Ctenopharyngodon idella PKZ facilitates cell apoptosis through phosphorylating eIF2α
• PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK ce...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wu, Chuxin [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
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| Schlagwörter: |
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| Umfang: |
11 |
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| Übergeordnetes Werk: |
Enthalten in: Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls - Gayda, Mathieu ELSEVIER, 2015, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:69 ; year:2016 ; pages:13-23 ; extent:11 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.molimm.2015.11.006 |
|---|
| Katalog-ID: |
ELV035049359 |
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| 245 | 1 | 0 | |a Ctenopharyngodon idella PKZ facilitates cell apoptosis through phosphorylating eIF2α |
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| 520 | |a • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. | ||
| 520 | |a • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. | ||
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| 650 | 7 | |a Phosphorylation |2 Elsevier | |
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| 650 | 7 | |a Apoptosis |2 Elsevier | |
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| 700 | 1 | |a Fan, Lihua |4 oth | |
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10.1016/j.molimm.2015.11.006 doi GBVA2016003000011.pica (DE-627)ELV035049359 (ELSEVIER)S0161-5890(15)30116-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Wu, Chuxin verfasserin aut Ctenopharyngodon idella PKZ facilitates cell apoptosis through phosphorylating eIF2α 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. eIF2α Elsevier Phosphorylation Elsevier PKR Elsevier PKZ Elsevier Apoptosis Elsevier Hu, Yousheng oth Fan, Lihua oth Wang, Haizhou oth Sun, Zhicheng oth Deng, Shoulong oth Liu, Yong oth Hu, Chengyu oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:69 year:2016 pages:13-23 extent:11 https://doi.org/10.1016/j.molimm.2015.11.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 69 2016 13-23 11 045F 570 |
| spelling |
10.1016/j.molimm.2015.11.006 doi GBVA2016003000011.pica (DE-627)ELV035049359 (ELSEVIER)S0161-5890(15)30116-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Wu, Chuxin verfasserin aut Ctenopharyngodon idella PKZ facilitates cell apoptosis through phosphorylating eIF2α 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. eIF2α Elsevier Phosphorylation Elsevier PKR Elsevier PKZ Elsevier Apoptosis Elsevier Hu, Yousheng oth Fan, Lihua oth Wang, Haizhou oth Sun, Zhicheng oth Deng, Shoulong oth Liu, Yong oth Hu, Chengyu oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:69 year:2016 pages:13-23 extent:11 https://doi.org/10.1016/j.molimm.2015.11.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 69 2016 13-23 11 045F 570 |
| allfields_unstemmed |
10.1016/j.molimm.2015.11.006 doi GBVA2016003000011.pica (DE-627)ELV035049359 (ELSEVIER)S0161-5890(15)30116-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Wu, Chuxin verfasserin aut Ctenopharyngodon idella PKZ facilitates cell apoptosis through phosphorylating eIF2α 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. eIF2α Elsevier Phosphorylation Elsevier PKR Elsevier PKZ Elsevier Apoptosis Elsevier Hu, Yousheng oth Fan, Lihua oth Wang, Haizhou oth Sun, Zhicheng oth Deng, Shoulong oth Liu, Yong oth Hu, Chengyu oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:69 year:2016 pages:13-23 extent:11 https://doi.org/10.1016/j.molimm.2015.11.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 69 2016 13-23 11 045F 570 |
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10.1016/j.molimm.2015.11.006 doi GBVA2016003000011.pica (DE-627)ELV035049359 (ELSEVIER)S0161-5890(15)30116-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Wu, Chuxin verfasserin aut Ctenopharyngodon idella PKZ facilitates cell apoptosis through phosphorylating eIF2α 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. eIF2α Elsevier Phosphorylation Elsevier PKR Elsevier PKZ Elsevier Apoptosis Elsevier Hu, Yousheng oth Fan, Lihua oth Wang, Haizhou oth Sun, Zhicheng oth Deng, Shoulong oth Liu, Yong oth Hu, Chengyu oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:69 year:2016 pages:13-23 extent:11 https://doi.org/10.1016/j.molimm.2015.11.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 69 2016 13-23 11 045F 570 |
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10.1016/j.molimm.2015.11.006 doi GBVA2016003000011.pica (DE-627)ELV035049359 (ELSEVIER)S0161-5890(15)30116-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 630 640 610 VZ Wu, Chuxin verfasserin aut Ctenopharyngodon idella PKZ facilitates cell apoptosis through phosphorylating eIF2α 2016transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. • PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. eIF2α Elsevier Phosphorylation Elsevier PKR Elsevier PKZ Elsevier Apoptosis Elsevier Hu, Yousheng oth Fan, Lihua oth Wang, Haizhou oth Sun, Zhicheng oth Deng, Shoulong oth Liu, Yong oth Hu, Chengyu oth Enthalten in Elsevier Gayda, Mathieu ELSEVIER Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls 2015 Amsterdam [u.a.] (DE-627)ELV012849286 volume:69 year:2016 pages:13-23 extent:11 https://doi.org/10.1016/j.molimm.2015.11.006 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_40 GBV_ILN_227 GBV_ILN_674 AR 69 2016 13-23 11 045F 570 |
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Enthalten in Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls Amsterdam [u.a.] volume:69 year:2016 pages:13-23 extent:11 |
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Letter regarding the article: Changes in BNP and cardiac troponin I after high-intensity interval and endurance exercise in heart failure patients and healthy controls |
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ctenopharyngodon idella pkz facilitates cell apoptosis through phosphorylating eif2α |
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Ctenopharyngodon idella PKZ facilitates cell apoptosis through phosphorylating eIF2α |
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• PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. |
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• PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. |
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• PKZ and PKR were up-regulated by poly I:C in a time-dependent manner. • Both PKZ and Caspase-3 mRNA came with a high degree of consistency in CIK cells either after treatment with poly I:C or transfection with siRNA against PKZ gene. • Overexpression of wild type PKZ but not mutant K198R in CIK cells resulted in higher apoptotic rate and a significantly reduced viability rate. • Overexpression of wild type eIF2α induced apoptosis, whereas phosphodeficient eIF2α (S51A) blocked induction of apoptosis. • Mutant of eIF2α (S51A) would block the induction of apoptosis and PKZ could elicit apoptosis via phosphorylating eIF2α at Ser51 excluding the effects of endogenous PKZ/PKR largely. |
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