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  1. Article ; Online: Biochanin A impedes STAT3 activation by upregulating p38δ MAPK phosphorylation in IL-6-stimulated macrophages.

    Basu, Anandita / Das, Anindhya Sundar / Borah, Pallab Kumar / Duary, Raj Kumar / Mukhopadhyay, Rupak

    Inflammation research : official journal of the European Histamine Research Society ... [et al.

    2020  Volume 69, Issue 11, Page(s) 1143–1156

    Abstract: Objective: IL-6-induced STAT3 activation is associated with various chronic inflammatory diseases. In this study, we investigated the anti-STAT3 mechanism of the dietary polyphenol, biochanin A (BCA), in IL-6-treated macrophages.: Methods: The effect ...

    Abstract Objective: IL-6-induced STAT3 activation is associated with various chronic inflammatory diseases. In this study, we investigated the anti-STAT3 mechanism of the dietary polyphenol, biochanin A (BCA), in IL-6-treated macrophages.
    Methods: The effect of BCA on STAT3 and p38 MAPK was analyzed by immunoblot. The localization of both these transcription factors was determined by immunofluorescence and fractionation studies. The impact on DNA-binding activity of STAT3 was studied by luciferase assay. To understand which of the isoforms of p38 MAPK was responsible for BCA-mediated regulation of STAT3, overexpression of the proteins, site-directed mutagenesis, pull-down assays and computational analysis were performed. Finally, adhesion-migration assays and semi-quantitative PCR were employed to understand the biological effects of BCA-mediated regulation of STAT3.
    Results: BCA prevented STAT3 phosphorylation (Tyr
    Conclusion: This differential regulation of STAT3 and p38 MAPK in macrophages establishes a novel anti-inflammatory mechanism of BCA which could be important for the prevention of IL-6-associated chronic inflammatory diseases.
    MeSH term(s) Anti-Inflammatory Agents/pharmacology ; Cell Adhesion/drug effects ; Cell Movement/drug effects ; Cell Survival/drug effects ; Genistein/pharmacology ; HEK293 Cells ; Humans ; Interleukin-6/pharmacology ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/physiology ; Macrophages/drug effects ; Macrophages/physiology ; Mitogen-Activated Protein Kinase 13/genetics ; Mitogen-Activated Protein Kinase 13/metabolism ; Phosphorylation/drug effects ; STAT3 Transcription Factor/metabolism ; THP-1 Cells
    Chemical Substances Anti-Inflammatory Agents ; Interleukin-6 ; STAT3 Transcription Factor ; STAT3 protein, human ; Genistein (DH2M523P0H) ; Mitogen-Activated Protein Kinase 13 (EC 2.7.1.-) ; biochanin A (U13J6U390T)
    Language English
    Publishing date 2020-08-27
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1221794-3
    ISSN 1420-908X ; 1023-3830
    ISSN (online) 1420-908X
    ISSN 1023-3830
    DOI 10.1007/s00011-020-01387-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 675: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Post-transcriptional regulation of C-C motif chemokine ligand 2 expression by ribosomal protein L22 during LPS-mediated inflammation.

    Das, Anindhya Sundar / Basu, Anandita / Kumar, Ravi / Borah, Pallab Kumar / Bakshi, Subhojit / Sharma, Manoj / Duary, Raj Kumar / Ray, Partho Sarothi / Mukhopadhyay, Rupak

    The FEBS journal

    2020  Volume 287, Issue 17, Page(s) 3794–3813

    Abstract: Monocyte infiltration to the site of pathogenic invasion is critical for inflammatory response and host defence. However, this process demands precise regulation as uncontrolled migration of monocytes to the site delays resolution of inflammation and ... ...

    Abstract Monocyte infiltration to the site of pathogenic invasion is critical for inflammatory response and host defence. However, this process demands precise regulation as uncontrolled migration of monocytes to the site delays resolution of inflammation and ultimately promotes chronic inflammation. C-C motif chemokine ligand 2 (CCL2) plays a key role in monocyte migration, and hence, its expression should be tightly regulated. Here, we report a post-transcriptional regulation of CCL2 involving the large ribosomal subunit protein L22 (RPL22) in LPS-activated, differentiated THP-1 cells. Early events following LPS treatment include transcriptional upregulation of RPL22 and its nuclear accumulation. The protein binds to the first 20 nt sequence of the 5'UTR of ccl2 mRNA. Simultaneous nuclear translocation of up-frameshift-1 protein and its interaction with RPL22 results in cytoplasmic degradation of the ccl2 mRNA at a later stage. Removal of RPL22 from cells results in increased expression of CCL2 in response to LPS causing disproportionate migration of monocytes. We propose that post-transcriptional regulation of CCL2 by RPL22 fine-tunes monocyte infiltration during a pathogenic insult and maintains homeostasis of the immune response critical to resolution of inflammation. DATABASES: Microarray data are available in NCBI GEO database (Accession No GSE126525).
    MeSH term(s) 5' Untranslated Regions ; Active Transport, Cell Nucleus ; Base Sequence ; CRISPR-Cas Systems ; Cell Movement ; Chemokine CCL2/biosynthesis ; Chemokine CCL2/genetics ; Humans ; Inflammation/chemically induced ; Inflammation/genetics ; Inflammation/metabolism ; Lipopolysaccharides/toxicity ; MCF-7 Cells ; Models, Molecular ; Neoplasm Proteins/metabolism ; Protein Conformation ; Protein Interaction Mapping ; Protein Processing, Post-Translational ; RNA Helicases/metabolism ; RNA Stability ; RNA, Messenger/metabolism ; RNA-Binding Proteins/physiology ; Ribosomal Proteins/deficiency ; Ribosomal Proteins/physiology ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; THP-1 Cells ; Trans-Activators/metabolism
    Chemical Substances 5' Untranslated Regions ; CCL2 protein, human ; Chemokine CCL2 ; Lipopolysaccharides ; Neoplasm Proteins ; RNA, Messenger ; RNA-Binding Proteins ; Ribosomal Proteins ; Trans-Activators ; RPL22 protein, human (135844-68-7) ; RNA Helicases (EC 3.6.4.13) ; UPF1 protein, human (EC 3.6.4.13)
    Language English
    Publishing date 2020-05-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.15362
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 260: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Antiatherogenic Roles of Dietary Flavonoids Chrysin, Quercetin, and Luteolin.

    Basu, Anandita / Das, Anindhya S / Majumder, Munmi / Mukhopadhyay, Rupak

    Journal of cardiovascular pharmacology

    2016  Volume 68, Issue 1, Page(s) 89–96

    Abstract: Cardiovascular diseases (CVDs) are the commonest cause of global mortality and morbidity. Atherosclerosis, the fundamental pathological manifestation of CVDs, is a complex process and is poorly managed both in terms of preventive and therapeutic ... ...

    Abstract Cardiovascular diseases (CVDs) are the commonest cause of global mortality and morbidity. Atherosclerosis, the fundamental pathological manifestation of CVDs, is a complex process and is poorly managed both in terms of preventive and therapeutic intervention. Aberrant lipid metabolism and chronic inflammation play critical roles in the development of atherosclerosis. These processes can be targeted for effective management of the disease. Although managing lipid metabolism is in the forefront of current therapeutic approaches, controlling inflammation may also prove to be crucial for an efficient treatment regimen of the disease. Flavonoids, the plant-derived polyphenols, are known for their antiinflammatory properties. This review discusses the possible antiatherogenic role of 3 flavonoids, namely, chrysin, quercetin, and luteolin primarily known for their antiinflammatory properties.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/administration & dosage ; Anti-Inflammatory Agents/pharmacokinetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/physiopathology ; Atherosclerosis/prevention & control ; Biological Availability ; Flavonoids/administration & dosage ; Flavonoids/pharmacokinetics ; Healthy Diet ; Humans ; Inflammation/metabolism ; Inflammation/pathology ; Inflammation/physiopathology ; Inflammation/prevention & control ; Inflammation Mediators/metabolism ; Intestinal Absorption ; Lipid Metabolism/drug effects ; Luteolin/administration & dosage ; Luteolin/pharmacokinetics ; Quercetin/administration & dosage ; Quercetin/pharmacokinetics
    Chemical Substances Anti-Inflammatory Agents ; Flavonoids ; Inflammation Mediators ; chrysin (3CN01F5ZJ5) ; Quercetin (9IKM0I5T1E) ; Luteolin (KUX1ZNC9J2)
    Language English
    Publishing date 2016-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 391970-5
    ISSN 1533-4023 ; 0160-2446
    ISSN (online) 1533-4023
    ISSN 0160-2446
    DOI 10.1097/FJC.0000000000000380
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1471: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Post‐transcriptional regulation of C‐C motif chemokine ligand 2 expression by ribosomal protein L22 during LPS‐mediated inflammation

    Das, Anindhya Sundar / Basu, Anandita / Kumar, Ravi / Borah, Pallab Kumar / Bakshi, Subhojit / Sharma, Manoj / Duary, Raj Kumar / Ray, Partho Sarothi / Mukhopadhyay, Rupak

    FEBS journal. 2020 Sept., v. 287, no. 17

    2020  

    Abstract: Monocyte infiltration to the site of pathogenic invasion is critical for inflammatory response and host defence. However, this process demands precise regulation as uncontrolled migration of monocytes to the site delays resolution of inflammation and ... ...

    Abstract Monocyte infiltration to the site of pathogenic invasion is critical for inflammatory response and host defence. However, this process demands precise regulation as uncontrolled migration of monocytes to the site delays resolution of inflammation and ultimately promotes chronic inflammation. C‐C motif chemokine ligand 2 (CCL2) plays a key role in monocyte migration, and hence, its expression should be tightly regulated. Here, we report a post‐transcriptional regulation of CCL2 involving the large ribosomal subunit protein L22 (RPL22) in LPS‐activated, differentiated THP‐1 cells. Early events following LPS treatment include transcriptional upregulation of RPL22 and its nuclear accumulation. The protein binds to the first 20 nt sequence of the 5′UTR of ccl2 mRNA. Simultaneous nuclear translocation of up‐frameshift‐1 protein and its interaction with RPL22 results in cytoplasmic degradation of the ccl2 mRNA at a later stage. Removal of RPL22 from cells results in increased expression of CCL2 in response to LPS causing disproportionate migration of monocytes. We propose that post‐transcriptional regulation of CCL2 by RPL22 fine‐tunes monocyte infiltration during a pathogenic insult and maintains homeostasis of the immune response critical to resolution of inflammation. DATABASES: Microarray data are available in NCBI GEO database (Accession No GSE126525).
    Keywords databases ; homeostasis ; immune response ; inflammation ; ligands ; microarray technology ; monocytes ; ribosomal proteins ; transcription (genetics)
    Language English
    Dates of publication 2020-09
    Size p. 3794-3813.
    Publishing place John Wiley & Sons, Ltd
    Document type Article
    Note NAL-AP-2-clean ; JOURNAL ARTICLE
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.15362
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 2006/704: Show issues

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  5. Article: STAT3 and NF-κB are common targets for kaempferol-mediated attenuation of COX-2 expression in IL-6-induced macrophages and carrageenan-induced mouse paw edema.

    Basu, Anandita / Das, Anindhya Sundar / Sharma, Manoj / Pathak, Manash Pratim / Chattopadhyay, Pronobesh / Biswas, Kaushik / Mukhopadhyay, Rupak

    Biochemistry and biophysics reports

    2017  Volume 12, Page(s) 54–61

    Abstract: Cycloxygenase-2 (COX-2) is the inducible isoform of cycloxygenase enzyme family that catalyzes synthesis of inflammatory mediators, prostanoids and prostaglandins, and therefore, can be targeted by anti-inflammatory drugs. Here, we showed a plant ... ...

    Abstract Cycloxygenase-2 (COX-2) is the inducible isoform of cycloxygenase enzyme family that catalyzes synthesis of inflammatory mediators, prostanoids and prostaglandins, and therefore, can be targeted by anti-inflammatory drugs. Here, we showed a plant polyphenol, kaempferol, attenuated IL-6-induced COX-2 expression in human monocytic THP-1 cells suggesting its beneficial role in chronic inflammation. Kaempferol deactivated and prevented nuclear localization of two major transcription factors STAT3 and NF-κB, mutually responsible for COX-2 induction in response to IL-6. Moreover, STAT3 and NF-κB were simultaneously deactivated by kaempferol in acute inflammation, as shown by carrageenan-induced mouse paw edema model. The concomitant reduction in COX-2 expression in paw tissues suggested kaempferol's role in mitigation of inflammation by targeting STAT3 and NF-κB.
    Language English
    Publishing date 2017-08-26
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2831046-9
    ISSN 2405-5808
    ISSN 2405-5808
    DOI 10.1016/j.bbrep.2017.08.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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