Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes
Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hT...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Zhdanov, D. D. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Schlagwörter: |
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| Anmerkung: |
© Pleiades Publishing, Ltd. 2017 |
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| Übergeordnetes Werk: |
Enthalten in: Biochemistry (Moscow) - Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007, 11(2017), 3 vom: Juli, Seite 251-264 |
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| Übergeordnetes Werk: |
volume:11 ; year:2017 ; number:3 ; month:07 ; pages:251-264 |
| Links: |
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| DOI / URN: |
10.1134/S199075081703012X |
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| Katalog-ID: |
SPR022602224 |
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| 100 | 1 | |a Zhdanov, D. D. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes |
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| 520 | |a Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. These cells have phenotype of T lymphoblastic leukemic cells and are able to form tumors and cause death in experimental mice. | ||
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| 650 | 4 | |a telomerase |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a hTERT |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a alternative splicing |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a malignant transformation |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Vasina, D. A. |4 aut | |
| 700 | 1 | |a Orlova, E. V. |4 aut | |
| 700 | 1 | |a Orlova, V. S. |4 aut | |
| 700 | 1 | |a Pokrovsky, V. S. |4 aut | |
| 700 | 1 | |a Pokrovskaya, M. V. |4 aut | |
| 700 | 1 | |a Aleksandrova, S. S. |4 aut | |
| 700 | 1 | |a Sokolov, N. N. |4 aut | |
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10.1134/S199075081703012X doi (DE-627)SPR022602224 (SPR)S199075081703012X-e DE-627 ger DE-627 rakwb eng Zhdanov, D. D. verfasserin aut Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2017 Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. These cells have phenotype of T lymphoblastic leukemic cells and are able to form tumors and cause death in experimental mice. cisplatin (dpeaa)DE-He213 EndoG (dpeaa)DE-He213 telomerase (dpeaa)DE-He213 hTERT (dpeaa)DE-He213 alternative splicing (dpeaa)DE-He213 malignant transformation (dpeaa)DE-He213 Vasina, D. A. aut Orlova, E. V. aut Orlova, V. S. aut Pokrovsky, V. S. aut Pokrovskaya, M. V. aut Aleksandrova, S. S. aut Sokolov, N. N. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 11(2017), 3 vom: Juli, Seite 251-264 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:11 year:2017 number:3 month:07 pages:251-264 https://dx.doi.org/10.1134/S199075081703012X lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 11 2017 3 07 251-264 |
| spelling |
10.1134/S199075081703012X doi (DE-627)SPR022602224 (SPR)S199075081703012X-e DE-627 ger DE-627 rakwb eng Zhdanov, D. D. verfasserin aut Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2017 Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. These cells have phenotype of T lymphoblastic leukemic cells and are able to form tumors and cause death in experimental mice. cisplatin (dpeaa)DE-He213 EndoG (dpeaa)DE-He213 telomerase (dpeaa)DE-He213 hTERT (dpeaa)DE-He213 alternative splicing (dpeaa)DE-He213 malignant transformation (dpeaa)DE-He213 Vasina, D. A. aut Orlova, E. V. aut Orlova, V. S. aut Pokrovsky, V. S. aut Pokrovskaya, M. V. aut Aleksandrova, S. S. aut Sokolov, N. N. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 11(2017), 3 vom: Juli, Seite 251-264 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:11 year:2017 number:3 month:07 pages:251-264 https://dx.doi.org/10.1134/S199075081703012X lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 11 2017 3 07 251-264 |
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10.1134/S199075081703012X doi (DE-627)SPR022602224 (SPR)S199075081703012X-e DE-627 ger DE-627 rakwb eng Zhdanov, D. D. verfasserin aut Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2017 Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. These cells have phenotype of T lymphoblastic leukemic cells and are able to form tumors and cause death in experimental mice. cisplatin (dpeaa)DE-He213 EndoG (dpeaa)DE-He213 telomerase (dpeaa)DE-He213 hTERT (dpeaa)DE-He213 alternative splicing (dpeaa)DE-He213 malignant transformation (dpeaa)DE-He213 Vasina, D. A. aut Orlova, E. V. aut Orlova, V. S. aut Pokrovsky, V. S. aut Pokrovskaya, M. V. aut Aleksandrova, S. S. aut Sokolov, N. N. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 11(2017), 3 vom: Juli, Seite 251-264 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:11 year:2017 number:3 month:07 pages:251-264 https://dx.doi.org/10.1134/S199075081703012X lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 11 2017 3 07 251-264 |
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10.1134/S199075081703012X doi (DE-627)SPR022602224 (SPR)S199075081703012X-e DE-627 ger DE-627 rakwb eng Zhdanov, D. D. verfasserin aut Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2017 Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. These cells have phenotype of T lymphoblastic leukemic cells and are able to form tumors and cause death in experimental mice. cisplatin (dpeaa)DE-He213 EndoG (dpeaa)DE-He213 telomerase (dpeaa)DE-He213 hTERT (dpeaa)DE-He213 alternative splicing (dpeaa)DE-He213 malignant transformation (dpeaa)DE-He213 Vasina, D. A. aut Orlova, E. V. aut Orlova, V. S. aut Pokrovsky, V. S. aut Pokrovskaya, M. V. aut Aleksandrova, S. S. aut Sokolov, N. N. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 11(2017), 3 vom: Juli, Seite 251-264 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:11 year:2017 number:3 month:07 pages:251-264 https://dx.doi.org/10.1134/S199075081703012X lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 11 2017 3 07 251-264 |
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10.1134/S199075081703012X doi (DE-627)SPR022602224 (SPR)S199075081703012X-e DE-627 ger DE-627 rakwb eng Zhdanov, D. D. verfasserin aut Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2017 Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. These cells have phenotype of T lymphoblastic leukemic cells and are able to form tumors and cause death in experimental mice. cisplatin (dpeaa)DE-He213 EndoG (dpeaa)DE-He213 telomerase (dpeaa)DE-He213 hTERT (dpeaa)DE-He213 alternative splicing (dpeaa)DE-He213 malignant transformation (dpeaa)DE-He213 Vasina, D. A. aut Orlova, E. V. aut Orlova, V. S. aut Pokrovsky, V. S. aut Pokrovskaya, M. V. aut Aleksandrova, S. S. aut Sokolov, N. N. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 11(2017), 3 vom: Juli, Seite 251-264 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:11 year:2017 number:3 month:07 pages:251-264 https://dx.doi.org/10.1134/S199075081703012X lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 11 2017 3 07 251-264 |
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Zhdanov, D. D. @@aut@@ Vasina, D. A. @@aut@@ Orlova, E. V. @@aut@@ Orlova, V. S. @@aut@@ Pokrovsky, V. S. @@aut@@ Pokrovskaya, M. V. @@aut@@ Aleksandrova, S. S. @@aut@@ Sokolov, N. N. @@aut@@ |
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D.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Pleiades Publishing, Ltd. 2017</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. 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Zhdanov, D. D. |
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Zhdanov, D. D. misc cisplatin misc EndoG misc telomerase misc hTERT misc alternative splicing misc malignant transformation Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes |
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Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes cisplatin (dpeaa)DE-He213 EndoG (dpeaa)DE-He213 telomerase (dpeaa)DE-He213 hTERT (dpeaa)DE-He213 alternative splicing (dpeaa)DE-He213 malignant transformation (dpeaa)DE-He213 |
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misc cisplatin misc EndoG misc telomerase misc hTERT misc alternative splicing misc malignant transformation |
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Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes |
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Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes |
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Zhdanov, D. D. |
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Zhdanov, D. D. Vasina, D. A. Orlova, E. V. Orlova, V. S. Pokrovsky, V. S. Pokrovskaya, M. V. Aleksandrova, S. S. Sokolov, N. N. |
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Zhdanov, D. D. |
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cisplatin-induced apoptotic endonuclease endog inhibits telomerase activity and causes malignant transformation of human $ cd4^{+} $ t lymphocytes |
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Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes |
| abstract |
Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. These cells have phenotype of T lymphoblastic leukemic cells and are able to form tumors and cause death in experimental mice. © Pleiades Publishing, Ltd. 2017 |
| abstractGer |
Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. These cells have phenotype of T lymphoblastic leukemic cells and are able to form tumors and cause death in experimental mice. © Pleiades Publishing, Ltd. 2017 |
| abstract_unstemmed |
Abstract Alternative splicing of telomerase catalytic subunit hTERT pre-mRNA (human Telomerase Reverse Transcriptase) regulates telomerase activity. Increased expression of non-active splice variant hTERT results in inhibition of telomerase. Apoptotic endonuclease EndoG is known to participate in hTERT alternative splicing. Expression of EndoG can be induced in response to DNA damages. The aim of this study was to determine the ability of a DNA-damaging compound, cisplatin, to induce EndoG and its influence on alternative splicing of hTERT and telomerase activity in human $ CD4^{+} $ Т lymphocytes. Overexpression of EndoG in $ CD4^{+} $ T cells downregulated expression of the active full-length hTERT variant and upregulated its non-active spliced variant. Reduction of full-length hTERT caused downregulation of telomerase activity, shortening of telomeres length during cell divisions, converting cells to the replicative senescence state, activation of apoptosis and finally cell death. Few cells survived and underwent malignant transformation. Transformed cells have increased telomerase activity and proliferative potential compare to initial $ CD4^{+} $ T cells. These cells have phenotype of T lymphoblastic leukemic cells and are able to form tumors and cause death in experimental mice. © Pleiades Publishing, Ltd. 2017 |
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Cisplatin-induced apoptotic endonuclease EndoG inhibits telomerase activity and causes malignant transformation of human $ CD4^{+} $ T lymphocytes |
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https://dx.doi.org/10.1134/S199075081703012X |
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Vasina, D. A. Orlova, E. V. Orlova, V. S. Pokrovsky, V. S. Pokrovskaya, M. V. Aleksandrova, S. S. Sokolov, N. N. |
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Vasina, D. A. Orlova, E. V. Orlova, V. S. Pokrovsky, V. S. Pokrovskaya, M. V. Aleksandrova, S. S. Sokolov, N. N. |
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2024-07-03T13:57:21.298Z |
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| score |
7.399349 |