Dr engohang_resume

330 University Drive NE New Philadelphia, OH 44663
EDUCATION AND Assistant Professor, Kent State University at Tuscarawas,
President of International Actions Against Buruli Ulcer (IAABU)
Visiting Assistant Professor of Biology,
Post-doctoral fellow, Public Health Research Institute,
Ph.D., Medical Microbiology, University of Sciences and

My research focuses mainly on fighting infectious diseases in general and INTERESTS
mycobacterial diseases in particular including tuberculosis and Buruli ulcer. Tuberculosis is caused by Mycobacterium tuberculosis. It is the first and the most deadly mycobacterial disease. In 2012, about 8.8 million new cases of tuberculosis were diagnosed and 1.5 millions tuberculosis patients died, most of these occurring in developing countries. The increased number of multi-drug resistant and extensively drug resistant tuberculosis cases urges the need to find or develop new anti-tuberculosis drugs. During the past decade, I have worked on unraveling possible mechanisms through which treatment of tuberculosis could be improved using ethionamide, a second-line tuberculosis drug. I have also worked on identifying M. tuberculosis genes that could be used as potential drug targets, including the Iron-dependent Regulator (IdeR) which is essential for M. tuberculosis and involved in acquisition and storage of iron. During the past three years, I have broadened my research interest to Buruli ulcer. Unlike tuberculosis, Buruli ulcer is a neglected disease with about 6000 new cases reported each year from 33 tropical countries. However, it is believed that much more cases occur in endemic areas and that the disease is largely underreported for multiple reasons including cultural believes. Buruli ulcer is a necrotizing and debilitating skin disease that affects with the same chances both males and females. More than 50% of Buruli ulcer patients are children under 15 years old. Buruli ulcer is endemic in Central and Western Africa, in the Americas, in Southeast Asia, and in Western Pacific. However, sub-Saharan African countries record the highest incidence of the disease. Buruli ulcer is caused by Mycobacterium ulcerans, which produces a single toxin called mycolactone and responsible for skin necrosis observed in Buruli ulcer patients.
Molecular mechanisms of Bacterial Pathogenesis
The major M. ulcerans genes responsible for mycolactone production (mlsA1,
mlsA2 and mlsB) were identified during the past decade. Nevertheless, the
complete mechanisms of mycolactone production and its regulation are still
unclear. Additionally, the mechanisms through which the toxin is exported from
the cell are still to be clarified. In my laboratory, using modern molecular
biology, genetic and biochemical techniques, I am interested in understanding
these different mechanisms of M. ulcerans pathogenesis. To this date, I am
currently studying the level of expression of key mycolactone genes during
different stages of M. ulcerans growth. This would allow me to determine if
these key mycolactone genes are expressed constitutively or not. In silico
analyses I recently performed along with several workbench observations
made between last year and now suggest that mycolactone production may be
regulated. Thus, I am actively engaged in identifying conditions under which
mycolactone production may be affected including the role of population
density, iron, temperature and lipids.

Drug Discovery

Currently, the best treatment for medium size and large size Buruli ulcers
consists of a traumatic surgical removal of infected skin tissues followed by skin
grafting while small ulcers can be treated with a combination of streptomycin
and rifampicin for eight weeks. Nevertheless, in spite of the use of streptomycin
and rifampicin for treating small Buruli ulcers, the success of the
chemotherapeutic treatment is not always guaranteed. It was recently shown
that secondary infections occur often before, during and even after the eight-
week treatment with the current chemotherapeutic regimen. Therefore, I am
investigating on new Buruli ulcer treatments by testing antimicrobial activities of
new anti-tuberculosis drugs on M ulcerans.
Jean Engohang-Ndong, Frenois F., Locht C., Villeret V. and 2003
Baulard A.R. 2003. Patent N° 0312801 (PCT/FR2004/002721
CNRS/INSERM/IPL, France) “Ligands of the mycobacterial repressor EthR: selection processes and applications.” Research/Creative Activity Summer Appointment.
$6,500 (Awarded)
Electron beam treatment of sewage sludge.
$52,350 (Awarded by Haley & Aldrich Inc./Arlington County,
Research/Creative Activity Summer Appointment.
$6,500 (Awarded)
Academic Research Enhancement Award (NIH-R15).
Project title: Mycolactone production: Role of mup045 and mup038 and regulation of its synthesis. Post-doctoral grant provided by The New York Community 2004-2006
Trust in the context of The Heiser Program For Research in
Leprosy and Tuberculosis. $80,000 (Awarded)

Member of the American Society for Microbiology (ASM)
Member of the Mycobacterium tuberculosis Structural
Genomics Consortium

Research papers
Jean Engohang-Ndong. Control of microbial population in sludge using electron
beam irradiation. (In preparation for submission)
Jean Engohang-Ndong and Donald G. Gerbig. 2013. Making basic microbiology
laboratory an exciting and engaging experience. Journal of Microbiology and
Biology Education
. 14(1): 125-126
Jean Engohang-Ndong. 2012. Antimycobacterial drugs currently in phase II
clinical trials and preclinical Phase for tuberculosis treatment. Expert Opinion on
Investigational Drugs
. 21(12):1789-800
Wang S., Jean Engohang-Ndong, Issar Smith. 2007. Structure of the DNA-
Binding Domain of the Response Regulator PhoP from Mycobacterium
Biochemistry. 46(51):14751-61
Fréderic Frénois, Jean Engohang-Ndong, Camille Locht, Alain R. Baulard and
Vincent Villeret. 2004. Crystal structure of the regulator EthR in a ligand bound
conformation reveals therapeutic perspectives against tuberculosis and leprosy.
Molecular Cell. 16(2): 301-307.

Jean Engohang-Ndong
, David Baillat, Marc Aumercier, Flore Bellefontaine,
Gurdyal S. Besra, Camille Locht and Alain R. Baulard. 2004. EthR, a repressor of
the TetR/CamR family implicated in ethionamide resistance in mycobacteria,
hexamerizes cooperatively on its operator. Molecular Microbiology. 51(1): 175-
Alain R. Baulard, Sudagar S. Gurcha, Jean Engohang-Ndong, Kamila Gouffi,
Camille Locht, and Gurdyal S. Besra. 2003. In vivo interaction between the
polyprenol phosphate mannose synthase Ppm1 and the integral membrane
protein Ppm2 from Mycobacterium smegmatis revealed by a bacterial two-hybrid
system. Journal of Biological Chemistry. 278(4): 2242-2248.
Alain R. Baulard, Joanna C. Betts, Jean Engohang-Ndong, Selwyn Quan, Ruth
A. McAdam, Patrick J. Brennan, Camille Locht, and Gurdyal S. Besra. 2000.
Activation of the pro-drug ethionamide is regulated in mycobacteria. Journal of
Biological Chemistry
. 275(36): 28326-28331.
Books (Co-author)
Jean Engohang-Ndong, S. Allred, D. Cox, and Wendy Ribeiro. 2009. Test bank
for Biology Today and Tomorrow, third edition. Belmont CA. Brooks/Cole
Cengage Learning.

COMMUNICATIONS Invited speaker
Africa Belle Conference 2012 – Atlanta, Georgia INTERNATIONAL
Fighting Neglected Tropical Diseases in Africa: A Global
The Brown Bag series, Kent State University at Tuscarawas Tuberculosis Survey in Ohio from 1999 to 2010.
The Brown Bag series, Kent State University at Tuscarawas IAABU: A partner of choice for fighting Buruli ulcer.
2nd Annual Biological Sciences Day. Université des Sciences May, 2009 et Mycobacterium ulcerans infection.
1st Annual Biological Sciences Day. Université des Sciences et Jun 08, 2008
Techniques de Masuku, Franceville, GABON. Mycobacterial
infections: A challenge for the present and the future.
Honor Program, Brigham Young University Hawaii, Laie HI. Jan 16, 2008
We are all connected by the air we breathe.

Source: http://buruli.org/Resume.pdf


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