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  1. Home
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Browsing by Author "Pranjali Pandey"

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    PublicationConference Paper
    Comparison between Fingerprint-Based Biometric Recognition Systems and QR Code-Based Authentication Systems: Challenges, Solutions, and Applications
    (Institute of Electrical and Electronics Engineers Inc., 2021) Pranjali Pandey; Jai Prakash Kumar; Arun Kumar Agariya
    This paper aims to reflect upon the limitations of the fingerprint-based biometric system and a way to overcome them with the help of a QR Code based system. Primary data was collected through a questionnaire to get the insight of people having exposure to both the systems, and it was backed with secondary data to get an overall comparison. The research showed that QR Codes fared better than fingerprint biometrics in parameters like accuracy, cost-effectiveness, maintenance, and future scope. The study has attempted to apply the findings with the help of an android application, which would help the Indian MSMEs manage their employees. © 2021 IEEE.
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    PublicationArticle
    Maheshvara regulates JAK/STAT signaling by interacting and stabilizing hopscotch transcripts which leads to apoptosis in Drosophila melanogaster
    (Springer Nature, 2021) Bhawana Maurya; Satya Surabhi; Rituparna Das; Pranjali Pandey; Ashim Mukherjee; Mousumi Mutsuddi
    Maheshvara (mahe), an RNA helicase that is widely conserved across taxa, regulates Notch signaling and neuronal development in Drosophila. In order to identify novel components regulated by mahe, transcriptome profiling of ectopic mahe was carried out and this revealed striking upregulation of JAK/STAT pathway components like upd1, upd2, upd3, and socs36E. Further, significant downregulation of the pathway components in mahe loss-of-function mutant as well as upon lowering the level of mahe by RNAi, supported and strengthened our transcriptome data. Parallelly, we observed that mahe, induced caspase-dependent apoptosis in photoreceptor neurons, and this phenotype was significantly modulated by JAK/STAT pathway components. RNA immunoprecipitation unveiled the presence of JAK/STAT tyrosine kinase hopscotch (hop) transcripts in the complex immunoprecipitated with Mahe, which ultimately resulted in stabilization and elevation of hop transcripts. Additionally, we also observed the surge in activity of downstream transcription factor Stat92E, which is indicative of activation of the JAK/STAT signaling, and this in turn led to apoptosis via upregulation of hid. Taken together, our data provide a novel regulation of JAK/STAT pathway by RNA helicase Maheshvara, which ultimately promotes apoptosis. © 2021, The Author(s).
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    PublicationArticle
    RNA helicase maheshvara interacts with TDP-43 and exacerbates neurodegeneration in Drosophila model of amyotrophic lateral sclerosis
    (Academic Press Inc., 2025) Pranjali Pandey; Rituparna Das; Harshita Yadav; Ashim Mukherjee; M. Mutsuddi
    Drosophila maheshvara (mahe) encodes a conserved DEAD box RNA helicase that regulates various important signaling pathways like Notch and JAK/STAT, pathways that have been functionally implicated in neuronal development. In order to identify novel modulators of mahe as well as to unravel its role in neurodegenerative disorders, a genetic modifier screen using Drosophila models of neurodegenerative disorders was carried out. From this screen, we identified mahe to be a potent modifier of TDP-43 mediated proteinopathy in Drosophila model of Amyotrophic Lateral Sclerosis (ALS). We demonstrate that Mahe genetically interacts and associates with cytosolic hyperphosphorylated toxic aggregates of TDP-43 leading to enhanced TDP-43 mediated neurodegenerative phenotype. Increased autophagy, cytoskeletal disruption, and FMRP-mediated translational repression of neuronal target Futsch were observed, potentially contributing to neuronal dysfunction. The current study indicates a strong interaction of mahe and TDP-43 (TARDBP) resulting in augmentation of TDP-43 mediated neurodegenerative phenotypes which parallels ALS clinical pathology. © 2025
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    PublicationArticle
    Spoonbill positively regulates JNK signalling mediated apoptosis in Drosophila melanogaster
    (Elsevier GmbH, 2023) Rituparna Das; Pranjali Pandey; Bhawana Maurya; Priyadarshika Pradhan; Devanjan Sinha; Ashim Mukherjee; Mousumi Mutsuddi
    A-kinase anchoring protein (AKAP) comprises a family of scaffold proteins, which decides the subcellular localisation of a combination of signalling molecules. Spoonbill (Spoon) is a putative A-kinase anchoring protein in Drosophila. We have earlier reported that Spoon suppresses ribonuclear foci formed by trinucleotide repeat expanded transcripts associated with Spinocerebellar Ataxia 8 neurodegeneration in Drosophila. However, the role of Spoonbill in cellular signalling was unexplored. In this report, we have unravelled a novel function of Spoon protein in the regulation of the apoptotic pathway. The Drosophila TNFα homolog, Eiger, induces apoptosis via activation of the JNK pathway. We have shown here that Spoonbill is a positive regulator of the Eiger-induced JNK signalling. Further genetic interaction studies show that the spoon interacts with components of the JNK pathway, TGF-β activated kinase 1 (Tak1 - JNKKK), hemipterous (hep - JNKK) and basket (bsk - JNK). Interestingly, Spoonbill alone can also induce ectopic activation of the JNK pathway in a context-specific manner. To understand the molecular mechanism underlying Spoonbill-mediated modulation of the JNK pathway, the interaction between Spoon and Drosophila JNK was assessed. basket encodes the only known JNK in Drosophila. This serine/threonine-protein kinase phosphorylates Jra/Kay, which transcriptionally regulate downstream targets like Matrix metalloproteinase 1 (Mmp1), puckered (puc), and proapoptotic genes hid, reaper and grim. Interestingly, we found that Spoonbill colocalises and co-immunoprecipitates with the Basket protein in the developing photoreceptor neurons. Hence, we propose that Spoon plays a vital role in JNK-induced apoptosis. Furthermore, stress-induced JNK activation underlying Parkinson's Disease was also examined. In the Parkinson's Drosophila model of neurodegeneration, depletion of Spoonbill leads to a partial reduction of JNK pathway activation, along with improvement in adult motor activity. These observations suggest that the putative scaffold protein Spoonbill is a functional and physical interacting partner of the Drosophila JNK protein, Basket. Spoon protein is localised on the outer mitochondrial membrane (OMM), which may perhaps provide a suitable subcellular niche for activation of Drosophila Basket protein by its kinases which induce apoptosis. © 2023
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    PublicationBook Chapter
    The expanding role of RNA-binding proteins in neurodegeneration
    (Springer Singapore, 2019) Bhawana Maurya; Satya Surabhi; Pranjali Pandey; Ashim Mukherjee; Mousumi Mutsuddi
    In eukaryotic cells, gene expression is regulated at various levels after generation of a primary RNA transcript, including mRNA processing, transport, stability, and co-and post-transcriptional regulation. These processes are tightly controlled by the action of a multitude of RNA-binding proteins (RBPs). As soon as an RNA is transcribed, RBPs regulate the RNA at every step, starting from processing up to its final degradation. RNA processing plays a fundamental role in regulating multiple events during nervous system development. So far, RBPs have been shown to be important for neurogenesis, neurite outgrowth, maintaining neural stem cells, synapse formation, and plasticity. In addition, studies have depicted that several neurological diseases are associated with deregulated genes involved in RNA metabolism. Moreover, alterations in RNA-binding proteins are associated with many neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), fragile X syndrome (FXS), spinal muscular atrophy (SMA), and many others. Drosophila has been one of the best model organisms to understand neurodegeneration at the molecular level. In this chapter, we report the use of Drosophila in comprehending recent advances that link RBPs with neurodegenerative processes. This will help in advancing our knowledge as to how RBP dysfunction contributes to neurological diseases. © Springer Nature Singapore Pte Ltd. 2019.
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