Rituparna Kundu Chaudhuri

National Brain Research Centre

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Co-Authors

Dipankar Chakraborti

University of Calcutta

Sanatan Ghosh

University of Calcutta

Arnab Purohit

Indian Statistical Institute

Shreeparna Ganguly

St Xavier’s College

Anurag Agrawal

Ashoka University

Tanveer Ahmad

Jamia Millia Islamia

Anjan Hazra

University of Calcutta

Sujata Mohanty

All India Institute of Medical Sciences

Balaram Ghosh

Institute of Genomics and Integrative Biology

Bijay Pattnaik

All India Institute of Medical Sciences

Cooperative Institutions

All India Institute of Medical Sciences

Institute of Genomics and Integrative Biology

Jamia Millia Islamia

University of Calcutta

Academy of Scientific and Innovative Research

Council of Scientific and Industrial Research

National Institutes of Health

Indian Council of Agricultural Research

Bahauddin Zakariya University

University of Agriculture Faisalabad

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Fusarium Dieback: Scientific Challenges and Priorities to Safeguard Indian tea Industry

National Academy Science Letters (2024)

Anjan Hazra Rituparna Kundu Chaudhuri Dipankar Chakraborti

Safeguard

10.1007/s40009-024-01413-4

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Citations (0)

Contributors

Elsevier eBooks (2018)

Anurag Agrawal MaryEllen Antkowiak Melinda A. Beck Sapna Bhatia Ellen E. Blaak

10.1016/b978-0-12-813553-2.09994-2

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Regulation of NF-κB Activation through a Novel PI-3K-Independent and PKA/Akt-Dependent Pathway in Human Umbilical Vein Endothelial Cells

PLoS ONE (2012)

Sakshi Balwani Rituparna Kundu Chaudhuri Debkumar Nandi Parasuraman Jaisankar Anurag Agrawal

The transcription factor NF-κB regulates numerous inflammatory diseases, and proteins involved in the NF-κB-activating signaling pathway are important therapeutic targets. In human umbilical vein endothelial cells (HUVECs), TNF-α-induced IκBα degradation and p65/RelA phosphorylation regulate NF-κB activation. These are mediated by IKKs (IκB kinases) viz. IKKα, β and γ which receive activating signals from upstream kinases such as Akt. Akt is known to be positively regulated by PI-3K (phosphoinositide-3-kinase) and differentially regulated via Protein kinase A (PKA) in various cell types. However, the involvement of PKA/Akt cross talk in regulating NF-κB in HUVECs has not been explored yet. Here, we examined the involvement of PKA/Akt cross-talk in HUVECs using a novel compound, 2-methyl-pyran-4-one-3-O-β-D-2′,3′,4′,6′-tetra-O-acetyl glucopyranoside (MPTAG). We observed that MPTAG does not directly inhibit IKK-β but prevents TNF-α-induced activation of IKK-β by blocking its association with Akt and thereby inhibits NF-κB activation. Interestingly, our results also revealed that inhibitory effect of MPTAG on Akt and NF-κB activation was unaffected by wortmannin, and was completely abolished by H-89 treatment in these cells. Thus, MPTAG-mediated inhibition of TNF-α-induced Akt activation was independent of PI-3K and dependent on PKA. Most importantly, MPTAG restores the otherwise repressed activity of PKA and inhibits the TNF-α-induced Akt phosphorylation at both Thr308 and Ser473 residues. Thus, we demonstrate for the first time the involvement of PKA/Akt cross talk in NF-κB activation in HUVECs. Also, MPTAG could be useful as a lead molecule for developing potent therapeutic molecules for diseases where NF-κB activation plays a key role.

IκB kinase

Wortmannin

Phosphoinositide 3-kinase

10.1371/journal.pone.0046528

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Citations (31)

Novel nuclear translocation of inositol polyphosphate 4-phosphatase is associated with cell cycle, proliferation and survival

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (2018)

Rituparna Kundu Chaudhuri Kritika Khanna D B Koundinya Bijay Pattnaik Damini Vatsa

Compartmentalization (fire protection)

Nuclear export signal

10.1016/j.bbamcr.2018.07.013

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Citations (7)

Variability among isolates of Fusarium udum and the effect on progression of wilt in pigeonpea

European Journal of Plant Pathology (2017)

Arnab Purohit Sanjib Ganguly GautamKumar Ghosh Rituparna Kundu Chaudhuri Siraj Datta

10.1007/s10658-017-1167-z

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Citations (17)

Global transcriptome analysis reveals fungal disease responsive core gene regulatory landscape in tea

Scientific Reports (2023)

Anjan Hazra Sanatan Ghosh S. K. Naskar P. F. Rahaman Chitralekha Roy

Abstract Fungal infections are the inevitable limiting factor for productivity of tea. Transcriptome reprogramming recruits multiple regulatory pathways during pathogen infection. A comprehensive meta-analysis was performed utilizing previously reported, well-replicated transcriptomic datasets from seven fungal diseases of tea. The study identified a cumulative set of 18,517 differentially expressed genes (DEGs) in tea, implicated in several functional clusters, including the MAPK signaling pathway, transcriptional regulation, and the biosynthesis of phenylpropanoids. Gene set enrichment analyses under each pathogen stress elucidated that DEGs were involved in ethylene metabolism, secondary metabolism, receptor kinase activity, and various reactive oxygen species detoxification enzyme activities. Expressional fold change of combined datasets highlighting 2258 meta-DEGs shared a common transcriptomic response upon fungal stress in tea. Pervasive duplication events caused biotic stress-responsive core DEGs to appear in multiple copies throughout the tea genome. The co-expression network of meta-DEGs in multiple modules demonstrated the coordination of appropriate pathways, most of which involved cell wall organization. The functional coordination was controlled by a number of hub genes and miRNAs, leading to pathogenic resistance or susceptibility. This first-of-its-kind meta-analysis of host–pathogen interaction generated consensus candidate loci as molecular signatures, which can be associated with future resistance breeding programs in tea.

Secondary metabolism

Biotic stress

Gene regulatory network

Reprogramming

10.1038/s41598-023-44163-x

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Citations (1)

Novel role of mortalin in attenuating HIV-1 Tat-mediated astrogliosis

Journal of Neuroinflammation (2020)

Priyanka Renu Wadhwa Rituparna Kundu Chaudhuri Tapas Chandra Nag Pankaj Seth

Abstract Background In human immunodeficiency virus-1 (HIV-1) infection, activation of astrocytes induces imbalance in physiological functions due to perturbed astrocytic functions that unleashes toxicity on neurons. This leads to inflammatory response finally culminating into neurocognitive dysfunction. In neuroAIDS, HIV-1 protein, transactivator of transcription (Tat) is detected in the cerebrospinal fluid of infected patients. Mortalin, a multifunctional protein, has anti-inflammatory role following its activation in various stress conditions. Recent studies demonstrate downregulation of mortalin in neurodegenerative diseases. Here, we explored the mechanisms of mortalin in modulating HIV-1 Tat-mediated neuroinflammation. Methods Expression of mortalin in autopsy section in normal and diseased individuals were examined using immunohistochemistry. To decipher the role of mortalin in HIV-1 Tat-induced activation, human fetal brain-derived astrocytes were transiently transfected with Tat and mortalin using expression vectors. HIV-1 Tat-mediated damage was analyzed using RT-PCR and western blotting. Modulatory role of mortalin was examined by coexpressing it with Tat, followed by examination of mitochondrial morphodynamics using biochemical assay and confocal and electron microscopy. Extracellular ATP release was monitored using luciferase assay. Neuroinflammation in astrocytes was examined using flow cytometry, dye based study, immunocytochemistry, immunoprecipitation, and western blotting. Indirect neuronal damage was also analyzed. Results HIV-1 Tat downregulates the expression of mortalin in astrocytes, and this is corroborated with autopsy sections of HIV-1 patients. We found that overexpression of mortalin with Tat reduced inflammation and also rescued astrocytic-mediated neuronal death. Using bioinformatics, we discovered that binding of mortalin with Tat leads to Tat degradation and rescues the cell from neuroinflammation. Blocking of proteosomal pathway rescued the Tat degradation and revealed the ubiquitination of Tat. Conclusion Overall, our data demonstrated the protective role of mortalin in combating HIV-1 Tat-mediated damage. We also showed that mortalin could degrade Tat through direct binding with HIV-1 Tat. Overexpression of mortalin in the presence of Tat could significantly reduce cytotoxic effects of Tat in astrocytes. Indirect neuronal death was also found to be rescued. Our in vitro findings were validated as we found attenuated expression of mortalin in the autopsy sections of HIV-1 patients.

Astrogliosis

Immunoprecipitation

Chromatin immunoprecipitation

10.1186/s12974-020-01912-3

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Citations (13)

Genomic Design for Abiotic Stress Resistance in Pigeonpea

Springer eBooks (2022)

B. Nandini S Venkatesh Uday G. Reddy Bingi Pujari Mallikarjuna B. Manu

Germ plasm

Marker-Assisted Selection

Plant Breeding

Molecular breeding

10.1007/978-3-030-91039-6_6

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Citations (2)

Graphene Nanofiber Composites for Enhanced Neuronal Differentiation of Human Mesenchymal Stem Cells

Nanomedicine (2021)

Sonali Rawat Krishan Gopal Jain Deepika Gupta Pawan Kumar Raghav Rituparna Kundu Chaudhuri

Aim: To differentiate mesenchymal stem cells into functional dopaminergic neurons using an electrospun polycaprolactone (PCL) and graphene (G) nanocomposite. Methods: A one-step approach was used to electrospin the PCL nanocomposite, with varying G concentrations, followed by evaluating their biocompatibility and neuronal differentiation. Results: PCL with exiguous graphene demonstrated an ideal nanotopography with an unprecedented combination of guidance stimuli and substrate cues, aiding the enhanced differentiation of mesenchymal stem cells into dopaminergic neurons. These newly differentiated neurons were seen to exhibit unique neuronal arborization, enhanced intracellular Ca2+ influx and dopamine secretion. Conclusion: Having cost-effective fabrication and room-temperature storage, the PCL-G nanocomposites could pave the way for enhanced neuronal differentiation, thereby opening a new horizon for an array of applications in neural regenerative medicine.

Nanotopography

Regenerative Medicine

Biocompatibility

Neural tissue engineering

Polycaprolactone

10.2217/nnm-2021-0121

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Citations (13)

Clean gene technology to develop selectable marker-free pod borer-resistant transgenic pigeon pea events involving the constitutive expression of Cry1Ac

Applied Microbiology and Biotechnology (2022)

Shreeparna Ganguly Arnab Purohit Sanatan Ghosh Rituparna Kundu Chaudhuri Sampa Das

Cry1Ac

Selectable marker

Marker gene

10.1007/s00253-022-11922-1

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Citations (4)