کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1929163 | 1050447 | 2012 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Role of km23-1 in RhoA/actin-based cell migration Role of km23-1 in RhoA/actin-based cell migration](/preview/png/1929163.png)
km23-1 was originally identified as a TGFß receptor-interacting protein that plays an important role in TGFß signaling. Moreover, km23-1 is actually part of an ancient superfamily of NTPase-regulatory proteins, widely represented in archaea and bacteria. To further elucidate the function of km23-1, we identified novel protein interacting partners for km23-1 by using tandem affinity purification (TAP) and tandem mass spectrometry (MS). Here we show that km23-1 interacted with a class of proteins involved in actin-based cell motility and modulation of the actin cytoskeleton. We further showed that km23-1 modulates the formation of a highly organized stress fiber network. More significantly, we demonstrated that knockdown (KD) of km23-1 decreased RhoA activation in Mv1Lu epithelial cells. Finally, our results demonstrated for the first time that depletion of km23-1 inhibited cell migration of human colon carcinoma cells (HCCCs) in wound-healing assays. Overall, our findings demonstrate that km23-1 regulates RhoA and motility-associated actin modulating proteins, suggesting that km23-1 may represent a novel target for anti-metastatic therapy.
► We identified several motility-related km23-1-interacting proteins.
► km23-1 overexpression increases actin stress fiber formation in epithelial cells.
► Depletion of km23-1 inhibits RhoA activation in epithelial cells.
► km23-1 depletion inhibits cell migration of human colon carcinoma cells.
Journal: Biochemical and Biophysical Research Communications - Volume 428, Issue 3, 23 November 2012, Pages 333–338