Structural highlights
Disease
[RUSC2_HUMAN] The disease is caused by mutations affecting the gene represented in this entry.
Function
[RAB35_HUMAN] The small GTPases Rab are key regulators of intracellular membrane trafficking, from the formation of transport vesicles to their fusion with membranes. Rabs cycle between an inactive GDP-bound form and an active GTP-bound form that is able to recruit to membranes different sets of downstream effectors directly responsible for vesicle formation, movement, tethering and fusion. That Rab is involved in the process of endocytosis and is an essential rate-limiting regulator of the fast recycling pathway back to the plasma membrane. During cytokinesis, required for the postfurrowing terminal steps, namely for intercellular bridge stability and abscission, possibly by controlling phosphatidylinositol 4,5-bis phosphate (PIP2) and SEPT2 localization at the intercellular bridge. May indirectly regulate neurite outgrowth.[1] [2]
References
- ↑ Kouranti I, Sachse M, Arouche N, Goud B, Echard A. Rab35 regulates an endocytic recycling pathway essential for the terminal steps of cytokinesis. Curr Biol. 2006 Sep 5;16(17):1719-25. PMID:16950109 doi:http://dx.doi.org/10.1016/j.cub.2006.07.020
- ↑ Rahajeng J, Giridharan SS, Cai B, Naslavsky N, Caplan S. MICAL-L1 is a tubular endosomal membrane hub that connects Rab35 and Arf6 with Rab8a. Traffic. 2012 Jan;13(1):82-93. doi: 10.1111/j.1600-0854.2011.01294.x. Epub 2011, Oct 24. PMID:21951725 doi:http://dx.doi.org/10.1111/j.1600-0854.2011.01294.x
