Dr. Pradeepkiran Jangampalli Adi, PhD - Internal medicine/Texas Tech Health Sciences Center - Postdoc

Dr. Pradeepkiran Jangampalli Adi

PhD

Internal medicine/Texas Tech Health Sciences Center

Postdoc

Lubbock, TX | United States

Main Specialties: Biochemical Genetics, Biology, Endocrinology Diabetes & Metabolism, Neurology, Pharmacology

Additional Specialties: Bioinformatics

ORCID logohttps://orcid.org/0000-0003-4678-6443


Top Author

Dr. Pradeepkiran Jangampalli Adi, PhD - Internal medicine/Texas Tech Health Sciences Center - Postdoc

Dr. Pradeepkiran Jangampalli Adi

PhD

Introduction

Currently works at the Department of Internal Medicine, Texas Tech University Health Sciences Center. Working on Alzheimer's Disease hyperphosphorylated Tau (p-Tau) interactions of AD neurons. Discovery of new lead molecules against the pathological targeted proteins in AD and other neurological disorders.

Primary Affiliation: Internal medicine/Texas Tech Health Sciences Center - Lubbock, TX , United States

Specialties:

Additional Specialties:

Research Interests:


View Dr. Pradeepkiran Jangampalli Adi’s Resume / CV

Education

Jun 2016
Sri Venkateswara University
PhD
Jul 2007
Sri Venkateswara Institute of Medical Sciences
MSc

Experience

Oct 2016
Postdoctoral Research Associate
Sep 2014
The Research Fellowship in Sciences for meritorious students BSR(UGC)
Jun 2013
Senior Research Fellow DBT Project
Apr 2011
Junior Research Fellow DBT Project

Publications

20Publications

676Reads

72Profile Views

91PubMed Central Citations

Phenotypic and transcriptomic changes in zebrafish (Danio rerio) embryos/larvae following cypermethrin exposure.

Chemosphere 2020 Jun 7;249:126148. Epub 2020 Feb 7.

Department of Internal Medicine, Texas Tech University of Health Science Centre, Lubbock, 79413, TX, USA. Electronic address:

Cypermethrin is one of the widely used type-II pyrethroid and the indiscriminate use of this pesticide leads to life threatening effects and in particular showed developmental effects in sensitive populations such as children and pregnant woman. However, the molecular mechanisms underlying cypermethrin-induced development toxicity is not well defined. To address this gap, the present study was designed to investigate the phenotypic and transcriptomic (next generation RNA-Seq method) impact of cypermethrin in zebrafish embryos as a model system. Zebrafish embryos at two time points, 24 h postfertilization (hpf) and 48 hpf were exposed to cypermethrin at a concentration of 10 ?g/L. Respective control groups were maintained. Cypermethrin induced both phenotypic and transcriptomic changes in zebrafish embryos at 48 hpf. The phenotypic anomalies such as delayed hatching rate, increased heartbeat rate and deformed axial spinal curvature in cypermethrin exposed zebrafish embryos at 48 hpf as compared to its respective controls. Transcriptomic analysis indicated that cypermethrin exposure altered genes associated with visual/eye development and gene functional profiling also revealed that cypermethrin stress over a period of 48 h disrupts phototransduction pathway in zebrafish embryos. Interestingly, cypermethrin exposure resulted in up regulation of only one gene, tnnt3b, fast muscle troponin isoform 3T in 24 hpf embryos as compared to its respective controls. The present model system, cypermethrin exposed zebrafish embryos elaborates the toxic consequences of cypermethrin exposure during developmental stages, especially in fishes. The present findings paves a way to understand the visual impairment in sensitive populations such as children exposed to cypermethrin during their embryonic period and further research is warranted.

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http://dx.doi.org/10.1016/j.chemosphere.2020.126148DOI Listing
June 2020
5.108 Impact Factor

Synthesis, Biological Evaluation and Molecular Docking Studies of Novel Di-hydropyridine Analogs as Potent Antioxidants.

Curr Top Med Chem 2019 ;19(29):2676-2686

Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati-517502, AP, India.

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http://dx.doi.org/10.2174/1568026619666191105100959DOI Listing
February 2020
10 Reads
3.402 Impact Factor

Protective effects of BACE1 inhibitory ligand molecules against amyloid beta-induced synaptic and mitochondrial toxicities in Alzheimer's disease.

Hum Mol Genet 2020 01;29(1):49-69

Internal Medicine Department, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430, USA.

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http://dx.doi.org/10.1093/hmg/ddz227DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7001603PMC
January 2020
18 Reads
6.393 Impact Factor

Structure Based Design and Molecular Docking Studies for Phosphorylated Tau Inhibitors in Alzheimer's Disease.

Cells 2019 03 19;8(3). Epub 2019 Mar 19.

Internal Medicine Department, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430, USA.

The purpose of our study is to identify phosphorylated tau (p-tau) inhibitors. P-tau has recently received great interest as a potential drug target in Alzheimer's disease (AD). The continuous failure of A?-targeted therapeutics recommends an alternative drug target to treat AD. There is increasing evidence and growing awareness of tau, which plays a central role in AD pathophysiology, including tangles formation, abnormal activation of phosphatases/kinases, leading p-tau aggregation in AD neurons. In the present study, we performed computational pharmacophore models, molecular docking, and simulation studies for p-tau in order to identify hyperphosphorylated sites. We found multiple serine sites that altered the R1/R2 repeats flanking sequences in the tau protein, affecting the microtubule binding ability of tau. The ligand molecules exhibited the p-O ester scaffolds with inhibitory and/or blocking actions against serine residues of p-tau. Our molecular docking results revealed five ligands that showed high docking scores and optimal protein-ligand interactions of p-tau. These five ligands showed the best pharmacokinetic and physicochemical properties, including good absorption, distribution, metabolism, and excretion (ADME) and admetSAR toxicity tests. The p-tau pharmacophore based drug discovery models provide the comprehensive and rapid drug interventions in AD, and tauopathies are expected to be the prospective future therapeutic approach in AD.

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http://dx.doi.org/10.3390/cells8030260DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468864PMC
March 2019
29 Reads
7 Citations
5.600 Impact Factor

Pharmacophore-based models for therapeutic drugs against phosphorylated tau in Alzheimer's disease.

Drug Discov Today 2019 02 16;24(2):616-623. Epub 2018 Nov 16.

Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Cell Biology & Biochemistry Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Pharmacology & Neuroscience Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Neurology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Speech, Language and Hearing Sciences Departments, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, 6630 S. Quaker Suite E, MS 7495, Lubbock, TX 79413, USA. Electronic address:

Phosphorylated tau (P-tau) has received much attention in the field of Alzheimer's disease (AD), as a potential therapeutic target owing to its involvement with synaptic damage and neuronal dysfunction. The continuous failure of amyloid ? (A?)-targeted therapeutics highlights the urgency to consider alternative therapeutic strategies for AD. The present review describes the latest developments in tau biology and function. It also explains abnormal interactions between P-tau with A? and the mitochondrial fission protein Drp1, leading to excessive mitochondrial fragmentation and synaptic damage in AD neurons. This article also addresses 3D pharmacophore-based drug models designed to treat patients with AD and other tauopathies.

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http://dx.doi.org/10.1016/j.drudis.2018.11.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6397090PMC
February 2019
32 Reads
5 Citations
6.691 Impact Factor

Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease.

J Alzheimers Dis 2018 ;61(3):843-866

Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, USA.

The purpose of our article is to assess the current understanding of Indian spice, curcumin, against amyloid-? (A?)-induced toxicity in Alzheimer's disease (AD) pathogenesis. Natural products, such as ginger, curcumin, and gingko biloba have been used as diets and dietary supplements to treat human diseases, including cancer, cardiovascular, respiratory, infectious, diabetes, obesity, metabolic syndromes, and neurological disorders. Products derived from plants are known to have protective effects, including anti-inflammatory, antioxidant, anti-arthritis, pro-healing, and boosting memory cognitive functions. In the last decade, several groups have designed and synthesized curcumin and its derivatives and extensively tested using cell and mouse models of AD. Recent research on A? and curcumin has revealed that curcumin prevents A? aggregation and crosses the blood-brain barrier, reach brain cells, and protect neurons from various toxic insults of aging and A? in humans. Recent research has also reported that curcumin ameliorates cognitive decline and improves synaptic functions in mouse models of AD. Further, recent groups have initiated studies on elderly individuals and patients with AD and the outcome of these studies is currently being assessed. This article highlights the beneficial effects of curcumin on AD. This article also critically assesses the current limitations of curcumin's bioavailability and urgent need for new formulations to increase its brain levels to treat patients with AD.

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http://dx.doi.org/10.3233/JAD-170512DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5796761PMC
January 2019
53 Reads
22 Citations
4.151 Impact Factor

Three Novel Mutations I65S, R66S, and G86R Divulge Significant Conformational Variations in the PTB Domain of the IRS1 Gene.

ACS Omega 2019 Jan 29;4(1):2217-2224. Epub 2019 Jan 29.

Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati 517502, India.

Insulin receptor substrate 1 (IRS1) is one of the major substrates for the IR, and their interaction mediates several downstream insulin signaling pathways. In this study, we have identified three novel mutations in the IRS1 gene of type 2 diabetic (T2D) patients, which reflected in the amino acid changes as I65S, R66S, and G86R in the phosphotyrosine binding domain of the IRS1 protein. The impact of these mutations on the structure and function of the IRS1 protein was evaluated through molecular modeling studies, and distinct conformational fluctuations were recorded. The variable binding affinities and positional displacement of these mutant models were observed in the ligand-binding cleft of IR. The mutant IRS1 models triggered conformational changes in the L1 domain of IR upon their binding. Such structural variations in IRS1 and IR structures due to mutations resulted in variable molecular interactions that could lead to altered insulin transduction, followed by insulin resistance and T2D.

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http://dx.doi.org/10.1021/acsomega.8b01712DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6814177PMC
January 2019
4 Reads
2.584 Impact Factor

Current Status of Healthy Aging and Dementia Research: A Symposium Summary.

J Alzheimers Dis 2019 ;72(s1):S11-S35

Arizona State University, Tempe, AZ, USA.

The purpose of the 'First Regional Healthy Aging and Dementia Research Symposium' was to discuss the latest research in healthy aging and dementia research, public health trends related to neurodegenerative diseases of aging, and community-based programs and research studying health, nutrition, and cognition. This symposium was organized by the Garrison Institute on Aging (GIA) of the Texas Tech University Health Sciences Center (TTUHSC), and was held in Lubbock, Texas, October 24-25, 2018. The Symposium joined experts from educational and research institutions across the United States. The two-day Symposium included all GIA staff and researchers. Students, postdoctoral fellows, and faculty members involved in dementia research presented at the Symposium. Healthcare professionals, from geriatricians to social workers working with patients with neurodegenerative diseases, also presented. In addition, experts traveled from across the United States to participate. This event was comprised of multiple sessions, each with several oral presentations, followed by questions and answers, and discussion.

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http://dx.doi.org/10.3233/JAD-190252DOI Listing
January 2019
39 Reads
1 Citation
4.151 Impact Factor

Conformational transition pathway of R308K mutant glucokinase in the presence of the glucokinase activator YNKGKA4.

FEBS Open Bio 2018 Aug 6;8(8):1202-1208. Epub 2018 Jul 6.

Garrison Institute on Aging Texas Tech University of Health Science Centre Lubbock TX USA.

Glucokinase (GK) plays a vital role in the control of blood glucose levels and its altered activity can lead to the development of forms of diabetes. We have previously identified a mutant GK (R308K) in patients with type 2 diabetes with reduced enzyme activity. In the present study, the activation mechanism of GK from super-open to the closed state under wild-type and mutant conditions in the presence of the novel aminophosphonate derivative YNKGKA4 (an allosteric activator of GK) was characterized via a series of molecular dynamics simulations. A reliable conformational transition pathway of GK was observed from super-open to closed state during trajectory analysis. Glucose was also observed to modulate its binding orientation in the active site but with stable moments in the cavity. These observations provide insights into the complicated conformational transitions in the presence of YNKGKA4 and the molecular mechanism of GK activators for the allosteric regulation of mutant forms of GK.

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http://dx.doi.org/10.1002/2211-5463.12255DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6070654PMC
August 2018
17 Reads
1.959 Impact Factor

Mutant APP and amyloid beta-induced defective autophagy, mitophagy, mitochondrial structural and functional changes and synaptic damage in hippocampal neurons from Alzheimer's disease.

Hum Mol Genet 2018 07;27(14):2502-2516

Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, USA.

The purpose of our study was to determine the toxic effects of hippocampal mutant APP (mAPP) and amyloid beta (A?) in human mAPP complementary DNA (cDNA) transfected with primary mouse hippocampal neurons (HT22). Hippocampal tissues are the best source of studying learning and memory functions in patients with Alzheimer's disease (AD) and healthy controls. However, investigating immortalized hippocampal neurons that express AD proteins provide an excellent opportunity for drug testing. Using quantitative reverse transcriptase-polymerase chain reaction, immunoblotting & immunofluorescence and transmission electron microscopy, we assessed messenger RNA (mRNA) and protein levels of synaptic, autophagy, mitophagy, mitochondrial dynamics, biogenesis, dendritic protein MAP2 and assessed mitochondrial number and length in mAPP-HT22 cells that express Swedish/Indiana mutations. Mitochondrial function was assessed by measuring the levels of hydrogen peroxide, lipid peroxidation, cytochrome c oxidase activity and mitochondrial adenosine triphosphate. Increased levels of mRNA and protein levels of mitochondrial fission genes, Drp1 and Fis1 and decreased levels fusion (Mfn1, Mfn2 and Opa1) biogenesis (PGC1?, NRF1, NRF2 & TFAM), autophagy (ATG5 & LC3BI, LC3BII), mitophagy (PINK1 & TERT, BCL2 & BNIPBL), synaptic (synaptophysin & PSD95) and dendritic (MAP2) genes were found in mAPP-HT22 cells relative to WT-HT22 cells. Cell survival was significantly reduced mAPP-HT22 cells. GTPase-Drp1 enzymatic activity was increased in mAPP-HT22 cells. Transmission electron microscopy revealed significantly increased mitochondrial numbers and reduced mitochondrial length in mAPP-HT22 cells. These findings suggest that hippocampal accumulation of mAPP and A? is responsible for abnormal mitochondrial dynamics and defective biogenesis, reduced MAP2, autophagy, mitophagy and synaptic proteins & reduced dendritic spines and mitochondrial structural and functional changes in mAPP hippocampal cells. These observations strongly suggest that accumulation of mAPP and A? causes mitochondrial, synaptic and autophagy/mitophagy abnormalities in hippocampal neurons, leading to neuronal dysfunction.

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http://dx.doi.org/10.1093/hmg/ddy154DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031001PMC
July 2018
44 Reads
19 Citations
6.393 Impact Factor

Discovery of small molecules through pharmacophore modeling, docking and molecular dynamics simulation against Vivapain-3 (VP-3).

Heliyon 2018 May 8;4(5):e00612. Epub 2018 May 8.

Sri Venkateswara University, Tirupati, 517502, Andhra Pradesh, India.

Vivapain-3(VP-3) protein is a family of cysteine rich proteases of malaria parasite is extensively reported to participate in a range of wide cellular processes including survival. VP-3 of plasmodium recognized as an attractive drug target in vector-borne diseases like malaria. In the present study we robust a homology model of VP-3 protein and generated the pharmacophore based models adapted to screen the best drug like compounds from PubChem database. Our results finds the fourteen best lead molecules were mapped with core pharmacophore features of VP-3 and top hits were further evaluated by molecular dynamics simulation and docking studies. Based on the molecular dynamics simulation and docking results and binding vicinity of ligand molecules, top five i.e., CID 74427945, CID 74427946, CID 360883, CID193721 and CID 51416859 showed the best docking scores with good molecular interactions against VP-3. Furthermore ADMET and assays clearly exhibited that out of five three CID74427946, CID74427945 and CID360883 ligand molecules showed the best promising inhibition against VP-3. The present study believed to provide significant information of potential ligand inhibitors against VP-3 to design and develop the next generation malaria therapeutics through computational approach.

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http://dx.doi.org/10.1016/j.heliyon.2018.e00612DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5944417PMC
May 2018
22 Reads
3 Citations

Multiplex quantification of Escherichia coli, Salmonella typhi and Vibrio cholera with three DNA targets in single reaction assay.

Microb Pathog 2017 Sep 9;110:50-55. Epub 2017 Jun 9.

Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati 517502, India.

Escherichia coli (E. coli), Salmonella typhi and Vibrio cholera harmful pathogens, which causes various diseases in humans. Rapid diagnosis of bacterial infection is an important for patient management and appropriate therapy during the early phase of the bacterial infected diseases. Among the existing techniques for identifying pathogens were less sensitive and time-consuming processes. In the present study total, 48 clinical 31 blood and 17 urine samples of patients suspected with the infections were collected from SVRR Hospital and used to detect the pathogens. Multiplex polymerase chain reaction (PCR) assay was set to design for the identification of Escherichia coli, Salmonella typhi and Vibrio cholera from the different clinical samples. Rapid diagnosis of Escherichia coli (E. coli), Salmonella and Vibrio cholera pathogens can be done with simultaneously in a single multiplex PCR assay by using specific primers with adjusted PCR conditions. Through this approach, the results represented with out of 31 blood samples 1-15 shows the positive with E. coli and remaining 14 only 11 were correlated with multiplex results of Vibrio cholera, remaining the urine samples all are positive with 17 samples correlate with the Salmonella typhi. Through the high specificity benefits of excellent sensitivity, with high resolution and reproducibility. This method of results proved and illustrates the best potential system for diagnosing the infectious disease with modern trendy.

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http://dx.doi.org/10.1016/j.micpath.2017.06.010DOI Listing
September 2017
62 Reads
3 Citations
2.581 Impact Factor

Novel 1, 4-dihydropyridines for L-type calcium channel as antagonists for cadmium toxicity.

Sci Rep 2017 03 27;7:45211. Epub 2017 Mar 27.

Division of Bioinformatics, Department of Zoology, Sri Venkateswara University, Tirupati, 517502, A.P., India.

The present study, we design and synthesize the novel dihydropyridine derivatives, i.e., 3 (a-e) and 5 (a-e) and evaluated, anticonvulsant activity. Initially due to the lacuna of LCC, we modeled the protein through modeller 9.15v and evaluated through servers. Docking studies were performed with the synthesized compounds and resulted two best compounds, i.e., 5a, 5e showed the best binding energies. The activity of intracellular Ca measurements was performed on two cell lines: A7r5 (rat aortic smooth muscle cells) and SH-SY5Y (human neuroblastoma cells). The 5a and 5e compounds was showing the more specific activity on L-type calcium channels, i.e. A7r5 (IC?=?0.18?±?0.02 and 0.25?±?0.63??g/ml, respectively) (containing only L-type channels) than SH-SY5Y (i.e. both L-type and T-type channels) (IC?=?8?±?0.23 and 10?±?0.18??g/ml, respectively) with intracellular calcium mobility similar to amlodipine. Finally, both in silico and in vitro results exploring two derivatives 5a and 5e succeeded to treat cadmium toxicity.

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http://dx.doi.org/10.1038/srep45211DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5366925PMC
March 2017
22 Reads
7 Citations
5.078 Impact Factor

Modeling, molecular docking, probing catalytic binding mode of acetyl-CoA malate synthase G in 16M.

Biochem Biophys Rep 2016 Dec 22;8:192-199. Epub 2016 Aug 22.

Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati 517502, Andhra Pradesh, India.

There are enormous evidences and previous reports standpoint that the enzyme of glyoxylate pathway malate synthase G (MSG) is a potential virulence factor in several pathogenic organisms, including 16M. Where the lack of crystal structures for best candidate proteins like MSG of 16M creates big lacuna to understand the molecular pathogenesis of brucellosis. In the present study, we have constructed a 3-D structure of MSG of 16M in MODELLER with the help of crystal structure of malate synthase (PDB ID: 2GQ3) as template. The stereo chemical quality of the restrained model was evaluated by SAVES server; remarkably we identified the catalytic functional core domain located at 4 cleft with conserved catalytic amino acids, start at ILE 59 to VAL 586 manifest the function of the protein. Furthermore, virtual screening and docking results reveals that best leadmolecules binds at the core domain pocket of MSG catalytic residues and these ligand leads could be the best prospective inhibitors to treat brucellosis.

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http://dx.doi.org/10.1016/j.bbrep.2016.08.020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5613768PMC
December 2016
19 Reads
2 Citations

Modeling, molecular dynamics, and docking assessment of transcription factor rho: a potential drug target in Brucella melitensis 16M.

Drug Des Devel Ther 2015 31;9:1897-912. Epub 2015 Mar 31.

Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati, India.

The zoonotic disease brucellosis, a chronic condition in humans affecting renal and cardiac systems and causing osteoarthritis, is caused by Brucella, a genus of Gram-negative, facultative, intracellular pathogens. The mode of transmission and the virulence of the pathogens are still enigmatic. Transcription regulatory elements, such as rho proteins, play an important role in the termination of transcription and/or the selection of genes in Brucella. Adverse effects of the transcription inhibitors play a key role in the non-successive transcription challenges faced by the pathogens. In the investigation presented here, we computationally predicted the transcription termination factor rho (TtFRho) inhibitors against Brucella melitensis 16M via a structure-based method. In view the unknown nature of its crystal structure, we constructed a robust three-dimensional homology model of TtFRho's structure by comparative modeling with the crystal structure of the Escherichia coli TtFRho (Protein Data Bank ID: 1PVO) as a template in MODELLER (v 9.10). The modeled structure was optimized by applying a molecular dynamics simulation for 2 ns with the CHARMM (Chemistry at HARvard Macromolecular Mechanics) 27 force field in NAMD (NAnoscale Molecular Dynamics program; v 2.9) and then evaluated by calculating the stereochemical quality of the protein. The flexible docking for the interaction phenomenon of the template consists of ligand-related inhibitor molecules from the ZINC (ZINC Is Not Commercial) database using a structure-based virtual screening strategy against minimized TtFRho. Docking simulations revealed two inhibitors compounds - ZINC24934545 and ZINC72319544 - that showed high binding affinity among 2,829 drug analogs that bind with key active-site residues; these residues are considered for protein-ligand binding and unbinding pathways via steered molecular dynamics simulations. Arg215 in the model plays an important role in the stability of the protein-ligand complex via a hydrogen bonding interaction by aromatic-? contacts, and the ADMET (absorption, distribution, metabolism, and excretion) analysis of best leads indicate nontoxic in nature with good potential for drug development.

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http://dx.doi.org/10.2147/DDDT.S77020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4386771PMC
September 2016
44 Reads
6 Citations
3.028 Impact Factor

Calcium, zinc and vitamin E ameliorate cadmium-induced renal oxidative damage in albino Wistar rats.

Toxicol Rep 2016 29;3:591-597. Epub 2016 Jul 29.

Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati - 517502, Andhra Pradesh, India.

This study was aimed to examine the protective effects of supplementation with calcium + zinc (Ca + Zn) or vitamin E (Vit-E) on Cd-induced renal oxidative damage. Young albino Wistar rats (180 ± 10 g) (n = 6) control rats, Cd, Cd + Ca + Zn, and Cd + Vit-E experimental groups and the experimental period was 30 days. Rats were exposed to Cd (20 mg/kg body weight) alone treated as Cd treated group and the absence or presence of Ca + Zn (2 mg/kg each) or Vit-E (20 mg/kg body weight) supplementation treated as two separate groups. The activities of the stress marker enzymes superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and lipid peroxidase (LPx) were determined in renal mitochondrial fractions of experimental rats. We observed quantitative changes in SOD isoenzymatic patterns by non-denaturing PAGE analysis, and quantified band densities. These results showed that Cd exposure leads to decreases in SOD, CAT, GR, and GPx activities and a concomitant increase in LPx and GST activities. Ca + Zn and Vit-E administration with Cd significantly reversed Cd-induced perturbations in oxidative stress marker enzymes. However, Vit-E showed more inhibitory activity against Cd than did Ca + Zn, and it protected against Cd-induced nephrotoxicity.

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http://dx.doi.org/10.1016/j.toxrep.2016.07.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5616016PMC
July 2016
17 Reads
7 Citations

Complete genome-wide screening and subtractive genomic approach revealed new virulence factors, potential drug targets against bio-war pathogen Brucella melitensis 16M.

Drug Des Devel Ther 2015 19;9:1691-706. Epub 2015 Mar 19.

Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati, India.

Brucella melitensis 16M is a Gram-negative coccobacillus that infects both animals and humans. It causes a disease known as brucellosis, which is characterized by acute febrile illness in humans and causes abortions in livestock. To prevent and control brucellosis, identification of putative drug targets is crucial. The present study aimed to identify drug targets in B. melitensis 16M by using a subtractive genomic approach. We used available database repositories (Database of Essential Genes, Kyoto Encyclopedia of Genes and Genomes Automatic Annotation Server, and Kyoto Encyclopedia of Genes and Genomes) to identify putative genes that are nonhomologous to humans and essential for pathogen B. melitensis 16M. The results revealed that among 3 Mb genome size of pathogen, 53 putative characterized and 13 uncharacterized hypothetical genes were identified; further, from Basic Local Alignment Search Tool protein analysis, one hypothetical protein showed a close resemblance (50%) to Silicibacter pomeroyi DUF1285 family protein (2RE3). A further homology model of the target was constructed using MODELLER 9.12 and optimized through variable target function method by molecular dynamics optimization with simulating annealing. The stereochemical quality of the restrained model was evaluated by PROCHECK, VERIFY-3D, ERRAT, and WHATIF servers. Furthermore, structure-based virtual screening was carried out against the predicted active site of the respective protein using the glycerol structural analogs from the PubChem database. We identified five best inhibitors with strong affinities, stable interactions, and also with reliable drug-like properties. Hence, these leads might be used as the most effective inhibitors of modeled protein. The outcome of the present work of virtual screening of putative gene targets might facilitate design of potential drugs for better treatment against brucellosis.

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http://dx.doi.org/10.2147/DDDT.S76948DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4371898PMC
May 2016
28 Reads
2 Citations
3.028 Impact Factor

CGMD: An integrated database of cancer genes and markers.

Sci Rep 2015 Jul 10;5:12035. Epub 2015 Jul 10.

Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati-517502, Andhra Pradesh, India.

Integrating cancer genes and markers with experimental evidence might provide valuable information for the further investigation of crosstalk between tumor genes and markers in cancer biology. To achieve this objective, we developed a database known as the Cancer Gene Marker Database (CGMD), which integrates data on tumor genes and markers based on experimental evidence. The major goal of CGMD is to provide the following: 1) current systematic treatment approaches and recent advances in different cancer treatments; 2) the aggregation of different genes and markers by their molecular characteristics and pathway associations; and 3) free access to the data compiled by CGMD at http://cgmd.in/. The database consists of 309 genes and 206 markers, as well as a list of 40 different human cancers, with detailed descriptions of all characterized markers. CGMD provides complete cancer annotations and molecular descriptions of cancer genes and markers such as CpG islands, promoters, exons, PDB structures, active sites and domains.

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http://dx.doi.org/10.1038/srep12035DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4498195PMC
July 2015
167 Reads
4 Citations
5.078 Impact Factor

Comparison and correlation of Simple Sequence Repeats distribution in genomes of Brucella species.

Bioinformation 2011 26;6(5):179-82. Epub 2011 May 26.

Division of Animal Biotechnology, Department of Zoology, S. V. University, Tirupati-517502, Andhra Pradesh, India.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3124796PMC
http://dx.doi.org/10.6026/97320630006179DOI Listing
July 2011
18 Reads
1 Citation

Top co-authors

Matcha Bhaskar
Matcha Bhaskar

Sri Venkateswara University

5
Arubala P Reddy
Arubala P Reddy

Oregon National Primate Research Center

5
Maria Manczak
Maria Manczak

Garrison Institute on Aging

4
Bhaskar Matcha
Bhaskar Matcha

Sri Venkateswara University

4
Ramesh Kandimalla
Ramesh Kandimalla

Postgraduate Institute of Medical Education and Research

4
Xiangling Yin
Xiangling Yin

Garrison Institute on Aging

3
Yellapu Nanda Kumar
Yellapu Nanda Kumar

Sri Venkateswara University

3
Subodh Kumar
Subodh Kumar

Texas Tech University Health Sciences Center

3