eIF6 anti-association activity is required for ribosome biogenesis, translational control and tumor progression
Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence show...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Brina, Daniela [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Umfang: |
6 |
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| Übergeordnetes Werk: |
Enthalten in: Homogeneous coating of ionomer on electrocatalyst assisted by polybenzimidazole as an adhesive layer and its effect on fuel cell performance - Yang, Zehui ELSEVIER, 2015transfer abstract, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:1849 ; year:2015 ; number:7 ; pages:830-835 ; extent:6 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.bbagrm.2014.09.010 |
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ELV039764737 |
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| 520 | |a Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. | ||
| 520 | |a Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. | ||
| 700 | 1 | |a Miluzio, Annarita |4 oth | |
| 700 | 1 | |a Ricciardi, Sara |4 oth | |
| 700 | 1 | |a Biffo, Stefano |4 oth | |
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10.1016/j.bbagrm.2014.09.010 doi GBVA2015011000007.pica (DE-627)ELV039764737 (ELSEVIER)S1874-9399(14)00252-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 690 VZ 50.92 bkl Brina, Daniela verfasserin aut eIF6 anti-association activity is required for ribosome biogenesis, translational control and tumor progression 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Miluzio, Annarita oth Ricciardi, Sara oth Biffo, Stefano oth Enthalten in Elsevier Yang, Zehui ELSEVIER Homogeneous coating of ionomer on electrocatalyst assisted by polybenzimidazole as an adhesive layer and its effect on fuel cell performance 2015transfer abstract Amsterdam [u.a.] (DE-627)ELV01314085X volume:1849 year:2015 number:7 pages:830-835 extent:6 https://doi.org/10.1016/j.bbagrm.2014.09.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_40 50.92 Meerestechnik VZ AR 1849 2015 7 830-835 6 045F 570 |
| spelling |
10.1016/j.bbagrm.2014.09.010 doi GBVA2015011000007.pica (DE-627)ELV039764737 (ELSEVIER)S1874-9399(14)00252-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 690 VZ 50.92 bkl Brina, Daniela verfasserin aut eIF6 anti-association activity is required for ribosome biogenesis, translational control and tumor progression 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Miluzio, Annarita oth Ricciardi, Sara oth Biffo, Stefano oth Enthalten in Elsevier Yang, Zehui ELSEVIER Homogeneous coating of ionomer on electrocatalyst assisted by polybenzimidazole as an adhesive layer and its effect on fuel cell performance 2015transfer abstract Amsterdam [u.a.] (DE-627)ELV01314085X volume:1849 year:2015 number:7 pages:830-835 extent:6 https://doi.org/10.1016/j.bbagrm.2014.09.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_40 50.92 Meerestechnik VZ AR 1849 2015 7 830-835 6 045F 570 |
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10.1016/j.bbagrm.2014.09.010 doi GBVA2015011000007.pica (DE-627)ELV039764737 (ELSEVIER)S1874-9399(14)00252-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 690 VZ 50.92 bkl Brina, Daniela verfasserin aut eIF6 anti-association activity is required for ribosome biogenesis, translational control and tumor progression 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Miluzio, Annarita oth Ricciardi, Sara oth Biffo, Stefano oth Enthalten in Elsevier Yang, Zehui ELSEVIER Homogeneous coating of ionomer on electrocatalyst assisted by polybenzimidazole as an adhesive layer and its effect on fuel cell performance 2015transfer abstract Amsterdam [u.a.] (DE-627)ELV01314085X volume:1849 year:2015 number:7 pages:830-835 extent:6 https://doi.org/10.1016/j.bbagrm.2014.09.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_40 50.92 Meerestechnik VZ AR 1849 2015 7 830-835 6 045F 570 |
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10.1016/j.bbagrm.2014.09.010 doi GBVA2015011000007.pica (DE-627)ELV039764737 (ELSEVIER)S1874-9399(14)00252-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 690 VZ 50.92 bkl Brina, Daniela verfasserin aut eIF6 anti-association activity is required for ribosome biogenesis, translational control and tumor progression 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Miluzio, Annarita oth Ricciardi, Sara oth Biffo, Stefano oth Enthalten in Elsevier Yang, Zehui ELSEVIER Homogeneous coating of ionomer on electrocatalyst assisted by polybenzimidazole as an adhesive layer and its effect on fuel cell performance 2015transfer abstract Amsterdam [u.a.] (DE-627)ELV01314085X volume:1849 year:2015 number:7 pages:830-835 extent:6 https://doi.org/10.1016/j.bbagrm.2014.09.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_40 50.92 Meerestechnik VZ AR 1849 2015 7 830-835 6 045F 570 |
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10.1016/j.bbagrm.2014.09.010 doi GBVA2015011000007.pica (DE-627)ELV039764737 (ELSEVIER)S1874-9399(14)00252-1 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 690 VZ 50.92 bkl Brina, Daniela verfasserin aut eIF6 anti-association activity is required for ribosome biogenesis, translational control and tumor progression 2015transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. Miluzio, Annarita oth Ricciardi, Sara oth Biffo, Stefano oth Enthalten in Elsevier Yang, Zehui ELSEVIER Homogeneous coating of ionomer on electrocatalyst assisted by polybenzimidazole as an adhesive layer and its effect on fuel cell performance 2015transfer abstract Amsterdam [u.a.] (DE-627)ELV01314085X volume:1849 year:2015 number:7 pages:830-835 extent:6 https://doi.org/10.1016/j.bbagrm.2014.09.010 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_40 50.92 Meerestechnik VZ AR 1849 2015 7 830-835 6 045F 570 |
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Enthalten in Homogeneous coating of ionomer on electrocatalyst assisted by polybenzimidazole as an adhesive layer and its effect on fuel cell performance Amsterdam [u.a.] volume:1849 year:2015 number:7 pages:830-835 extent:6 |
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Enthalten in Homogeneous coating of ionomer on electrocatalyst assisted by polybenzimidazole as an adhesive layer and its effect on fuel cell performance Amsterdam [u.a.] volume:1849 year:2015 number:7 pages:830-835 extent:6 |
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Homogeneous coating of ionomer on electrocatalyst assisted by polybenzimidazole as an adhesive layer and its effect on fuel cell performance |
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eIF6 anti-association activity is required for ribosome biogenesis, translational control and tumor progression |
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Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. |
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Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. |
| abstract_unstemmed |
Here we discuss the function of eukaryotic initiation factor 6 (eIF6; Tif6 in yeast). eIF6 binds 60S ribosomal subunits and blocks their joining to 40S. In this context, we propose that eIF6 impedes unproductive 80S formation, namely, the formation of 80S subunits without mRNA. Genetic evidence shows that eIF6 has a dual function: in yeast and mammals, nucleolar eIF6 is necessary for the biogenesis of 60S subunits. In mammals, cytoplasmic eIF6 is required for insulin and growth factor-stimulated translation. In contrast to other translation factors, eIF6 activity is not under mTOR control. The physiological significance of eIF6 impacts on cancer and on inherited Shwachman–Bodian–Diamond syndrome. eIF6 is overexpressed in specific human tumors. In a murine model of lymphomagenesis, eIF6 depletion leads to a striking increase of survival, without adverse effects. Shwachman–Bodian–Diamond syndrome is caused by loss of function of SBDS protein. In yeast, point mutations of Tif6, the yeast homolog of eIF6, rescue the quasi-lethal effect due to the loss of the SBDS homolog, Sdo1. We propose that eIF6 is a node regulator of ribosomal function and predict that prioritizing its pharmacological targeting will be of benefit in cancer and Shwachman–Bodian–Diamond syndrome. This article is part of a Special Issue entitled: Translation and Cancer. |
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