1z22
GDP-Bound Rab23 GTPase crystallized in C222(1) space groupGDP-Bound Rab23 GTPase crystallized in C222(1) space group
Structural highlights
DiseaseRAB23_MOUSE Note=Defects in Rab23 are the cause of the open brain phenotype. Mice suffer from exencephaly and severe malformations of the spinal cord and the dorsal root ganglia, leading to complete embryonic lethality. In addition, mice display poorly developed eyes and polydactyly.[1] FunctionRAB23_MOUSE 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 set of downstream effectors directly responsible for vesicle formation, movement, tethering and fusion (By similarity). Plays a role in autophagic vacuole assembly, and mediates defense against pathogens, such as S.aureus, by promoting their capture by autophagosomes that then merge with lysosomes (By similarity). Together with SUFU, prevents nuclear import of GLI1, and thereby inhibits GLI1 transcription factor activity. Regulates GLI1 in differentiating chondrocytes. Likewise, regulates GLI3 proteolytic processing and modulates GLI2 and GLI3 transcription factor activity.[2] [3] [4] [5] [6] Evolutionary Conservation Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. See AlsoReferences
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