TY - JOUR
T1 - Rab family of small GTPases
T2 - an updated view on their regulation and functions
AU - Homma, Yuta
AU - Hiragi, Shu
AU - Fukuda, Mitsunori
N1 - Funding Information:
This work was supported in part by Grant‐in‐Aid for Young Scientists from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan (grant number 18K14692 to YH), Grant‐in‐Aid for Scientific Research(B) from the MEXT (grant number 19H03220 to MF), and by Japan Science and Technology Agency (JST) CREST (grant number JPMJCR17H4 to MF).
Publisher Copyright:
© 2020 The Authors. The FEBS Journal published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies
PY - 2021/1
Y1 - 2021/1
N2 - The Rab family of small GTPases regulates intracellular membrane trafficking by orchestrating the biogenesis, transport, tethering, and fusion of membrane-bound organelles and vesicles. Like other small GTPases, Rabs cycle between two states, an active (GTP-loaded) state and an inactive (GDP-loaded) state, and their cycling is catalyzed by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Because an active form of each Rab localizes on a specific organelle (or vesicle) and recruits various effector proteins to facilitate each step of membrane trafficking, knowing when and where Rabs are activated and what effectors Rabs recruit is crucial to understand their functions. Since the discovery of Rabs, they have been regarded as one of the central hubs for membrane trafficking, and numerous biochemical and genetic studies have revealed the mechanisms of Rab functions in recent years. The results of these studies have included the identification and characterization of novel GEFs, GAPs, and effectors, as well as post-translational modifications, for example, phosphorylation, of Rabs. Rab functions beyond the simple effector-recruiting model are also emerging. Furthermore, the recently developed CRISPR/Cas technology has enabled acceleration of knockout analyses in both animals and cultured cells and revealed previously unknown physiological roles of many Rabs. In this review article, we provide the most up-to-date and comprehensive lists of GEFs, GAPs, effectors, and knockout phenotypes of mammalian Rabs and discuss recent findings in regard to their regulation and functions.
AB - The Rab family of small GTPases regulates intracellular membrane trafficking by orchestrating the biogenesis, transport, tethering, and fusion of membrane-bound organelles and vesicles. Like other small GTPases, Rabs cycle between two states, an active (GTP-loaded) state and an inactive (GDP-loaded) state, and their cycling is catalyzed by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Because an active form of each Rab localizes on a specific organelle (or vesicle) and recruits various effector proteins to facilitate each step of membrane trafficking, knowing when and where Rabs are activated and what effectors Rabs recruit is crucial to understand their functions. Since the discovery of Rabs, they have been regarded as one of the central hubs for membrane trafficking, and numerous biochemical and genetic studies have revealed the mechanisms of Rab functions in recent years. The results of these studies have included the identification and characterization of novel GEFs, GAPs, and effectors, as well as post-translational modifications, for example, phosphorylation, of Rabs. Rab functions beyond the simple effector-recruiting model are also emerging. Furthermore, the recently developed CRISPR/Cas technology has enabled acceleration of knockout analyses in both animals and cultured cells and revealed previously unknown physiological roles of many Rabs. In this review article, we provide the most up-to-date and comprehensive lists of GEFs, GAPs, effectors, and knockout phenotypes of mammalian Rabs and discuss recent findings in regard to their regulation and functions.
KW - GAP
KW - GEF
KW - Rab small GTPases
KW - effector
KW - knockout
KW - membrane traffic
KW - organelle
KW - post-translational modification
UR - http://www.scopus.com/inward/record.url?scp=85087302230&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85087302230&partnerID=8YFLogxK
U2 - 10.1111/febs.15453
DO - 10.1111/febs.15453
M3 - Review article
C2 - 32542850
AN - SCOPUS:85087302230
SN - 1742-464X
VL - 288
SP - 36
EP - 55
JO - FEBS Journal
JF - FEBS Journal
IS - 1
ER -