PRADEESH BABU

Dr. PRADEESH BABU

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Research Focus & Metrics

Academic Career Length

15Years (2012-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 May 2012 in Current Cancer Drug Targets
Verified
Journal Article
Closed access
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KNK. Neelakandan
K. Neelakandan
PBPRADEESH BABU
PRADEESH BABU
SNSujit Nair
Sujit Nair
MiRNAs are small endogenous non-coding RNAs, approximately 21-nucleotides in length, which are shown to regulate an array of cellular processes such as differentiation, cell cycle, cell proliferation, apoptosis, and angiogenesis which are important in cancer. miRNAs can function as both tumor promoters (oncomiRs) or tumor suppressors by their ability to target numerous biomolecules that are important in carcinogenesis. Aberrant expression of miRNAs is correlated with the development and progression of tumors, and the reversal of their expression has been shown to modulate the cancer phenotype suggesting the potential of miRNAs as targets for anti-cancer drugs. Several chemopreventive phytochemicals like epigallocatechin-3-gallate, curcumin, isoflavones, indole-3-carbinol, resveratrol, and isothiocyanate have been shown to modulate the expression of numerous miRNAs in cancer cells that lead to either abrogation of tumor growth or sensitization of cancer cells to chemotherapeutic agents. This review focuses on the putative role(s) of miRNAs in different aspects of tumorigenesis and at various stages of early drug discovery that makes them a promising class of drug targets for chemopreventive intervention in cancer. We summarize the current progress in the development of strategies for miRNA-based anti-cancer therapies. We also explore the modulation of miRNAs by various cancer chemopreventive agents and the role of miRNAs in drug metabolism. We will discuss the role of miRNAs in cancer stem cells and epithelial-to-mesenchymal transition; and talk about how modulation of miRNA expression relates to altered glycosylation patterns in cancer cells. In addition, we consider the role of altered miRNA expression in carcinogenesis induced by various agents including genotoxic and epigenetic carcinogens. Finally, we will end with a discussion on the potential involvement of miRNAs in the development of cancer chemoresistance. Taken together, a better understanding of the complex role(s) of miRNAs in cancer may help in designing better strategies for biomarker discovery or drug targeting of miRNAs and/or their putative protein targets.

1 April 2018 in International Journal of Biological Macromolecules
Verified
Journal Article
Open access
CPChandni Porayath
Chandni Porayath
ASAmrita Salim
Amrita Salim
AVArchana Palillam Veedu
Archana Palillam Veedu
PBPRADEESH BABU
PRADEESH BABU
BNBipin G Nair
Bipin G Nair
SPSanjay Pal
Sanjay Pal
Recent literature has suggested a novel symbiotic relationship between bacteriophage and metazoan host that provides antimicrobial defense protecting mucosal surface by binding to host matrix mucin glycoproteins. Here, we isolated and studied different bacteriophages that specifically interact with human extracellular matrix molecules such as fibronectin, gelatin, heparin and demonstrated their potency for protection to host against microbial infections. We showed that subpopulations of bacteriophages that work against clinical isolates of Escherichia coli can bind to pure gelatin, fibronectin and heparin and reduced bacterial load in human colon cell line HT29. The bacteriophages were characterized with respect to their genome sizes, melting curve patterns and host tropism (cross-reactivity with different hosts). Since, the bacteriophages are non-toxic to the host and can effectively reduce bacterial load in HT29 cell line their therapeutic potency against bacterial infection could be explored.

1 August 2021 in Journal of Environmental Chemical Engineering
Verified
Journal Article
Closed access
ASAmrita Salim
Amrita Salim
AMAjith Madhavan
Ajith Madhavan
PBPRADEESH BABU
PRADEESH BABU
CPChandni Porayath
Chandni Porayath
MKManjumol Kesavan
Manjumol Kesavan
SPSanjay Pal
Sanjay Pal

5 January 2022 in Water
Verified
Journal Article
Open access
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SSSuja Subhash
Suja Subhash
PBPRADEESH BABU
PRADEESH BABU
AVAmrutha Vijayakumar
Amrutha Vijayakumar
RSReshma Alookaran Suresh
Reshma Alookaran Suresh
AMAjith Madhavan
Ajith Madhavan
SPSanjay Pal
Sanjay Pal
Robust control of pathogens in sewage facilitates safe reuse of wastewater rich in valuable nutrients for potential valorization through biological means. Aspergillus niger is widely reported in bioremediation of wastewater but studies on control of enteric pathogens in sewage are very sparse. So, this study aimed at exploring the antibacterial and nematicidal activity of A. niger culture filtrate (ACF). Antibacterial activity of ACF on enteric pathogens (Klebsiella pneumoniae, Pseudomonas aeruginosa, Vibrio cholerae, Salmonella enterica, Shigella dysenteriae, Escherichia coli, Staphylococcus aureus, Klebsiella variicola) was determined by spectrophotometric growth analysis, resazurin based viability assay and biofilm formation assay. ACF showed inhibition against all enteric pathogens except Pseudomonas aeruginosa. Nematicidal studies on Caenorhabditis elegans showed 85% egg hatch inhibition and 52% mortality of L1 larvae. Sewage treatment with ACF at 1:1 (v/v) showed 2–3 log reduction in coliforms, Klebsiella, Shigella, Salmonella, S. aureus and Vibrio except Pseudomonas, indicating significant alteration of complex microbial dynamics in wastewater. Application of ACF can potentially be used as a robust biocontrol strategy against infectious microbes in wastewater and subsequent valorization by cultivating beneficial Pseudomonas.

3 July 2019 in Microbiology Resource Announcements
Verified
Journal Article
Open access
PDF file
ASAmrita Salim
Amrita Salim
PBPRADEESH BABU
PRADEESH BABU
KMKeerthi Mohan
Keerthi Mohan
MMManju Moorthy
Manju Moorthy
DRDevika Raj
Devika Raj
SPSanjay Pal
Sanjay Pal
We report the draft genome sequence of Escherichia coli ASBT-1, a representative of E. coli sequence type 155 (ST155), obtained from India. Considering the known wide variety of pathogenic and antibiotic resistance potentials, this strain should be of great interest for detailed comparative genomic analysis.

Verified
Journal Article
Open access
PDF file
AMArjun M Menon
Arjun M Menon
GBGopichand Boinapalli
Gopichand Boinapalli
STShwetha Susan Thomas
Shwetha Susan Thomas
AKAbhinand Kuniyil
Abhinand Kuniyil
BNBipin G Nair
Bipin G Nair
AMAravind Madhavan
Aravind Madhavan
Rv1899c, a previously identified HDAC1–ZBTB25-interacting protein of Mycobacterium tuberculosis, plays a crucial role in bacterial adaptation and immune modulation. Recombinant M. smegmatis-expressing Rv1899c (MS_ Rv1899c) showed enhanced survival under acidic and oxidative stress compared to vector controls, along with improved early intracellular growth in THP1-derived macrophages. This was accompanied by reduced reactive oxygen species (ROS), diminished cytokines associated with inflammation and downregulation of autophagy proteins ATG5, Beclin, and LC3, which ultimately skewed the immune response, suppressing the pro-inflammatory M1 macrophage population. Targeting Rv1899c with 3-aminobenzamide (3-AB) impaired intracellular bacterial survival and restored IL-12B expression, while its combination with the HDAC inhibitor C1994 significantly enhanced bacterial clearance. Structural modelling confirmed the high stereochemical quality of the Rv1899c macrodomain, and computational studies identified 3-AB as the strongest ligand (−5.75 kcal/mol), stabilized through hydrogen bonding and hydrophobic interactions with key residues. Molecular dynamics simulations conducted for 200 ns demonstrated stable protein–ligand interactions with consistent parameters, while MM/GBSA analysis indicated favourable binding energy (ΔG_bind = −6.6 kcal/mol), largely influenced by van der Waals and electrostatic forces. Together, these findings highlight Rv1899c as a mediator of stress resistance and immune evasion and propose it as a potential therapeutic target against M. tuberculosis.