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  1. Article ; Online: KIFC1 Regulates the Trajectory of Neuronal Migration.

    Muralidharan, Hemalatha / Guha, Shrobona / Madugula, Kiran / Patil, Ankita / Bennison, Sarah A / Sun, Xiaohuan / Toyo-Oka, Kazuhito / Baas, Peter W

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2022  Volume 42, Issue 11, Page(s) 2149–2165

    Abstract: During neuronal migration, forces generated by cytoplasmic dynein yank on microtubules extending from the centrosome into the leading process and move the nucleus along microtubules that extend behind the centrosome. Scaffolds, such as radial glia, guide ...

    Abstract During neuronal migration, forces generated by cytoplasmic dynein yank on microtubules extending from the centrosome into the leading process and move the nucleus along microtubules that extend behind the centrosome. Scaffolds, such as radial glia, guide neuronal migration outward from the ventricles, but little is known about the internal machinery that ensures that the soma migrates along its proper path rather than moving backward or off the path. Here we report that depletion of KIFC1, a minus-end-directed kinesin called HSET in humans, causes neurons to migrate off their appropriate path, suggesting that this molecular motor is what ensures fidelity of the trajectory of migration. For these studies, we used rat migratory neurons
    MeSH term(s) Animals ; Cell Movement ; Cytoplasmic Dyneins/metabolism ; Kinesins/genetics ; Mice ; Microtubules/metabolism ; Neurons/physiology ; Rats ; beta Karyopherins
    Chemical Substances Kifc1 protein, rat ; beta Karyopherins ; Cytoplasmic Dyneins (EC 3.6.4.2) ; Kinesins (EC 3.6.4.4)
    Language English
    Publishing date 2022-01-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.1708-21.2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Human T-cell Leukemia Virus Type 1 and Strongyloides stercoralis: Partners in Pathogenesis

    Dykie, Adam / Wijesinghe, Tharaka / Rabson, Arnold B / Madugula, Kiran / Farinas, Christian / Wilson, Sydney / Abraham, David / Jain, Pooja

    Pathogens. 2020 Oct. 29, v. 9, no. 11

    2020  

    Abstract: Infection with human T-cell leukemia/lymphoma virus type 1 (HTLV-1) has been associated with various clinical syndromes including co-infection with Strongyloides stercoralis, which is an intestinal parasitic nematode and the leading cause of ... ...

    Abstract Infection with human T-cell leukemia/lymphoma virus type 1 (HTLV-1) has been associated with various clinical syndromes including co-infection with Strongyloides stercoralis, which is an intestinal parasitic nematode and the leading cause of strongyloidiasis in humans. Interestingly, HTLV-1 endemic areas coincide with regions citing high prevalence of S. stercoralis infection, making these communities optimal for elucidating the pathogenesis of co-infection and its clinical significance. HTLV-1 co-infection with S. stercoralis has been observed for decades in a number of published patient cases and case series; however, the implications of this co-infection remain elusive. Thus far, data suggest that S. stercoralis increases proviral load in patients co-infected with HTLV-1 compared to HTLV-1 infection alone. Furthermore, co-infection with HTLV-1 has been associated with shifting the immune response from Th2 to Th1, affecting the ability of the immune system to address the helminth infection. Thus, despite this well-known association, further research is required to fully elucidate the impact of each pathogen on disease manifestations in co-infected patients. This review provides an analytical view of studies that have evaluated the variation within HTLV-1 patients in susceptibility to S. stercoralis infection, as well as the effects of strongyloidiasis on HTLV-1 pathogenesis. Further, it provides a compilation of available clinical reports on the epidemiology and pathology of HTLV-1 with parasitic co-infection as well as data from mechanistic studies suggesting possible immunopathogenic mechanisms. Furthermore, specific areas of potential future research have been highlighted to facilitate advancing understanding of the complex interactions between these two pathogens.
    Keywords Strongyloides stercoralis ; T-lymphocytes ; epidemiology ; humans ; immune response ; intestines ; leukemia ; lymphoma ; mixed infection ; pathogenesis ; pathogens ; patients ; prevalence ; research ; strongyloidiasis ; viruses
    Language English
    Dates of publication 2020-1029
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    Note NAL-light
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens9110904
    Database NAL-Catalogue (AGRICOLA)

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  3. Article: Human T-cell Leukemia Virus Type 1 and

    Dykie, Adam / Wijesinghe, Tharaka / Rabson, Arnold B / Madugula, Kiran / Farinas, Christian / Wilson, Sydney / Abraham, David / Jain, Pooja

    Pathogens (Basel, Switzerland)

    2020  Volume 9, Issue 11

    Abstract: Infection with human T-cell leukemia/lymphoma virus type 1 (HTLV-1) has been associated with various clinical syndromes including co-infection ... ...

    Abstract Infection with human T-cell leukemia/lymphoma virus type 1 (HTLV-1) has been associated with various clinical syndromes including co-infection with
    Language English
    Publishing date 2020-10-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2695572-6
    ISSN 2076-0817
    ISSN 2076-0817
    DOI 10.3390/pathogens9110904
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: MEF-2 isoforms' (A-D) roles in development and tumorigenesis.

    Madugula, Kiran / Mulherkar, Ria / Khan, Zafar K / Chigbu, DeGaulle I / Patel, Dip / Harhaj, Edward W / Jain, Pooja

    Oncotarget

    2019  Volume 10, Issue 28, Page(s) 2755–2787

    Abstract: Myocyte enhancer factor (MEF)-2 plays a critical role in proliferation, differentiation, and development of various cell types in a tissue specific manner. Four isoforms of MEF-2 (A-D) differentially participate in controlling the cell fate during the ... ...

    Abstract Myocyte enhancer factor (MEF)-2 plays a critical role in proliferation, differentiation, and development of various cell types in a tissue specific manner. Four isoforms of MEF-2 (A-D) differentially participate in controlling the cell fate during the developmental phases of cardiac, muscle, vascular, immune and skeletal systems. Through their associations with various cellular factors MEF-2 isoforms can trigger alterations in complex protein networks and modulate various stages of cellular differentiation, proliferation, survival and apoptosis. The role of the MEF-2 family of transcription factors in the development has been investigated in various cell types, and the evolving alterations in this family of transcription factors have resulted in a diverse and wide spectrum of disease phenotypes, ranging from cancer to infection. This review provides a comprehensive account on MEF-2 isoforms (A-D) from their respective localization, signaling, role in development and tumorigenesis as well as their association with histone deacetylases (HDACs), which can be exploited for therapeutic intervention.
    Language English
    Publishing date 2019-04-12
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.26763
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Regulation of human T-cell leukemia virus type 1 antisense promoter by myocyte enhancer factor-2C in the context of adult T-cell leukemia and lymphoma.

    Madugula, Kiran K / Joseph, Julie / DeMarino, Catherine / Ginwala, Rashida / Teixeira, Vanessa / Khan, Zafar K / Sales, Dominic / Wilson, Sydney / Kashanchi, Fatah / Rushing, Amanda W / Lemasson, Isabelle / Harhaj, Edward W / Janakiram, Murali / Ye, B Hilda / Jain, Pooja

    Haematologica

    2022  Volume 107, Issue 12, Page(s) 2928–2943

    Abstract: Adult T-cell leukemia and lymphoma (ATLL) is an intractable T-cell neoplasia caused by a retrovirus, namely human T-cell leukemia virus type 1 (HTLV-1). Patients suffering from ATLL present a poor prognosis and have a dearth of treatment options. In ... ...

    Abstract Adult T-cell leukemia and lymphoma (ATLL) is an intractable T-cell neoplasia caused by a retrovirus, namely human T-cell leukemia virus type 1 (HTLV-1). Patients suffering from ATLL present a poor prognosis and have a dearth of treatment options. In contrast to the sporadic expression of viral transactivator protein Tax present at the 5' promoter region long terminal repeats (LTR), HTLV-1 bZIP gene (HBZ) is encoded by 3'LTR (the antisense promoter) and maintains its constant expression in ATLL cells and patients. The antisense promoter is associated with selective retroviral gene expression and has been an understudied phenomenon. Herein, we delineate the activity of transcription factor MEF (myocyte enhancer factor)-2 family members, which were found to be enriched at the 3'LTR and play an important role in the pathogenesis of ATLL. Of the four MEF isoforms (A to D), MEF-2A and 2C were highly overexpressed in a wide array of ATLL cell lines and in acute ATLL patients. The activity of MEF-2 isoforms were determined by knockdown experiments that led to decreased cell proliferation and regulated cell cycle progression. High enrichment of MEF-2C was observed at the 3'LTR along with cofactors Menin and JunD resulting in binding of MEF-2C to HBZ at this region. Chemical inhibition of MEF-2 proteins resulted in the cytotoxicity of ATLL cells in vitro and reduction of proviral load in a humanized mouse model. Taken together, this study provides a novel mechanism of 3'LTR regulation and establishes MEF-2 signaling a potential target for therapeutic intervention for ATLL.
    MeSH term(s) Animals ; Humans ; Mice ; Human T-lymphotropic virus 1/genetics ; Human T-lymphotropic virus 1/metabolism ; Leukemia-Lymphoma, Adult T-Cell/pathology ; Lymphoma/genetics ; MEF2 Transcription Factors/genetics ; MEF2 Transcription Factors/metabolism ; Promoter Regions, Genetic ; Viral Proteins/genetics ; Viral Proteins/metabolism
    Chemical Substances MEF2 Transcription Factors ; Viral Proteins
    Language English
    Publishing date 2022-12-01
    Publishing country Italy
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2021.279542
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.76: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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