tk]-cells, and the inhibition was greater in the lines that expressed higher levels of MAP4 or MTB.
To elucidate the types of transport events altered by overexpression of MAP4 or MTB, we used fluorescent markers to perform several assays of cell-sorting functions.
As before, we asked whether the inhibition of cellular activities dependent on organellar motility was attributable to the presence of extra MAP4 or MTB, or whether it was due to the MAP-induced alteration in MT stability.
In summary, we have used a system in which human MAP4 or its MT-binding domain is inducibly overexpressed in a cultured line of rodent cells to investigate the in vivo functions of MAP4.
Overexpression of MAP4 inhibits organelle motility in vivo.
Cellular microtubules heterogeneous in their content of MAP4 (210d MAP).
A second question is, do any of the motor molecules compete with MAP4 for binding sites on microtubules?