Veerendra Koppolu
Biography:Veerendra Koppolu M.Sc Ph.D C.Cy is a scientist in the Department of BiologicsDevelopment at AstraZeneca/Medimmune in Gaithersburg, Maryland, USA. Dr. Koppolu is alsoa honorary faculty member at non-profit organization Novel Global Community EducationFoundation (NGCEF) focused in guiding doctoral students. His lectures are highly valued andwas awarded Robert H Emmer award and Michael S Gaines awards for this teaching. Dr.Koppolu has published over 50 peer-reviewed papers including research article, review articles,abstracts, book chapters, and books. Dr. Koppolu is serving as reviewer of 30 peer-reviewedinternational journals including Biotechnology Journal, Journal of Bacteriology, Futuremicrobiology etc. Dr. Koppolu is Editorial advisory board member of International Journal ofApplied and Natural Sciences, Editor of Oncology Reports and Reviews, Editor of HolisticApproaches in Oncotherapy, Editor of Open Access Journal of Surgery, Associate Editor ofCancer Therapy and Oncology International Journal, Associate Editor of Research Reviews onhealthcare. Dr. Koppolu is a member in international scientific communities such as “Americanchemical society, American Society of Microbiology, American Association of cancer research,American Society of clinical oncology, and Internationally certified flow cytometry Association.His primary research interests include pre-clinical and clinical development ofimmunotherapeutic drugs including monoclonal antibodies, bispecifics, and antibody drugconjugates. At AstraZeneca, he helped in the development of drug Durvalumab, an FDAapproved drug that prevents tumor immune suppression in urinary bladder cancer. He alsoworked in the development of immunotherapeutic vaccines for triple negative breast cancer.Dr. Koppolu holds a BS and M.Sc (Biotech) from India, PhD from University of Kansas (USA), anda certification in Flow Cytometry (C.Cy)
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Papers by Veerendra Koppolu
survival of H. pylori is strongly influenced by the ability of bacteria to escape, disrupt and manipulate the host immune system. This bacterium can escape from recognition by innate immune receptors via altering its surface molecules. Moreover, H. pylori subverts adaptive immune response by modulation of effector T cell. In this review, we discuss the immunepathogenicity of H. pylori by focusing on its ability to manipulate the innate and acquired immune responses to increase its survival in the gastric mucosa, leading up to gastrointestinal disorders. We also highlight the mechanisms that resulted to the persistence of H. pylori in gastric mucosa.
to short‑lived clinical responses. Recent advances in our understanding of tumor‑immune signaling pathways, discovery of
immunosuppressive checkpoints, and subsequent development of antibodies that target these checkpoints reverses the situation
to some extent. Two antibodies ipilimumab and nivolumab gained Food and Drug administration approval for the treatment of
metastatic melanoma and target two major immunosuppressive checkpoints cytotoxic T lymphocyte antigen and programmed cell
death protein 1 (PD‑1), respectively. Nivolumab binds to PD‑1, prevents PD‑1 interaction with ligand Programmed death ligand 1
(PD‑L1), and thus releases the T‑cell exhaustion events (such as T cell apoptosis, decrease in T cell proliferation, etc.) leading to
buildup of potent tumor‑specific immune response. Successful Phase I–III results with remarkable antitumor activity and safety
led to approval of nivolumab against ipilimumab refractory metastatic melanoma. Nivolumab therapy is exciting in that it not only
provides substantial benefit but also provides durable responses. This review focuses on the evolution of immunotherapy leading to
nivolumab approval and its potential in treating melanoma either alone or in combination with other therapies.
targets for the development of novel antibacterial agents. Here, we describe an in vivo high
throughput screen to identify inhibitors of the AraC family activator protein RhaS. The screen
used two E. coli reporter fusions; one to identify potential RhaS inhibitors, and a second to
eliminate non-specific inhibitors from consideration. One compound with excellent selectivity,
OSSL_051168, was chosen for further study. OSSL_051168 inhibited in vivo transcription
activation by the RhaS DNA-binding domain to the same extent as the full-length protein,
indicating that this domain was the target of its inhibition. Growth curves showed that
OSSL_051168 did not impact bacterial cell growth at the concentrations used in this study. In
vitro DNA binding assays with purified protein suggest that OSSL_051168 inhibits DNA binding
by RhaS. In addition, we found that it inhibits DNA binding by a second AraC family protein,
RhaR, which shares 30% amino acid identity with RhaS. OSSL_051168 did not have a significant
impact on DNA binding by the non-AraC family proteins CRP and LacI, suggesting that the
inhibition is likely specific for RhaS, RhaR, and possibly additional AraC family activator
proteins.
and cell-to-cell spread by Shigella flexneri, including multiple components of the type three secretion system (T3SS) machinery
and effectors. We tested a small-molecule compound, SE-1 (formerly designated OSSL_051168), which we had identified as an
effective inhibitor of the AraC family proteins RhaS and RhaR, for its ability to inhibit VirF. Cell-based reporter gene assays with
Escherichia coli and Shigella, as well as in vitro DNA binding assays with purified VirF, demonstrated that SE-1 inhibited DNA
binding and transcription activation (likely by blocking DNA binding) by VirF. Analysis of mRNA levels using real-time quantitative
reverse transcription-PCR (qRT-PCR) further demonstrated that SE-1 reduced the expression of the VirF-dependent virulence
genes icsA, virB, icsB, and ipaB in Shigella.We also performed eukaryotic cell invasion assays and found that SE-1 reduced
invasion by Shigella. The effect of SE-1 on invasion required preincubation of Shigella with SE-1, in agreement with the hypothesis
that SE-1 inhibited the expression of VirF-activated genes required for the formation of the T3SS apparatus and invasion. We
found that the same concentrations of SE-1 had no detectable effects on the growth or metabolism of the bacterial cells or the
eukaryotic host cells, respectively, indicating that the inhibition of invasion was not due to general toxicity. Overall, SE-1 appears
to inhibit transcription activation by VirF, exhibits selectivity toward AraC family proteins, and has the potential to be
developed into a novel antibacterial agent.
choice for the production of biofuels. Here, we reviewed the microbial production of liquid biofuels that have the potential to be used either alone or in combination with the present-day fuels. We specifically highlighted the metabolic engineering and synthetic biology approaches used to improve the production of biofuels from E. coli over the past few years. We also discussed the challenges that still exist for the biofuel production from E. coli and their possible solutions.
Books by Veerendra Koppolu
survival of H. pylori is strongly influenced by the ability of bacteria to escape, disrupt and manipulate the host immune system. This bacterium can escape from recognition by innate immune receptors via altering its surface molecules. Moreover, H. pylori subverts adaptive immune response by modulation of effector T cell. In this review, we discuss the immunepathogenicity of H. pylori by focusing on its ability to manipulate the innate and acquired immune responses to increase its survival in the gastric mucosa, leading up to gastrointestinal disorders. We also highlight the mechanisms that resulted to the persistence of H. pylori in gastric mucosa.
to short‑lived clinical responses. Recent advances in our understanding of tumor‑immune signaling pathways, discovery of
immunosuppressive checkpoints, and subsequent development of antibodies that target these checkpoints reverses the situation
to some extent. Two antibodies ipilimumab and nivolumab gained Food and Drug administration approval for the treatment of
metastatic melanoma and target two major immunosuppressive checkpoints cytotoxic T lymphocyte antigen and programmed cell
death protein 1 (PD‑1), respectively. Nivolumab binds to PD‑1, prevents PD‑1 interaction with ligand Programmed death ligand 1
(PD‑L1), and thus releases the T‑cell exhaustion events (such as T cell apoptosis, decrease in T cell proliferation, etc.) leading to
buildup of potent tumor‑specific immune response. Successful Phase I–III results with remarkable antitumor activity and safety
led to approval of nivolumab against ipilimumab refractory metastatic melanoma. Nivolumab therapy is exciting in that it not only
provides substantial benefit but also provides durable responses. This review focuses on the evolution of immunotherapy leading to
nivolumab approval and its potential in treating melanoma either alone or in combination with other therapies.
targets for the development of novel antibacterial agents. Here, we describe an in vivo high
throughput screen to identify inhibitors of the AraC family activator protein RhaS. The screen
used two E. coli reporter fusions; one to identify potential RhaS inhibitors, and a second to
eliminate non-specific inhibitors from consideration. One compound with excellent selectivity,
OSSL_051168, was chosen for further study. OSSL_051168 inhibited in vivo transcription
activation by the RhaS DNA-binding domain to the same extent as the full-length protein,
indicating that this domain was the target of its inhibition. Growth curves showed that
OSSL_051168 did not impact bacterial cell growth at the concentrations used in this study. In
vitro DNA binding assays with purified protein suggest that OSSL_051168 inhibits DNA binding
by RhaS. In addition, we found that it inhibits DNA binding by a second AraC family protein,
RhaR, which shares 30% amino acid identity with RhaS. OSSL_051168 did not have a significant
impact on DNA binding by the non-AraC family proteins CRP and LacI, suggesting that the
inhibition is likely specific for RhaS, RhaR, and possibly additional AraC family activator
proteins.
and cell-to-cell spread by Shigella flexneri, including multiple components of the type three secretion system (T3SS) machinery
and effectors. We tested a small-molecule compound, SE-1 (formerly designated OSSL_051168), which we had identified as an
effective inhibitor of the AraC family proteins RhaS and RhaR, for its ability to inhibit VirF. Cell-based reporter gene assays with
Escherichia coli and Shigella, as well as in vitro DNA binding assays with purified VirF, demonstrated that SE-1 inhibited DNA
binding and transcription activation (likely by blocking DNA binding) by VirF. Analysis of mRNA levels using real-time quantitative
reverse transcription-PCR (qRT-PCR) further demonstrated that SE-1 reduced the expression of the VirF-dependent virulence
genes icsA, virB, icsB, and ipaB in Shigella.We also performed eukaryotic cell invasion assays and found that SE-1 reduced
invasion by Shigella. The effect of SE-1 on invasion required preincubation of Shigella with SE-1, in agreement with the hypothesis
that SE-1 inhibited the expression of VirF-activated genes required for the formation of the T3SS apparatus and invasion. We
found that the same concentrations of SE-1 had no detectable effects on the growth or metabolism of the bacterial cells or the
eukaryotic host cells, respectively, indicating that the inhibition of invasion was not due to general toxicity. Overall, SE-1 appears
to inhibit transcription activation by VirF, exhibits selectivity toward AraC family proteins, and has the potential to be
developed into a novel antibacterial agent.
choice for the production of biofuels. Here, we reviewed the microbial production of liquid biofuels that have the potential to be used either alone or in combination with the present-day fuels. We specifically highlighted the metabolic engineering and synthetic biology approaches used to improve the production of biofuels from E. coli over the past few years. We also discussed the challenges that still exist for the biofuel production from E. coli and their possible solutions.