified my belief that
protein ubiquitylation machinery will be an important drug target in the future.
2000-2003 MSc, Banting & Best Research Institute, University of
Toronto, Canada
Supervisor: Professor Bernard Schimmer
Project: Characterization of forskolin resistant Y1 mouse adrenocortical cell lines
Four mutant clones independently derived from the Y1 mouse adrenocortical tumour cell line
have adenylyl cyclase (AC) activities that are resistant to forskolin, a direct activator of AC. I
carried out experiments to determine the AC isoform composition of the forskolin-resistant
mutants in order to explore the underlying basis for the resistance to forskolin. As
determined by Western blot and RT-PCR analysis, the four forskolin-resistant mutants were
all deficient in AC-4; the levels of other AC isoforms (AC-1, AC-3 and AC-5/6) were
comparable to the levels in parent Y1 cells. Transfection of one of the mutant clones with an
AC-4 expression vector increased forskolin-stimulated cAMP signalling, and restored
forskolin-induced changes in cell morphology and growth. My work lead to the conclusion
that AC-4 deficiency is a hallmark of the forskolin-resistant phenotype of these mutants and
suggested that AC-4 is an important target of forskolin action in the Y1 adrenal cell line.

4. PUBLICATIONS
Manuscripts in press:
1. Abdallah K. Al-Hakim, Mikhail Bashkurov, Anne-Claude Gingras, Daniel Durocher and
Laurence Pelletier. Interaction proteomics identify NEURL4 and the HECT E3 ligase HERC2
as novel modulators of centrosome architecture. Molecular and Cellular
Proteomics mcp.M111.014233. First Published on January 19,
2012, doi:10.1074/mcp.M111.014233
2. Ceccarelli DF, Tang X, Pelletier B, Orlicky S, Xie W, Plantevin V, Neculai D, Chou YC,
Ogunjimi A, Al-Hakim A, Varelas X, Koszela J, Wasney GA, Vedadi M, Dhe-Paganon S,
Cox S, Xu S, Lopez-Girona A, Mercurio F, Wrana J, Durocher D, Meloche S, et al.An
allosteric inhibitor of the human cdc34 ubiquitin-conjugating enzyme. Cell. 2011 Jun
24;145(7):1075-87. Epub 2011 Jun 16
3. Al-Hakim A, Escribano-Diaz C, Landry MC, O'Donnell L, Panier S, Szilard RK, Durocher
D. The ubiquitous role of ubiquitin in the DNA damage response. DNA Repair (Amst). 2010
Dec 10;9(12):1229-40. Epub 2010 Nov 4. Review.
4. O'Donnell L, Panier S, Wildenhain J, Tkach JM, Al-Hakim A, Landry MC, Escribano-Diaz
C, Szilard RK, Young JT, Munro M, Canny MD, Kolas NK, Zhang W, Harding SM, Ylanko J,
Mendez M, Mullin M, Sun T, Habermann B, Datti A, Bristow RG, Gingras AC, et al. The
MMS22L-TONSL complex mediates recovery from replication stress and homologous
recombination. Mol Cell. 2010 Nov 24;40(4):619-31. Epub 2010 Nov 4.
5. Nakada S, Tai I, Panier S, Al-Hakim A, Iemura S, Juang YC, O'Donnell L, Kumakubo A,
Munro M, Sicheri F, Gingras AC, Natsume T, Suda T, Durocher D.Non-canonical inhibition
of DNA damage-dependent ubiquitination by OTUB1. Nature. 2010 Aug 19;466(7309):941-
6.
6. Stewart GS, Panier S, Townsend K, Al-Hakim AK, Kolas NK, Miller ES, Nakada S,
Ylanko J, Olivarius S, Mendez M, Oldreive C, Wildenhain J, Tagliaferro A, Pelletier L,
Taubenheim N, Durandy A, Byrd PJ, Stankovic T, Taylor AM, Durocher D.The RIDDLE
syndrome protein mediates a ubiquitin-dependent signaling cascade at sites of DNA
damage. Cell. 2009 Feb 6;136(3):420-34.
7. Al-Hakim AK, Zagorska A, Chapman L, Deak M, Peggie M, Alessi DR.Control of AMPK-
related kinases by USP9X and atypical Lys(29)/Lys(33)-linked polyubiquitin chains.
Biochem J. 2008 Apr 15;411(2):249-60.
8. Al-Hakim AK, Göransson O, Deak M, Toth R, Campbell DG, Morrice NA, Prescott AR,
Alessi DR.14-3-3 cooperates with LKB1 to regulate the activity and localization of QSK and
SIK. J Cell Sci. 2005 Dec 1;118(Pt 23):5661-73.
9. Al-Hakim A, Rui X, Tsao J, Albert PR, Schimmer BP.Forskolin-resistant Y1 adrenal cell
mutants are deficient in adenylyl cyclase type 4. Mol Cell Endocrinol. 2004 Feb 12;214(1-
2):155-65.
10. Al-Hakim A, Rui X, Tsao J, Albert PR, Schimmer BP.Expression of adenylyl cyclase-4
(AC-4) in Y1 and forskolin-resistant adrenal cells. Mol Cell Endocrinol. 2004 Feb 27;215(1-
2):101-8.

5. AWARDS AND ACHIEVEMENTS
2011 Review article “The ubiquitous role of ubiquitin in the DNA damage
response” is ranked #2 on a list of 25 hottest articles in Biochemistry,
genetics and molecular biology by the journal DNA repair
2009-2011 CIHR EIRR21st (Excellence in Radiation Research) post doctoral fellowship
($CA 48,000/yr)
2007-2009 TD post-doctoral research fellowship from Toronto Dominion bank of Canada
($CA 40,000/yr)
2004-2007 Doctoral Fellowship from Moffat Charity Trust ($CA 25,000/yr)
2001-2003 NSERC Fellowship Award from Natural Science and Engineering Research
Council of Canada to fund my MSc research project ($CA 17,500/yr)
2005 J Cell Sci. (2005) publication was featured in Science STKE as the article of the
week in the field of biochemistry
2000 Graduate award from the University of Toronto to commence my graduate
studies in pharmacology ($CA 1000)
1998-2000 Undergraduate fellowship from the University of Toronto in my 3rd and 4th year
of undergraduate studies ($CA 1000/year)
1997-2000 Golden Key honour Society member, awarded annually to top 15% of
students in undergraduate studies
EXPERTISE AND SKILLS
Management and Supervision: Comprehensive experience in managing complex scientific
projects, multiple deadlines and highly collaborative team efforts. Extensive experience in
supervising technicians, graduate and undergraduate students.
Biochemistry and biophysics: Expression and affinity purification of recombinant proteins
from bacterial, insect and mammalian cells, Tandem Affinity Purification (TAP) of protein
complexes, analysis of protein interactions in vivo and in vitro, BIAcore, immunoprecipitations,
protein kinase assays, ubiquitylation/deubiquitylation assays, SDS-PAGE, Western
immunoblotting, affinity chromatography, HPLC, proteomics approaches for mass spectral
identification of proteins and phosphorylation site mapping.
Molecular biology: Standard molecular biology techniques including PCR, RT-PCR, cloning
procedures, DNA/RNA isolation from cells/tissues, FACS cell sorting.
Cellular biology and genetics: Mammalian cell culture, transient transfections, generation of
stable cell lines, siRNA, immunofluoresence, confocal microscopy and imaging. Use of
Adenoviral and Retroviral vectors.
Bioinformatics: DNA and Protein sequence analysis. Multiple sequence alignment using
ClustalW and Tcoffee. Molecular modeling and protein structure analysis. Transcriptomics
and genomic analysis.
Web-based tools and social media: Proficient with many forms of social media such as
Linkedin, Facebook, twitter and blogging. Familiar with email clients program such as MailChimp
and webinar platforms such as Go2Webinar

6. Languages: Fluent in English and Arabic, basic French.
OTHER ACTIVITIES
2009-2011 Toronto Biotechnology Initiative (TBI)
• Co-organized a Professional Development event attended by > 30 people on
‘Design Thinking’ with keynote speaker Heather Fraser (Director of
Designworks™ and Rotman’s Design Initiative)
• Active in member recruitment and in attending to members concerns
• Co-organizer of the Pub night networking event held each month (between 50-
100 attendees)
2010 BioFinance Conference, Toronto, Canada
• Member of the volunteer team at the BioFinance conference where I assisted in
moderating some of the breakout sessions
2010 McMaster University innovation showcase, Hamilton, Canada
• Participated as a one of the judges for the posters’ competition
2006-2007 Cancer Research UK Fund raising, Dundee, UK
• Organized a team of staff, PhD students and post-docs to participate in
Dundee’s half-marathon where we raised over $1000 for Cancer Research UK
2006 Biotechnology YES Project Competition, Edinburgh, UK
• Participated in a team project: (http://www.biotechnologyyes.co.uk/) - project
was titled “BIOVERT – a bio-green alternative to automobile exhaust” where we
prepared a business plan outlining the project and pitched the idea to a panel of
investors. Our project idea was awarded 2nd place overall in Scotland
2001-2003 Banting & Best Research Institute’s student representative to the Graduate
Students council
1994-2004 Competitive Rowing, Hamilton and Toronto, Canada
• Committed over 30 hours per week to rowing at Club and University varsity
levels
• Competed in a number of national and international regattas (Boston, Austin,
Pittsburgh, Philadelphia, USA; Milan, Italy; I-Lan, Taiwan)
CONTINUING STUDIES
2010 Entrepreneurship 101, MaRS discovery district, Toronto, Canada
2010 Venture capital strategy course, Rotman School of Management, Toronto,
Canada
MEETINGS AND PRESENTATIONS
2009 Gordon Research Conference on Mammalian DNA repair-Ventura, California
(Poster presentation)
2007 Identification and characterization of the interacting proteins of the AMPK-
related family of kinases. PhD defence seminar, University of Dundee,
Dundee, UK (Oral presentation)
2006 Role of protein ubiquitylation in regulating kinase activity of NUAK1 and
MARK4 kinases, MRC institute Christmas symposium, St. Andrews, UK (Oral
presentation)

7. 2006 LKB1 activated protein kinases are modified by a unique Lys29 and 33 ubiquitin
linkage. Planning for Management Committee (PMC) for pharmaceutical
collaborations meeting, University of Dundee, Dundee, UK (Oral presentation)
2006 FEBS Special Meeting: Cellular Signalling–Dubrovnik, Croatia (Poster
presentation)
2006 XXXIst Symposium on Hormones and Regulation: Cancer Cell Signalling,
Hostellerie du Mont Sainte-Odile, France (Poster presentation)
2005 14-3-3 and LKB1 mediate activity and localization of SIK and QSK protein
kinases. PMC meeting, University of Dundee, Dundee, UK (Oral presentation)
2004 Role of 14-3-3 proteins in regulating the kinase activity of AMPK-related kinases.
MRC Institute Christmas symposium, Ayleth, Perthshire, UK (Oral presentation)