TY - JOUR
T1 - The adenomatous polyposis coli protein
T2 - In the limelight out at the edge
AU - Dikovskaya, D.
AU - Zumbrunn, J.
AU - Penman, G. A.
AU - Näthke, I. S.
PY - 2001/9/1
Y1 - 2001/9/1
N2 - Truncation mutations in the adenomatous polyposis coli protein (APC) are responsible for familial and sporadic colonic tumours. APC is best known for its role in regulating β-catenin, an important mediator of cell adhesion and a transcriptional activator. However, recent studies indicate that APC has additional roles in cytoskeletal regulation. It binds to microtubules directly and indirectly. Furthermore, indirect connections between APC and the actin cytoskeleton have also been described. Here, we integrate recent information describing the association between APC and the cytoskeleton to illustrate how this multifaceted protein might link different cytoskeletal elements to each other and to cellular signaling pathways.
AB - Truncation mutations in the adenomatous polyposis coli protein (APC) are responsible for familial and sporadic colonic tumours. APC is best known for its role in regulating β-catenin, an important mediator of cell adhesion and a transcriptional activator. However, recent studies indicate that APC has additional roles in cytoskeletal regulation. It binds to microtubules directly and indirectly. Furthermore, indirect connections between APC and the actin cytoskeleton have also been described. Here, we integrate recent information describing the association between APC and the cytoskeleton to illustrate how this multifaceted protein might link different cytoskeletal elements to each other and to cellular signaling pathways.
UR - http://www.scopus.com/inward/record.url?scp=0035445284&partnerID=8YFLogxK
U2 - 10.1016/S0962-8924(01)02069-4
DO - 10.1016/S0962-8924(01)02069-4
M3 - Review article
C2 - 11514192
AN - SCOPUS:0035445284
SN - 0962-8924
VL - 11
SP - 378
EP - 384
JO - Trends in Cell Biology
JF - Trends in Cell Biology
IS - 9
ER -