Suppressing ERK1/2 phosphorylation of TAN Line Component FHOD1 rescues defective nuclear movement in fibroblasts expressing muscular dystrophy lamin A mutants.

被引：0
|
作者：
Antoku, S. [1 ]
Wu, W. [2 ]
Ostlund, C. [2 ]
Worman, H. J. [2 ]
Gundersen, G. G. [1 ]
机构：
[1] Columbia Univ, Dept Pathol & Cell Biol, New York, NY USA
[2] Columbia Univ, Dept Med, New York, NY USA
来源：
MOLECULAR BIOLOGY OF THE CELL | 2016年 / 27卷
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D O I：
暂无
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
E115
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页数：1
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  • [1] Suppressing ERK1/2 phosphorylation of TAN Line Component FHOD1 rescues defective nuclear movement in fibroblasts expressing muscular dystrophy lamin A mutants.
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  • [2] FHOD1 interaction with nesprin-2G mediates TAN line formation and nuclear movement
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    Nature Cell Biology, 2014, 16 : 708 - 715
  • [3] FHOD1 interaction with nesprin-2G mediates TAN line formation and nuclear movement
    Kutscheidt, Stefan
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  • [4] The formin FHOD1 interacts with the TAN line component, nesprin-2Giant, and is required for actin-dependent nuclear movement during centrosome orientation in migrating fibroblasts.
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  • [5] Defective nuclear movement in lamin A deficient cells is rescued by reducing activity of Erk1/2 and Rho signaling.
    Antoku, S.
    Ostlund, C. A.
    Folker, E. S.
    Worman, H. J.
    Gundersen, G. G.
    MOLECULAR BIOLOGY OF THE CELL, 2014, 25
  • [6] The formin FHOD1 interacts with nesprin-2G to provide a branched connection to actin cables essential for TAN line formation and nuclear movement
    Zhu, R.
    Antoku, S.
    Kutscheidt, S.
    Luxton, G.
    Fackler, O.
    Gundersen, G. G.
    MOLECULAR BIOLOGY OF THE CELL, 2013, 24
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