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  1. Article ; Online: Prostate cancer immunotherapy: Improving clinical outcomes with a multi-pronged approach.

    Sridaran, Dhivya / Bradshaw, Elliot / DeSelm, Carl / Pachynski, Russell / Mahajan, Kiran / Mahajan, Nupam P

    Cell reports. Medicine

    2023  Volume 4, Issue 10, Page(s) 101199

    Abstract: Cancer immunotherapy has gained traction in recent years owing to remarkable tumor clearance in some patients. Despite the notable success of immune checkpoint blockade (ICB) in multiple malignancies, engagement of the immune system for targeted prostate ...

    Abstract Cancer immunotherapy has gained traction in recent years owing to remarkable tumor clearance in some patients. Despite the notable success of immune checkpoint blockade (ICB) in multiple malignancies, engagement of the immune system for targeted prostate cancer (PCa) therapy is still in its infancy. Multiple factors contribute to limited response, including the heterogeneity of PCa, the cold tumor microenvironment, and a low number of neoantigens. Significant effort is being invested in improving immune-based PCa therapies. This review is a summary of the status of immunotherapy in treating PCa, with a discussion of multiple immune modalities, including vaccines, adoptively transferred T cells, and bispecific T cell engagers, some of which are undergoing clinical trials. In addition, this review also focuses on emerging mechanism-based small-molecule tyrosine kinase inhibitors with immune modulatory properties that, either as single agents or in combination with other immunotherapies, have the potential to improve clinical outcomes.
    MeSH term(s) Male ; Humans ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/pathology ; Immunotherapy ; T-Lymphocytes/pathology ; Tumor Microenvironment
    Language English
    Publishing date 2023-09-21
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 2666-3791
    ISSN (online) 2666-3791
    DOI 10.1016/j.xcrm.2023.101199
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  2. Article ; Online: Prevention of mitochondrial genomic instability in yeast by the mitochondrial recombinase Mhr1.

    Ling, Feng / Bradshaw, Elliot / Yoshida, Minoru

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 5433

    Abstract: Mitochondrial (mt) DNA encodes factors essential for cellular respiration, therefore its level and integrity are crucial. ABF2 encodes a mitochondrial DNA-binding protein and its null mutation (Δabf2) induces mtDNA instability in Saccharomyces cerevisiae. ...

    Abstract Mitochondrial (mt) DNA encodes factors essential for cellular respiration, therefore its level and integrity are crucial. ABF2 encodes a mitochondrial DNA-binding protein and its null mutation (Δabf2) induces mtDNA instability in Saccharomyces cerevisiae. Mhr1 is a mitochondrial recombinase that mediates the predominant form of mtDNA replication and acts in mtDNA segregation and the repair of mtDNA double-stranded breaks (DSBs). However, the involvement of Mhr1 in prevention of mtDNA deletion mutagenesis is unknown. In this study we used Δabf2 mhr1-1 double-mutant cells, which lose mitochondrial function in media containing fermentable carbon sources, to investigate whether Mhr1 is a suppressor of mtDNA deletion mutagenesis. We used a suppresivity assay and Southern blot analysis to reveal that the Δabf2 mutation causes mtDNA deletions rather than an mtDNA-lacking (ρ
    MeSH term(s) Culture Media ; Fermentation ; Genome, Mitochondrial ; Genomic Instability ; Mutation ; Point Mutation ; Recombination, Genetic ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Culture Media ; MHR1 protein, S cerevisiae ; Saccharomyces cerevisiae Proteins ; Transcription Factors
    Language English
    Publishing date 2019-04-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-41699-9
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  3. Article ; Online: Regulation of Small Mitochondrial DNA Replicative Advantage by Ribonucleotide Reductase in

    Bradshaw, Elliot / Yoshida, Minoru / Ling, Feng

    G3 (Bethesda, Md.)

    2017  Volume 7, Issue 9, Page(s) 3083–3090

    Abstract: Small mitochondrial genomes can behave as selfish elements by displacing wild-type genomes regardless of their detriment to the host organism. In the budding ... ...

    Abstract Small mitochondrial genomes can behave as selfish elements by displacing wild-type genomes regardless of their detriment to the host organism. In the budding yeast
    MeSH term(s) DNA Replication ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; Gene Expression ; Gene Expression Regulation, Fungal ; Mutation ; Phenotype ; Ribonucleotide Reductases/genetics ; Ribonucleotide Reductases/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism
    Chemical Substances DNA, Mitochondrial ; SML1 protein, S cerevisiae ; Saccharomyces cerevisiae Proteins ; Ribonucleotide Reductases (EC 1.17.4.-) ; Rnr1 protein, S cerevisiae (EC 1.17.4.-)
    Language English
    Publishing date 2017--07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2629978-1
    ISSN 2160-1836 ; 2160-1836
    ISSN (online) 2160-1836
    ISSN 2160-1836
    DOI 10.1534/g3.117.043851
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Eukaryotic translation initiation factor 5A (eIF5A) is essential for HIF-1α activation in hypoxia.

    Tariq, Mohammad / Ito, Akihiro / Ishfaq, Muhammad / Bradshaw, Elliot / Yoshida, Minoru

    Biochemical and biophysical research communications

    2016  Volume 470, Issue 2, Page(s) 417–424

    Abstract: The eukaryotic initiation factor 5A (eIF5A) is an essential protein involved in translation elongation and cell proliferation. eIF5A undergoes several post-translational modifications including hypusination and acetylation. Hypusination is indispensable ... ...

    Abstract The eukaryotic initiation factor 5A (eIF5A) is an essential protein involved in translation elongation and cell proliferation. eIF5A undergoes several post-translational modifications including hypusination and acetylation. Hypusination is indispensable for the function of eIF5A. On the other hand, the precise function of acetylation remains unknown, but it may render the protein inactive since hypusination blocks acetylation. Here, we report that acetylation of eIF5A increases under hypoxia. During extended hypoxic periods an increase in the level of eIF5A acetylation correlated with a decrease in HIF-1α, suggesting involvement of eIF5A activity in HIF-1α expression under hypoxia. Indeed, suppression of eIF5A by siRNA oligo-mediated knockdown or treatment with GC7, a deoxyhypusine synthase inhibitor, led to significant reduction of HIF-1α activity. Furthermore, knockdown of eIF5A or GC7 treatment reduced tumor spheroid formation with a concomitant decrease in HIF-1α expression. Our results suggest that functional, hypusinated eIF5A is necessary for HIF-1α expression during hypoxia and that eIF5A is an attractive target for cancer therapy.
    MeSH term(s) Cell Hypoxia/physiology ; Cell Line, Tumor ; Cell Proliferation ; HeLa Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Oxygen/metabolism ; Peptide Initiation Factors/metabolism ; RNA-Binding Proteins/metabolism ; Spheroids, Cellular/metabolism ; Spheroids, Cellular/pathology ; Eukaryotic Translation Initiation Factor 5A
    Chemical Substances HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Peptide Initiation Factors ; RNA-Binding Proteins ; Oxygen (S88TT14065)
    Language English
    Publishing date 2016-01-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2016.01.024
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 116: Show issues Location:
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  5. Article ; Online: Identification of a T-bet

    Raju, Saravanan / Xia, Yu / Daniel, Bence / Yost, Kathryn E / Bradshaw, Elliot / Tonc, Elena / Verbaro, Daniel J / Kometani, Kohei / Yokoyama, Wayne M / Kurosaki, Tomohiro / Satpathy, Ansuman T / Egawa, Takeshi

    Journal of immunology (Baltimore, Md. : 1950)

    2021  Volume 206, Issue 12, Page(s) 2924–2936

    Abstract: Persistent Ag induces a dysfunctional CD8 T cell state known as "exhaustion" characterized by PD-1 expression. Nevertheless, exhausted CD8 T cells retain functionality through continued differentiation of progenitor into effector cells. However, it ... ...

    Abstract Persistent Ag induces a dysfunctional CD8 T cell state known as "exhaustion" characterized by PD-1 expression. Nevertheless, exhausted CD8 T cells retain functionality through continued differentiation of progenitor into effector cells. However, it remains ill-defined how CD8 T cell effector responses are sustained in situ. In this study, we show using the mouse chronic lymphocytic choriomeningitis virus infection model that CX3CR1
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes ; CX3C Chemokine Receptor 1/genetics ; Cell Differentiation ; Hepatitis A Virus Cellular Receptor 2 ; Lymphocytic Choriomeningitis ; Lymphocytic choriomeningitis virus ; Mice
    Chemical Substances CX3C Chemokine Receptor 1 ; Cx3cr1 protein, mouse ; Hepatitis A Virus Cellular Receptor 2
    Language English
    Publishing date 2021-06-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.2001348
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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.37: Show issues Location:
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    Zs.MG 28: Show issues

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  6. Article ; Online: Mitochondrial fission proteins Fis1 and Mdv1, but not Dnm1, play a role in maintenance of heteroplasmy in budding yeast.

    Bradshaw, Elliot / Yoshida, Minoru / Ling, Feng

    FEBS letters

    2012  Volume 586, Issue 8, Page(s) 1245–1251

    Abstract: In budding yeast, the mitochondrial DNA (mtDNA) replication pathway involving the homologous DNA pairing protein Mhr1 promotes mitochondrial allele segregation. Mitochondrial fusion facilitates the recombination-mediated replication pathway; however, the ...

    Abstract In budding yeast, the mitochondrial DNA (mtDNA) replication pathway involving the homologous DNA pairing protein Mhr1 promotes mitochondrial allele segregation. Mitochondrial fusion facilitates the recombination-mediated replication pathway; however, the role of fission remains largely unknown. By monitoring mitochondrial allele segregation during zygotic division, we found that the absence of fission proteins Fis1 or Mdv1, but not Dnm1, resulted in increased initial homoplasmy levels and decreased mtDNA copy number. However, decreases in mtDNA copy number alone were not sufficient for rapid establishment of homoplasmy, suggesting that inhibiting the activities of certain fission proteins promotes homoplasmy by reducing the number of mtDNA segregation units.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; DNA, Mitochondrial/metabolism ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Membrane Fusion/physiology ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; DNA, Mitochondrial ; FIS1 protein, S cerevisiae ; MDV1 protein, S cerevisiae ; Mitochondrial Proteins ; Saccharomyces cerevisiae Proteins ; GTP Phosphohydrolases (EC 3.6.1.-) ; DNM1 protein, S cerevisiae (EC 3.6.5.5)
    Language English
    Publishing date 2012-04-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2012.03.046
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    Zs.B 282: Show issues Location:
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  7. Article: Mitochondrial fission proteins Fis1 and Mdv1, but not Dnm1, play a role in maintenance of heteroplasmy in budding yeast

    Bradshaw, Elliot / Yoshida, Minoru / Ling, Feng

    FEBS letters. 2012 Apr. 24, v. 586, no. 8

    2012  

    Abstract: In budding yeast, the mitochondrial DNA (mtDNA) replication pathway involving the homologous DNA pairing protein Mhr1 promotes mitochondrial allele segregation. Mitochondrial fusion facilitates the recombination-mediated replication pathway; however, the ...

    Abstract In budding yeast, the mitochondrial DNA (mtDNA) replication pathway involving the homologous DNA pairing protein Mhr1 promotes mitochondrial allele segregation. Mitochondrial fusion facilitates the recombination-mediated replication pathway; however, the role of fission remains largely unknown. By monitoring mitochondrial allele segregation during zygotic division, we found that the absence of fission proteins Fis1 or Mdv1, but not Dnm1, resulted in increased initial homoplasmy levels and decreased mtDNA copy number. However, decreases in mtDNA copy number alone were not sufficient for rapid establishment of homoplasmy, suggesting that inhibiting the activities of certain fission proteins promotes homoplasmy by reducing the number of mtDNA segregation units.
    Keywords gene segregation ; mitochondrial DNA ; monitoring ; proteins ; yeasts
    Language English
    Dates of publication 2012-0424
    Size p. 1245-1251.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2012.03.046
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