KIF26A Is an Unconventional Kinesin and Regulates GDNF-Ret Signaling in Enteric Neuronal Development | Zendy

Ruyun Zhou | Zendy; Shinsuke Niwa | Zendy; Noriko Homma | Zendy; Yosuke Takei | Zendy; Nobutaka Hirokawa | Zendy

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KIF26A Is an Unconventional Kinesin and Regulates GDNF-Ret Signaling in Enteric Neuronal Development

Author(s) -

Ruyun Zhou,

Shinsuke Niwa,

Noriko Homma,

Yosuke Takei,

Nobutaka Hirokawa

Publication year - 2009

Publication title -

cell

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 26.304

H-Index - 776

eISSN - 1097-4172

pISSN - 0092-8674

DOI - 10.1016/j.cell.2009.10.023

Subject(s) - biology , glial cell line derived neurotrophic factor , kinesin , microbiology and biotechnology , signal transduction , proto oncogene proteins c ret , neuroscience , neurotrophic factors , microtubule , genetics , receptor

The kinesin superfamily proteins (KIFs) are motor proteins that transport organelles and protein complexes in a microtubule- and ATP-dependent manner. We identified KIF26A as a new member of the murine KIFs. KIF26A is a rather atypical member as it lacks ATPase activity. Mice with a homozygous deletion of Kif26a developed a megacolon with enteric nerve hyperplasia. Kif26a-/- enteric neurons showed hypersensitivity for GDNF-Ret signaling, and we find that KIF26A suppressed GDNF-Ret signaling by direct binding and inhibition of Grb2, an essential component of GDNF/Akt/ERK signaling. We therefore propose that the unconventional kinesin KIF26A plays a key role in enteric nervous system development by repressing a cell growth signaling pathway.

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