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  1. Article ; Online: Oncolytic Activity of the Vaccine Strain of Type 3 Poliovirus on the Model of Rat Glioma C6 Cells.

    Sosnovtseva, A O / Zheltukhin, A O / Lipatova, A V / Chumakov, P M / Chekhonin, V P

    Bulletin of experimental biology and medicine

    2019  Volume 167, Issue 1, Page(s) 111–115

    Abstract: Rat glioma cell line C6 expressing human poliovirus receptor (PVR) and susceptible to polioviruses (C6-PVR-BFP) was used to produce a clone with knockout of IFNα/β (Ifnar1) receptor subunit 1 gene (Ifnar1). The sensitivity of C6-PVR-BFP cells to the ... ...

    Abstract Rat glioma cell line C6 expressing human poliovirus receptor (PVR) and susceptible to polioviruses (C6-PVR-BFP) was used to produce a clone with knockout of IFNα/β (Ifnar1) receptor subunit 1 gene (Ifnar1). The sensitivity of C6-PVR-BFP cells to the vaccine strain of poliovirus type 3 (PV3) depended on the signaling pathways of the cell response to type 1 IFN. Using the model of subcutaneous tumor xenografts, we demonstrated oncolytic activity of PV3 against C6-PVR-BFP cells that depended on the expression of PVR and increased considerably upon disturbances in IFN response pathways.
    MeSH term(s) Animals ; Cell Line, Tumor ; Glioma/metabolism ; Glioma/therapy ; Glioma/virology ; Interferon-alpha/genetics ; Interferon-beta/genetics ; Mice ; Oncolytic Virotherapy/methods ; Oncolytic Viruses/physiology ; Poliovirus/physiology ; Rats ; Rats, Mutant Strains ; Receptor, Interferon alpha-beta/genetics ; Receptor, Interferon alpha-beta/metabolism
    Chemical Substances Interferon-alpha ; Receptor, Interferon alpha-beta (156986-95-7) ; Interferon-beta (77238-31-4)
    Language English
    Publishing date 2019-06-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 390407-6
    ISSN 1573-8221 ; 0007-4888 ; 0365-9615
    ISSN (online) 1573-8221
    ISSN 0007-4888 ; 0365-9615
    DOI 10.1007/s10517-019-04472-6
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    In stock of ZB MED Cologne/Königswinter

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  2. Article: O nekotorykh patogeneticheskikh mekhanizmakh dizenterii cheloveka

    Survillo, O N / Pavel'eva, N I / Zheltukhin, P A / Nepyshnevskaia, V V / Shelkovskaia, G A

    Arkhiv patologii

    1974  Volume 36, Issue 5, Page(s) 63–67

    Title translation Some pathogenetic mechanisms of human dysentery.
    MeSH term(s) Acid Phosphatase ; Autolysis ; Cell Nucleus ; Dysentery, Bacillary/etiology ; Dysentery, Bacillary/pathology ; Enterochromaffin Cells ; Erythrocytes ; Humans ; Intestinal Mucosa/pathology ; Jejunum/pathology ; Lymphocytes ; Macrophages ; Mast Cells ; Phagocytosis ; Plasma Cells
    Chemical Substances Acid Phosphatase (EC 3.1.3.2)
    Language Russian
    Publishing date 1974
    Publishing country Russia (Federation)
    Document type English Abstract ; Journal Article
    ZDB-ID 127285-8
    ISSN 0004-1955
    ISSN 0004-1955
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  3. Article ; Online: Constitutive and induced functions of the p53 gene.

    Zheltukhin, A O / Chumakov, P M

    Biochemistry. Biokhimiia

    2011  Volume 75, Issue 13, Page(s) 1692–1721

    Abstract: The p53 tumor suppressor serves to secure genetic stability of multicellular organisms. It suppresses the accumulation of mutations in somatic cells and substantially decreases the probability of malignant diseases. The p53 gene acts highly selectively ... ...

    Abstract The p53 tumor suppressor serves to secure genetic stability of multicellular organisms. It suppresses the accumulation of mutations in somatic cells and substantially decreases the probability of malignant diseases. The p53 gene acts highly selectively through multiple mechanisms. Under relatively favorable conditions, p53 helps to maintain intracellular homeostasis by balancing anabolic and catabolic processes and by timely elimination of reactive oxygen species. These functions of p53 facilitate maximal efficiency and survival of cells under conditions of physiological stresses. In the case of grave molecular damage caused by severe stress, a significant amount of highly active p53 is induced leading to irreversible growth arrest and programmed cell death. The induced functions of p53 secure the timely elimination from the organism of damaged and potentially dangerous cells. Collectively, the functions of p53 contribute to the prevention of malignant and other diseases and decelerate the aging process.
    MeSH term(s) Animals ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2011-03-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/s0006297910130110
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  4. Article ; Online: Mitochondrial localization of SESN2.

    Kovaleva, Irina E / Tokarchuk, Artem V / Zheltukhin, Andrei O / Dalina, Alexandra A / Safronov, Grigoriy G / Evstafieva, Alexandra G / Lyamzaev, Konstantin G / Chumakov, Peter M / Budanov, Andrei V

    PloS one

    2020  Volume 15, Issue 4, Page(s) e0226862

    Abstract: SESN2 is a member of the evolutionarily conserved sestrin protein family found in most of the Metazoa species. The SESN2 gene is transcriptionally activated by many stress factors, including metabolic derangements, reactive oxygen species (ROS), and DNA- ... ...

    Abstract SESN2 is a member of the evolutionarily conserved sestrin protein family found in most of the Metazoa species. The SESN2 gene is transcriptionally activated by many stress factors, including metabolic derangements, reactive oxygen species (ROS), and DNA-damage. As a result, SESN2 controls ROS accumulation, metabolism, and cell viability. The best-known function of SESN2 is the inhibition of the mechanistic target of rapamycin complex 1 kinase (mTORC1) that plays a central role in support of cell growth and suppression of autophagy. SESN2 inhibits mTORC1 activity through interaction with the GATOR2 protein complex preventing an inhibitory effect of GATOR2 on the GATOR1 protein complex. GATOR1 stimulates GTPase activity of the RagA/B small GTPase, the component of RagA/B:RagC/D complex, preventing mTORC1 translocation to the lysosomes and its activation by the small GTPase Rheb. Despite the well-established role of SESN2 in mTORC1 inhibition, other SESN2 activities are not well-characterized. We recently showed that SESN2 could control mitochondrial function and cell death via mTORC1-independent mechanisms, and these activities might be explained by direct effects of SESN2 on mitochondria. In this work, we examined mitochondrial localization of SESN2 and demonstrated that SESN2 is located on mitochondria and can be directly involved in the regulation of mitochondrial functions.
    MeSH term(s) A549 Cells ; Animals ; Caenorhabditis elegans/cytology ; Caenorhabditis elegans/metabolism ; Cell Fractionation ; Cell Respiration ; Cytosol/metabolism ; Humans ; Mitochondria/metabolism ; Nuclear Proteins/metabolism ; Reactive Oxygen Species
    Chemical Substances Nuclear Proteins ; Reactive Oxygen Species ; SESN2 protein, human
    Language English
    Publishing date 2020-04-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0226862
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  5. Article: Treatment of cancer cells with chemotherapeutic drugs results in profound changes in expression of genes encoding aldehyde-metabolizing enzymes.

    Zinovieva, Olga L / Grineva, Evgeniya N / Krasnov, George S / Karpov, Dmitry S / Zheltukhin, Andrei O / Snezhkina, Anastasiya V / Kudryavtseva, Anna V / Mashkova, Tamara D / Lisitsyn, Nikolai A

    Journal of Cancer

    2019  Volume 10, Issue 18, Page(s) 4256–4263

    Abstract: Using RNA-seq, RT-qPCR, and bioinformatics we have studied the influence of a wide spectrum of chemotherapeutic drugs on transcription ... ...

    Abstract Using RNA-seq, RT-qPCR, and bioinformatics we have studied the influence of a wide spectrum of chemotherapeutic drugs on transcription of
    Language English
    Publishing date 2019-07-10
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2573318-7
    ISSN 1837-9664
    ISSN 1837-9664
    DOI 10.7150/jca.32608
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  6. Article: Constitutive and induced functions of the p53 gene

    Zheltukhin, A. O / Chumakov, P. M

    Biochemistry. 2010 Dec., v. 75, no. 13

    2010  

    Abstract: The p53 tumor suppressor serves to secure genetic stability of multicellular organisms. It suppresses the accumulation of mutations in somatic cells and substantially decreases the probability of malignant diseases. The p53 gene acts highly selectively ... ...

    Abstract The p53 tumor suppressor serves to secure genetic stability of multicellular organisms. It suppresses the accumulation of mutations in somatic cells and substantially decreases the probability of malignant diseases. The p53 gene acts highly selectively through multiple mechanisms. Under relatively favorable conditions, p53 helps to maintain intracellular homeostasis by balancing anabolic and catabolic processes and by timely elimination of reactive oxygen species. These functions of p53 facilitate maximal efficiency and survival of cells under conditions of physiological stresses. In the case of grave molecular damage caused by severe stress, a significant amount of highly active p53 is induced leading to irreversible growth arrest and programmed cell death. The induced functions of p53 secure the timely elimination from the organism of damaged and potentially dangerous cells. Collectively, the functions of p53 contribute to the prevention of malignant and other diseases and decelerate the aging process.
    Language English
    Dates of publication 2010-12
    Size p. 1692-1721.
    Publisher SP MAIK Nauka/Interperiodica
    Publishing place Dordrecht
    Document type Article
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297910130110
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  7. Article ; Online: LINC00973 Induces Proliferation Arrest of Drug-Treated Cancer Cells by Preventing p21 Degradation.

    Karpov, Dmitry S / Spirin, Pavel V / Zheltukhin, Andrey O / Tutyaeva, Vera V / Zinovieva, Olga L / Grineva, Evgenia N / Matrosova, Vera A / Krasnov, George S / Snezhkina, Anastasiya V / Kudryavtseva, Anna V / Prassolov, Vladimir S / Mashkova, Tamara D / Lisitsyn, Nikolai A

    International journal of molecular sciences

    2020  Volume 21, Issue 21

    Abstract: Overcoming drug resistance of cancer cells is the major challenge in molecular oncology. Here, we demonstrate that long non-coding RNA LINC00973 is up-regulated in normal and cancer cells of different origins upon treatment with different ... ...

    Abstract Overcoming drug resistance of cancer cells is the major challenge in molecular oncology. Here, we demonstrate that long non-coding RNA LINC00973 is up-regulated in normal and cancer cells of different origins upon treatment with different chemotherapeutics. Bioinformatics analysis shows that this is a consequence of DNA damage response pathway activation or mitotic arrest. Knockdown of
    MeSH term(s) Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Drug Resistance, Neoplasm/genetics ; HCT116 Cells ; Humans ; Neoplasms/genetics ; RNA, Long Noncoding/genetics ; Signal Transduction/drug effects ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Antineoplastic Agents ; Cyclin-Dependent Kinase Inhibitor p21 ; RNA, Long Noncoding ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2020-11-06
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21218322
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  8. Article ; Online: Mitochondrial localization of SESN2.

    Irina E Kovaleva / Artem V Tokarchuk / Andrei O Zheltukhin / Alexandra A Dalina / Grigoriy G Safronov / Alexandra G Evstafieva / Konstantin G Lyamzaev / Peter M Chumakov / Andrei V Budanov

    PLoS ONE, Vol 15, Iss 4, p e

    2020  Volume 0226862

    Abstract: SESN2 is a member of the evolutionarily conserved sestrin protein family found in most of the Metazoa species. The SESN2 gene is transcriptionally activated by many stress factors, including metabolic derangements, reactive oxygen species (ROS), and DNA- ... ...

    Abstract SESN2 is a member of the evolutionarily conserved sestrin protein family found in most of the Metazoa species. The SESN2 gene is transcriptionally activated by many stress factors, including metabolic derangements, reactive oxygen species (ROS), and DNA-damage. As a result, SESN2 controls ROS accumulation, metabolism, and cell viability. The best-known function of SESN2 is the inhibition of the mechanistic target of rapamycin complex 1 kinase (mTORC1) that plays a central role in support of cell growth and suppression of autophagy. SESN2 inhibits mTORC1 activity through interaction with the GATOR2 protein complex preventing an inhibitory effect of GATOR2 on the GATOR1 protein complex. GATOR1 stimulates GTPase activity of the RagA/B small GTPase, the component of RagA/B:RagC/D complex, preventing mTORC1 translocation to the lysosomes and its activation by the small GTPase Rheb. Despite the well-established role of SESN2 in mTORC1 inhibition, other SESN2 activities are not well-characterized. We recently showed that SESN2 could control mitochondrial function and cell death via mTORC1-independent mechanisms, and these activities might be explained by direct effects of SESN2 on mitochondria. In this work, we examined mitochondrial localization of SESN2 and demonstrated that SESN2 is located on mitochondria and can be directly involved in the regulation of mitochondrial functions.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2020-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Expression of long non-coding RNA LINC00973 is consistently increased upon treatment of colon cancer cells with different chemotherapeutic drugs.

    Zinovieva, Olga L / Grineva, Evgenia N / Prokofjeva, Maria M / Karpov, Dmitry S / Zheltukhin, Andrei O / Krasnov, George S / Snezhkina, Anastasiya V / Kudryavtseva, Anna V / Chumakov, Peter M / Mashkova, Tamara D / Prassolov, Vladimir S / Lisitsyn, Nikolai A

    Biochimie

    2018  Volume 151, Page(s) 67–72

    Abstract: Early prediction of tumor relapse depends on the identification of new prognostic cancer biomarkers, which are suitable for monitoring tumor response to different chemotherapeutic drugs. Using RNA-Seq, RT-qPCR, bioinformatics, and studies utilizing the ... ...

    Abstract Early prediction of tumor relapse depends on the identification of new prognostic cancer biomarkers, which are suitable for monitoring tumor response to different chemotherapeutic drugs. Using RNA-Seq, RT-qPCR, bioinformatics, and studies utilizing the murine tumor xenograft model, we have found significant and consistent changes in the abundance of five lincRNAs (LINC00973, LINC00941, CASC19, CCAT1, and BCAR4) upon treatment of both HT-29 and HCT-116 cells with 5-fluorouracil, oxaliplatin, and irinotecan at different doses and durations; both in vitro and in vivo. The most frequent changes were detected for LINC00973, whose content is most strongly and consistently increased upon treatment of both colon cancer cell lines with all three chemotherapeutic drugs. Additional studies are required in order to determine the molecular mechanisms by which anticancer drugs affect LINC00973 expression and to define the consequences of its upregulation on drug resistance of cancer cells.
    MeSH term(s) Animals ; Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor ; Colonic Neoplasms/drug therapy ; HCT116 Cells ; HT29 Cells ; Humans ; Mice ; RNA, Long Noncoding/genetics ; Transcription, Genetic/drug effects ; Xenograft Model Antitumor Assays
    Chemical Substances Antineoplastic Agents ; Biomarkers, Tumor ; RNA, Long Noncoding
    Language English
    Publishing date 2018-06-02
    Publishing country France
    Document type Journal Article
    ZDB-ID 120345-9
    ISSN 1638-6183 ; 0300-9084
    ISSN (online) 1638-6183
    ISSN 0300-9084
    DOI 10.1016/j.biochi.2018.05.021
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  10. Article: O VOZRASTNO I STRUKTURE ZABOLEVAEMOSTI PRI VIRUSNOM GEPATITE (BOLEZN' BOTKINA)

    KARIMOV, Z K / NOGOVITSINA, P S / ZHELTUKHIN, E N

    Zhurnal mikrobiologii, epidemiologii i immunobiologii

    1963  Volume 40, Page(s) 136–139

    Title translation ON THE AGE STRUCTURE OF PATIENTS WITH VIRAL HEPATITIS (BOTKIN'S DISEASE).
    MeSH term(s) Aging ; Chlamydia Infections ; Communicable Diseases ; Hepatitis ; Hepatitis A ; Humans
    Language Russian
    Publishing date 1963-04
    Publishing country Russia (Federation)
    Document type Journal Article
    ZDB-ID 218354-7
    ISSN 0372-9311 ; 0049-8726 ; 0372-8714
    ISSN 0372-9311 ; 0049-8726 ; 0372-8714
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