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Mea6 controls VLDL transport through the coordinated regulation of COPII assembly
Yaqing Wang,Liang Liu,Hongsheng Zhang,Junwan Fan,Feng Zhang,Mei Yu,Lei Shi,Lin Yang,Sin Man Lam,Huimin Wang,Xiaowei Chen,Yingchun Wang,Fei Gao,Guanghou Shui and Zhiheng Xu
Cell Research
Abstract
Lipid accumulation, which may be caused by the disturbance in very low density lipoprotein (VLDL) secretion in the liver, can lead to fatty liver disease. VLDL is synthesized in endoplasmic reticulum (ER) and transported to Golgi apparatus for secretion into plasma. However, the underlying molecular mechanism for VLDL transport is still poorly understood. Here we show that hepatocyte-specific deletion ofmeningioma-expressed antigen 6 (Mea6)/cutaneous T cell lymphoma-associated antigen 5C (cTAGE5C) leads to severe fatty liver and hypolipemia in mice. Quantitative lipidomic and proteomic analyses indicate that Mea6/cTAGE5 deletion impairs the secretion of different types of lipids and proteins, including VLDL, from the liver. Moreover, we demonstrate that Mea6/cTAGE5 interacts with components of the ER coat protein complex II (COPII) which, when depleted, also cause lipid accumulation in hepatocytes. Our findings not only reveal several novel factors that regulate lipid transport, but also provide evidence that Mea6 plays a critical role in lipid transportation through the coordinated regulation of the COPII machinery. Keywords: Mea6; fatty liver; lipid transport and VLDL secretion; COPII machinery
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论文编号: |
DOI:10.1038/cr.2016.75 |
论文题目: |
Mea6 controls VLDL transport through the coordinated regulation of COPII assembly |
英文论文题目: |
Mea6 controls VLDL transport through the coordinated regulation of COPII assembly |
第一作者: |
Yaqing Wang,Liang Liu,Hongsheng Zhang,Junwan Fan,Feng Zhang,Mei Yu,Lei Shi,Lin Yang,Sin Man Lam,Huimin Wang,Xiaowei Chen,Yingchun Wang,Fei Gao,Guanghou Shui and Zhiheng Xu |
英文第一作者: |
Yaqing Wang,Liang Liu,Hongsheng Zhang,Junwan Fan,Feng Zhang,Mei Yu,Lei Shi,Lin Yang,Sin Man Lam,Huimin Wang,Xiaowei Chen,Yingchun Wang,Fei Gao,Guanghou Shui and Zhiheng Xu |
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2016-06-21 |
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摘要: |
Lipid accumulation, which may be caused by the disturbance in very low density lipoprotein (VLDL) secretion in the liver, can lead to fatty liver disease. VLDL is synthesized in endoplasmic reticulum (ER) and transported to Golgi apparatus for secretion into plasma. However, the underlying molecular mechanism for VLDL transport is still poorly understood. Here we show that hepatocyte-specific deletion ofmeningioma-expressed antigen 6 (Mea6)/cutaneous T cell lymphoma-associated antigen 5C (cTAGE5C) leads to severe fatty liver and hypolipemia in mice. Quantitative lipidomic and proteomic analyses indicate that Mea6/cTAGE5 deletion impairs the secretion of different types of lipids and proteins, including VLDL, from the liver. Moreover, we demonstrate that Mea6/cTAGE5 interacts with components of the ER coat protein complex II (COPII) which, when depleted, also cause lipid accumulation in hepatocytes. Our findings not only reveal several novel factors that regulate lipid transport, but also provide evidence that Mea6 plays a critical role in lipid transportation through the coordinated regulation of the COPII machinery. Keywords: Mea6; fatty liver; lipid transport and VLDL secretion; COPII machinery |
英文摘要: |
Lipid accumulation, which may be caused by the disturbance in very low density lipoprotein (VLDL) secretion in the liver, can lead to fatty liver disease. VLDL is synthesized in endoplasmic reticulum (ER) and transported to Golgi apparatus for secretion into plasma. However, the underlying molecular mechanism for VLDL transport is still poorly understood. Here we show that hepatocyte-specific deletion ofmeningioma-expressed antigen 6 (Mea6)/cutaneous T cell lymphoma-associated antigen 5C (cTAGE5C) leads to severe fatty liver and hypolipemia in mice. Quantitative lipidomic and proteomic analyses indicate that Mea6/cTAGE5 deletion impairs the secretion of different types of lipids and proteins, including VLDL, from the liver. Moreover, we demonstrate that Mea6/cTAGE5 interacts with components of the ER coat protein complex II (COPII) which, when depleted, also cause lipid accumulation in hepatocytes. Our findings not only reveal several novel factors that regulate lipid transport, but also provide evidence that Mea6 plays a critical role in lipid transportation through the coordinated regulation of the COPII machinery. Keywords: Mea6; fatty liver; lipid transport and VLDL secretion; COPII machinery |
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Cell Research |
英文刊物名称: |
Cell Research |
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其它备注: |
Yaqing Wang,Liang Liu,Hongsheng Zhang,Junwan Fan,Feng Zhang,Mei Yu,Lei Shi,Lin Yang,Sin Man Lam,Huimin Wang,Xiaowei Chen,Yingchun Wang,Fei Gao,Guanghou Shui and Zhiheng Xu. Mea6 controls VLDL transport through the coordinated regulation of COPII assembly. Cell Research. DOI:10.1038/cr.2016.75 |
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