Conventional kinesin

Two questions about yet another motor protein:

There are a few models that explain the movement of conventional kinesin along the microtubule, i.e., inchworm, hand-over-hand (which can further be classified into three models), and biased Brownian.

So can we determine which model best explains the movement of full-length human KHC dimer (with or without full-length human KLC’s) along the human microtubule using AFM in solution (preferably in non-contact mode)?

And can we further determine whether cargo-binding of KLC or KHC via binding proteins (Sunday driver protein, amyloid precursor protein, milton, etc) alters its movement using AFM in solution?


I will discuss huntingtin later.

Addendum primum:
Is hand-over-hand model predominant?