Remodelling of IFT trains is thought to occur at the ciliary tip (Iomini et al, 2001; Buisson et al, 2013; reviewed in Snell and Cole, 2009). Retrograde transport is driven by the multi-subunit dynein-2 motor in an ATP-dependent fashion (Hou et al, 2004; Pazour et al, 1999; Porter et al, 1999; reviewed in Cole and Snell, 2009; Ishikawa et al, 2011). Mutations in genes encoding members of the IFT A complex or the dynein-2 motor generally result in short, swollen cilia that abnormally acccumulate IFT components (Iomini et al, 2009; Piperno et al, 1998; Pazour et al, 1999). The subunit composition of the human dynein-2 complex has recently been analyzed and preliminary characterization of the IFT A complex has begun, but detailed understanding of the molecular architecture of the retrograde IFT trains is still lacking (Assante et al, 2014; Piperno et al, 1998; Mukhopadhyay et al, 2010; reviewed in Taschner et al, 2012).
Ishikawa, H, Marshall, WF
Witman, GB, Hou, Y, Pazour, GJ
Snell, WJ, Cole, DG
Witman, GB, Pazour, GJ, Wilkerson, CG
Babaev-Khaimov, V, Piperno, G, Iomini, C, Sassaroli, M
Piperno, G, Segil, M, Siuda, E, Vaananen, H, Henderson, S, Sassaroli, M
Dutcher, SK, Iomini, C, Esparza, JM, Li, L
Dentler, W, Bower, R, Porter, ME, Byrd, P, Knott, JA
Lane, WS, Scales, SJ, Wen, X, Chih, B, Jackson, PK, Nelson, CD, Mukhopadhyay, S
Blisnick, T, Buisson, J, Bastin, P, Olivo-Marin, JC, Lagache, T, Chenouard, N
Stephens, DJ, Stevenson, NL, Asante, D
Bhogaraju, S, Taschner, M, Lorentzen, E
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