| Educational
Qualification |
B.Sc
(Hons) Chemistry - Presidency College, Calcutta, Calcutta
University
M.Sc (Biochemistry) - Department of Biochemistry, Calcutta
University
M.Tech
(Biotechnology) - School of Life Sciences & Biotechnology,
Jadavpur University
Ph.D (Biochemistry) - Department of Biochemistry, Calcutta
University
1. Neutralizing a Surface Charge on the FMN Subdomain Increases the Activity of Neuronal Nitric Oxide Synthase by Enhancing the Oxygen Reactivity of the Enzyme Heme-Nitric oxide Complex.Haque M.M., Fadlalla M.A., Wang Z.Q., Sinha Ray S., Panda K, Stuehr D.J. Journal of Biological Chemistry. 2009 May 27.
2. Cellular and molecular mechanisms of cigarette smoke-induced lung damage and prevention by vitamin C. Banerjee, S., Chattopadhyay R , Ghosh, A, Panda, K. and Chatterjee, I.B. Journal of Inflammation 5:21, 2008
3. A Connecting Hinge Represses the Activity of Endothelial Nitric Oxide Synthase. Haque, M., Panda, K. (joint first author), Tejero, J., Aulak, K., Fadlalla, M., Mustovich, A. & Stuehr, D.J. Proc. Natl. Acad. Sci. USA. Vol.104 (22): pp.9254-9259. 2007
4. Versatile regulation of neuronal nitric oxide synthase by specific regions of its C-terminal tail. Tiso M, Tejero J, Panda K, Aulak K.S., Stuehr, D.J. Biochemistry. Vol. 46(50):pp-14418-28, 2007
5. Black tea prevents cigarette smoke-induced apoptosis and lung damage. Banerjee, S., Maity, P., Mukherjee,S., Sil, A.K., Panda, K., Chattopadhyay, D.J., and Chatterjee I.B. Journal of Inflammation, Biomed Central, Vol. 4, 3, 2007
6. Failure of Alpha-Tocopherol to Prevent Cigarette Smoke-Induced Protein Oxidation: Comparison with Other Antioxidant Vitamins. Panda K. and Chatterjee I.B. Encyclopedia of Vitamin E. Oxford University Press (CABI), Oxordshire, UK. Editor, Victor R. Preedy, Kings College, London, UK. Chapter 63.p-883-893, 2007
7. Surface Charge Interactions of Electron Transport Modules Govern Catalysis by Nitric-oxide Synthase. Panda K. Haque, M., Garcin-Hosfield, E. Deborah, D., Elizabeth D. Getzoff, E.D. and Stuehr, D.J. Journal of Biological Chemistry, Vol. 281 (48), pp. 36819–36827, 2006.
8. Regulation of Monomer-Dimer Equilibrium in Inducible Nitric Oxide Synthase by NO. Li, David, Hayden, E.Y, Panda, K., Stuehr, D.J., Rousseau, D.L. and Yeh, S. Journal of Biological Chemistry, Vol. 281(12), pp-8197-8204, 2006.
9. The Tetrahydrofolate to Tetrahydrobiopterin Dependence Transition in Nitric Oxide Synthase Evolution Panda, K. and Stuehr, D.J. Pterins, Folates and Neurotransmitters in Molecular Medicine. p-16-17. SPS Publications, Heilbronn, Germany. Editors; Nenad Blau & Beat Thony, University of Zurich, Switzerland. 2006
10. Visualizing Inducible Nitric-Oxide Synthase in Living Cells with a Heme-Binding Fluorescent Inhibitor. Panda K. (corresponding author), Chawla-Sarkar, M., Santos, C., Koeck, T., Erzurum, S.C, Parkinson, J.F. and Stuehr, D.J. Proc. Natl. Acad. Sci. USA. Vol. 102(29), pp- 10117-10122, 2005.
11. C-terminal Tail Residue Arg 1400 Enables NADPH to Regulate Electron Transfer in Neuronal Nitric-Oxide Synthase. Tiso, M., Konas, D., Panda, K., Garcin, E, Sharma, M., Getzoff, E.D and Stuehr, D.J. Journal of Biological Chemistry, Vol. 280(47), pp- 39208-39219, 2005.
12. A Tryptophan that Modulates Tetrahydrobiopterin-Dependent Electron Transfer in Nitric Oxide Synthase Regulates Enzyme Catalysis by Additional Mechanisms. Wang, Z.Q., Wei, C.C., Santolini, J., Panda, K., Wang, Q. and Stuehr, D.J. Biochemistry. Vol. 44(12), pp-4676-4690, 2005.
13. Imaging Inducible Nitric Oxide Synthase In Living Cells. Panda, K. and Stuehr, D.J. Methods in Enzymology, Nitric Oxide (Part G). Editor, Enrique Cadenas & Lester Packer, (in press) .
‘Innovator
Award’ for 2006 from the Cleveland Clinic Foundation,
USA for inventing a live probe for Nitric Oxide Synthase
an enzyme involved the pathogenesis of several degenerative
diseases like Parkinson’s and Alzheimer’s disease.
‘Gordon
Research Conference Best Young Investigator Award’ at the
Gordon Research Conference, Barga,
Italy
(2005).
‘Research
Star Award’ of the Cleveland Clinic Foundation, USA
for exceptional contribution to research. (2003).
‘Alois
Niederwieser Award’ for being selected the ‘Best Young
Scientist’ among 62 selected international speakers in the
13th International Conference on Pterins, Folates
and Related Biogenic Amines, Maui,
Hawaii,USA
(2003).
William
Lower Award (First Prize) of the Cleveland Clinic Foundation,
USA for
original investigation and professional excellence in the
preparation of scientific paper in basic science for the
year 2001.
‘Shining
Star’, lapel of distinction of the Dept. of Immunology,
Cleveland Clinic Foundation (2003).
Recipient
of the Indian Science Congress Association’s 'Young Scientists'
Award' (First Prize), 1999, in Biochemistry, Biophysics
and Molecular Biology.
Shanti
Bhakta Memorial Award for delivering the best Post-Graduate
talk in Biochemistry by the Department of Biochemistry,
University of Calcutta for the academic year 1991
Proteomic
Identification of Cigarette Smoke-induced Degraded Proteins
in Emphysema
 Oxidative damage
of proteins encountered during degenerative diseases like
emphysema (COPD), cancer, atherosclerosis etc) entails the
degradation of vital proteins oxidized during the disease
progression. Such protein damage is also encountered during
exposure to xenobiotics like cigarette smoke, the most common
cause of lung diseases. We are using state-of-the-art proteomic
approaches like Two-Dimensional Fluorescence Difference
Electrophoresis (DIGE) as well as traditional two-dimensional
gel electrophoresis coupled with MALDI-TOF/TOF and online
MS-MS mediated detection of the proteins oxidized as well
as undergoing degradation during such oxidative insult in
vivo as well as in suitable cellular and animal models.
This would greatly help in understanding the poorly understood
mechanism of the oxidative routes involved in oxidative
lung damage as in cigarette smoke-induced emphysema.
Study
of the Role of NO and Nitric Oxide Synthases In Inflammatory
Lung Damage
  Inflammatory lung
damage caused by diseases like emphysema, asthma or Chronic
Obstructive Lung Disease (COPD) is typically implicated
with lung macrophage activation and production of increased
nitric oxide (NO). The level of exhaled NO in patients of
such diseases are usually found to increase substantially
with the progression of the disease. With the use of a novel
non-toxic and highly specific fluorescent probe for inducible
nitric oxide synthase (iNOS) [Panda et.al. Proc. Natl.
Acad. Sci. USA . Vol. 102(29), pp- 10117-10122., Jul, 2005]
we have developed the capability to monitor and study the
expression of iNOS real time in live cells and animal models
of the disease. Though the over-expression of iNOS has been
implicated with inflammatory lung damage its possible role
and possible mechanism in the disease progression is still
not established. We therefore plan to study the possible
causal relation between nitric oxide synthase over-expression
and inflammatory lung damage using relevant cell culture
and animal models. The probe can also be used a clinical
bioimaging tool for evaluation of these diseases once the
exact relation between its dysfunctional expression and
etiology of the diseases is correctly evaluated.
 Development of
a novel drug for therapeutic inhibition of inducible nitric
oxide synthase (iNOS) for clinical control of diseases causally
related to its over-expression.
Using
contemporary drug designing techniques and Structure Activity
Relationship (SAR) Programs we are presently involved in
designing therapeutically efficacious drug molecules that
can act as potent inhibitors of Inducible Nitric Oxide Synthase
(iNOS) the over-expression of which has been implicated
with several degenerative diseases like atherosclerosis,
sepsis, arthritis and several neurodegenerative diseases
like Parkinson’s Disease, and Alzheimer’s Disease. We plan
to screen the most promising molecules with respect to specificity,
affinity and efficacy and promote them to necessary trials
after completing relevant cell-based and animal studies
with the drugs.
Elucidating
the molecular mechanism of Arsenicosis and its prevention
 The molecular mechanism
of arsenic poisoning or Arsenicosis is poorly understood
despite the relevance of the disease in terms of its severity
in several parts of the world including the Indo-Bangladesh
border which is considered to be one among the worst affected.
There are at present no disease biomarkers reported which
can be either detected or measured in order to monitor the
progression of the level of poisoning by arsenic in humans.
We have therefore initiated an effort to both understand
the molecular mechanism underlying Arsenicosis as well as
search for a dependable biomarker that can be used to monitor
and diagnose this disease. Our attempt would also extend
to devising possible means of therapeutically preventing
the disease once we have some success in unfolding the mechanism
by which arsenic poisons humans.
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Pamela
Banerjee
PhD
Student (Research fellow)
pamelabanerjee23@gmail.com
|
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Indranil
Gupta
PhD
Student (Research fellow)
2006.indranil@gmail.com
|
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Munmun
Biswas
PhD
Student (Research fellow)
biswas_munmun@yahoo.co.in
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Latika
Nagpal
PhD
Student (Research fellow)
latikanagpal@gmail.com
|
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Nandini
Sen
PhD
Student (Research fellow)
nsen1234@gmail.com
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