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  1. Article: Assessing Differential Binding of Aggregation-Induced Emission-Based Luminogens to Host Interacting Surface Proteins of SARS-CoV-2 and Influenza Virus-An

    Tanneeru, Karunakar / Bhatraju, Naveen Kumar / Bhosale, Rajesh S / Kalangi, Suresh K

    Frontiers in microbiology

    2021  Volume 12, Page(s) 766351

    Abstract: Early detection of asymptomatic cases through mass screening is essential to constrain the coronavirus disease 2019 (COVID-19) transmission. However, the existing diagnostic strategies are either resource-intensive, time-consuming, or less sensitive, ... ...

    Abstract Early detection of asymptomatic cases through mass screening is essential to constrain the coronavirus disease 2019 (COVID-19) transmission. However, the existing diagnostic strategies are either resource-intensive, time-consuming, or less sensitive, which limits their use in the development of rapid mass screening strategies. There is a clear pressing need for simple, fast, sensitive, and economical diagnostic strategy for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) screening even in resource-limited settings. In the current work, we assessed the
    Language English
    Publishing date 2021-12-03
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587354-4
    ISSN 1664-302X
    ISSN 1664-302X
    DOI 10.3389/fmicb.2021.766351
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The deleterious impact of a non-synonymous SNP on protein structure and function is apparent in hypertension.

    Sharma, Kavita / Hema, Kanipakam / Bhatraju, Naveen Kumar / Kukreti, Ritushree / Das, Rajat Subhra / Gupta, Mohit Dayal / Syed, Mansoor Ali / Pasha, M A Qadar

    Journal of molecular modeling

    2021  Volume 28, Issue 1, Page(s) 14

    Abstract: Essential hypertension (EH) is a significant health issue around the globe. The indifferent therapy regimen suggests varied physiological functions due to the lifestyle and genetic presentations of an individual. The endothelial nitric oxide synthase ( ... ...

    Abstract Essential hypertension (EH) is a significant health issue around the globe. The indifferent therapy regimen suggests varied physiological functions due to the lifestyle and genetic presentations of an individual. The endothelial nitric oxide synthase (NOS3) gene is a crucial vascular system marker in EH that contributes significantly to the phenotype. Hence, the present study aimed to employ the candidate gene approach and investigate the association between NOS3 single nucleotide polymorphism (SNP) E298D (G894T/rs1799983) by applying several in silico tools and validation through human samples screening. We corroborated computational findings through a case-control study comprising 294 controls and 299 patients; the 894T allele emerged significantly as the risk allele (odds ratio=2.07; P=6.38E-05). The in silico analyses highlighted the significance of E298D on the native structure and function of NOS3. The dynamics simulation study revealed that the variant type 298D caused structural destabilization of the protein to alter its function. Plasma nitrite levels were reduced in patients (P=0.0002), and the same correlated with the 894T allele. Furthermore, correlations were apparent between clinical, genotype, and routine biochemical parameters. To conclude, the study demonstrated a perceptible association between the SNP E298D and NOS3 protein structure stability that appears to have a bearing on the enzyme's function with a deleterious role in EH.
    MeSH term(s) Alleles ; Amino Acid Substitution ; Biomarkers ; Computational Biology/methods ; Genotype ; Humans ; Hypertension/etiology ; Models, Molecular ; Nitric Oxide Synthase Type III/chemistry ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/metabolism ; Polymorphism, Single Nucleotide ; Protein Conformation ; Proteins/chemistry ; Proteins/genetics ; Reproducibility of Results ; Structure-Activity Relationship
    Chemical Substances Biomarkers ; Proteins ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
    Language English
    Publishing date 2021-12-27
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1284729-X
    ISSN 0948-5023 ; 1610-2940
    ISSN (online) 0948-5023
    ISSN 1610-2940
    DOI 10.1007/s00894-021-04997-6
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  3. Article ; Online: Valproic Acid-Induced Upregulation of Multidrug Efflux Transporter ABCG2/BCRP via PPAR

    Kukal, Samiksha / Bora, Shivangi / Kanojia, Neha / Singh, Pooja / Paul, Priyanka Rani / Rawat, Chitra / Sagar, Shakti / Bhatraju, Naveen Kumar / Grewal, Gurpreet Kaur / Singh, Anju / Kukreti, Shrikant / Satyamoorthy, Kapaettu / Kukreti, Ritushree

    Molecular pharmacology

    2022  Volume 103, Issue 3, Page(s) 145–157

    Abstract: Despite the progress made in the development of new antiepileptic drugs (AEDs), poor response to them is a rising concern in epilepsy treatment. Of several hypotheses explaining AED treatment failure, the most promising theory is the overexpression of ... ...

    Abstract Despite the progress made in the development of new antiepileptic drugs (AEDs), poor response to them is a rising concern in epilepsy treatment. Of several hypotheses explaining AED treatment failure, the most promising theory is the overexpression of multidrug transporters belonging to ATP-binding cassette (ABC) transporter family at blood-brain barrier. Previous data show that AEDs themselves can induce these transporters, in turn affecting their own brain bioavailability. Presently, this induction and the underlying regulatory mechanism involved at human blood-brain barrier is not well elucidated. Herein, we sought to explore the effect of most prescribed first- and second-line AEDs on multidrug transporters in human cerebral microvascular endothelial cells, hCMEC/D3. Our work demonstrated that exposure of these cells to valproic acid (VPA) induced mRNA, protein, and functional activity of breast cancer resistance protein (BCRP/ABCG2). On examining the substrate interaction status of AEDs with BCRP, VPA, phenytoin, and lamotrigine were found to be potential BCRP substrates. Furthermore, we observed that siRNA-mediated knockdown of peroxisome proliferator-activated receptor alpha (PPAR
    MeSH term(s) Humans ; Female ; PPAR alpha/metabolism ; Valproic Acid/pharmacology ; ATP Binding Cassette Transporter, Subfamily G, Member 2/genetics ; ATP Binding Cassette Transporter, Subfamily G, Member 2/metabolism ; Anticonvulsants/pharmacology ; Up-Regulation ; Endothelial Cells/metabolism ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Brain/metabolism ; Membrane Transport Proteins/metabolism ; ATP-Binding Cassette Transporters/genetics ; ATP-Binding Cassette Transporters/metabolism ; Epilepsy/drug therapy ; Epilepsy/metabolism ; Breast Neoplasms/metabolism
    Chemical Substances PPAR alpha ; Valproic Acid (614OI1Z5WI) ; ATP Binding Cassette Transporter, Subfamily G, Member 2 ; Anticonvulsants ; Neoplasm Proteins ; Membrane Transport Proteins ; ATP-Binding Cassette Transporters ; ABCG2 protein, human
    Language English
    Publishing date 2022-11-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 124034-1
    ISSN 1521-0111 ; 0026-895X
    ISSN (online) 1521-0111
    ISSN 0026-895X
    DOI 10.1124/molpharm.122.000568
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 525: Show issues Location:
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  4. Article ; Online: Adhatoda vasica

    Gheware, Atish / Panda, Lipsa / Khanna, Kritika / Bhatraju, Naveen Kumar / Jain, Vaibhav / Sagar, Shakti / Kumar, Manish / Singh, Vijay Pal / Kannan, Sadasivam / Subramanian, Venkatesan / Mukerji, Mitali / Agrawal, Anurag / Prasher, Bhavana

    American journal of physiology. Lung cellular and molecular physiology

    2021  Volume 320, Issue 5, Page(s) L757–L769

    Abstract: Severe asthma is a chronic airway disease that exhibits poor response to conventional asthma therapies. Growing evidence suggests that elevated hypoxia increases the severity of asthmatic inflammation among patients and in model systems. In this study, ... ...

    Abstract Severe asthma is a chronic airway disease that exhibits poor response to conventional asthma therapies. Growing evidence suggests that elevated hypoxia increases the severity of asthmatic inflammation among patients and in model systems. In this study, we elucidate the therapeutic effects and mechanistic basis of
    MeSH term(s) Animals ; Asthma/drug therapy ; Asthma/etiology ; Asthma/metabolism ; Asthma/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Hypoxia/complications ; Justicia/chemistry ; Male ; Mice ; Mice, Inbred BALB C ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/pathology ; Phytochemicals/pharmacology ; Plant Extracts/pharmacology ; Pneumonia/etiology ; Pneumonia/metabolism ; Pneumonia/pathology ; Pneumonia/prevention & control
    Chemical Substances Phytochemicals ; Plant Extracts
    Language English
    Publishing date 2021-02-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00511.2020
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    Uc I Zs.89: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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    Zs.A 2749: Show issues Location:
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  5. Article ; Online: IL-4 promotes asymmetric dimethylarginine accumulation, oxo-nitrative stress, and hypoxic response-induced mitochondrial loss in airway epithelial cells.

    Pattnaik, Bijay / Bodas, Manish / Bhatraju, Naveen Kumar / Ahmad, Tanveer / Pant, Richa / Guleria, Randeep / Ghosh, Balaram / Agrawal, Anurag

    The Journal of allergy and clinical immunology

    2016  Volume 138, Issue 1, Page(s) 130–141.e9

    Abstract: Background: Obesity is known to increase asthma risk and severity. Increased levels of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, are associated with mitochondrial toxicity, asthma, and metabolic syndrome. IL-4 ... ...

    Abstract Background: Obesity is known to increase asthma risk and severity. Increased levels of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, are associated with mitochondrial toxicity, asthma, and metabolic syndrome. IL-4 upregulates the expression of protein arginine methyltransferases, which are essential for ADMA formation. Importantly, cross-talk between IL-4, ADMA, and mitochondrial dysfunction could explain how obesity and IL-4 can synergize to exacerbate allergic inflammation.
    Objective: We sought to investigate how IL-4, a key asthma-associated cytokine, can influence ADMA-related effects on lungs.
    Methods: BEAS2B (bronchial epithelial) cells were treated with IL-4 followed by ADMA and investigated for oxo-nitrative stress and resultant mitochondrial toxicity after 48 hours by using flow cytometry, confocal imaging, immunoblotting, and fluorimetric assays.
    Results: IL-4-induced mitotoxicity in BEAS2B cells was significantly higher in the presence of exogenous ADMA. IL-4 treatment led to proteolytic degradation of dimethylarginine dimethylaminohydrolase 2, which catabolizes ADMA. IL-4 pretreatment was associated with increased intracellular ADMA accumulation and increased ADMA-induced mitotoxicity. Airway epithelial cells treated with IL-4 followed by ADMA showed exaggerated oxo-nitrative stress and potent induction of the cellular hypoxic response, despite normoxic conditions. The hypoxic response was associated with reduced mitochondrial function but was reversible by overexpression of the mitochondrial biogenesis factor, mitochondrial transcription factor A.
    Conclusion: We conclude that IL-4 promotes intracellular ADMA accumulation, leading to mitochondrial loss through oxo-nitrative stress and hypoxic response. This provides a novel understanding of how obesity, with high ADMA levels, and asthma, with high IL-4 levels, might potentiate each other and highlights the potential of mitochondrial-targeted therapeutics in obese subjects with asthma.
    MeSH term(s) Amidohydrolases/metabolism ; Apoptosis ; Arginine/analogs & derivatives ; Arginine/metabolism ; Asthma/etiology ; Asthma/metabolism ; Asthma/pathology ; Calpain/metabolism ; Cell Line ; Cells, Cultured ; Cytokines/metabolism ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Humans ; Hypoxia/metabolism ; Inflammation Mediators/metabolism ; Interleukin-4/metabolism ; Interleukin-4/pharmacology ; Mitochondria/drug effects ; Mitochondria/metabolism ; Nitric Oxide ; Oxidative Stress ; Peroxynitrous Acid/metabolism ; Proteolysis ; Reactive Oxygen Species/metabolism ; Respiratory Mucosa/metabolism
    Chemical Substances Cytokines ; Inflammation Mediators ; Reactive Oxygen Species ; Peroxynitrous Acid (14691-52-2) ; Interleukin-4 (207137-56-2) ; Nitric Oxide (31C4KY9ESH) ; N,N-dimethylarginine (63CV1GEK3Y) ; Arginine (94ZLA3W45F) ; Calpain (EC 3.4.22.-) ; Amidohydrolases (EC 3.5.-) ; dimethylargininase (EC 3.5.3.18)
    Language English
    Publishing date 2016-02-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2015.11.036
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