| 2000 |
RAB6B localizes to the Golgi apparatus and ERGIC-53-positive vesicles. Unlike the ubiquitously expressed RAB6A, RAB6B shows cell-type-specific expression predominantly in brain (microglia, pericytes, Purkinje cells) and neuroblastoma cells. RAB6B displays lower GTP-binding activities than RAB6A and in overexpression distributes over both Golgi and ER membranes, whereas RAB6A is more restricted to Golgi. The GTP-bound form (Q72L mutant) interacts with all known RAB6A effectors including Rabkinesin-6, suggesting a cell-type-specific role in retrograde membrane traffic at the Golgi complex. |
Subcellular fractionation, immunofluorescence, northern blot, immunohistochemistry, overexpression of GTP-locked mutant (Q72L), co-immunoprecipitation with effectors |
Journal of cell science |
High |
10893188
|
| 2007 |
RAB6B interacts with Bicaudal-D1 (BICD1) in its GTP-bound (active) form. RAB6B and BICD1 co-localize at the Golgi and on vesicles aligning along microtubules, and both co-localize with dynein in neurites of SK-N-SH neuronal cells. Live cell imaging revealed bi-directional movement of EGFP-RAB6B structures in neurites. This places RAB6B, via BICD1, in the dynein/dynactin retrograde transport complex in neuronal cells. |
Yeast two-hybrid screen, co-immunoprecipitation, pull-down assays, confocal co-localization, live cell imaging (EGFP-RAB6B) |
Experimental cell research |
High |
17707369
|
| 2008 |
RAB6B directly interacts with the dynein light chain DYNLRB1. Pull-down experiments showed a preferred association of DYNLRB1 with GDP-bound RAB6B (and GDP-bound RAB6A'), in contrast to GTP-bound RAB6A. DYNLRB1 co-localizes with all three RAB6 isoforms at the Golgi. In vitro GTPase activity assays showed DYNLRB1 does NOT stimulate RAB6 GTPase activity. |
Yeast two-hybrid, co-immunoprecipitation, pull-down assays, immunofluorescence co-localization, in vitro GTPase activity assay |
Cell motility and the cytoskeleton |
High |
18044744
|
| 2006 |
Crystal structures of human neuronal RAB6B were solved in the GDP-bound ('inactive', 2.3 Å) and GTPγS-bound ('active', 1.8 Å) forms. Conformational changes between states are concentrated in the switch I and switch II regions. Additional changes were observed in the RAB6 subfamily-specific RabSF3 region, potentially contributing to effector specificity of RAB6 isoforms. |
X-ray crystallography (space group P2₁2₁2₁; 2.3 Å GDP-bound and 1.8 Å GTPγS-bound structures) |
Acta crystallographica. Section D, Biological crystallography |
High |
16790928
|
| 2013 |
RAB6B physically interacts with GDAP1 (an outer mitochondrial membrane protein implicated in Charcot-Marie-Tooth disease) and with caytaxin, suggesting RAB6B participates in mitochondrial movement within the cell. |
Co-immunoprecipitation (interaction between GDAP1 and RAB6B/caytaxin in SH-SY5Y cells) |
Neurobiology of disease |
Low |
23542510
|
| 2021 |
RAB6B is expressed in primary mouse macrophages and localizes to the Golgi complex. Mycobacterium bovis BCG infection dynamically alters RAB6B expression in macrophages in vitro and in vivo. RAB6B knockdown reduces TNF secretion from BCG-infected macrophages without affecting Tnf mRNA levels or intracellular TNF protein abundance, establishing RAB6B as a positive regulator of TNF vesicle trafficking and secretion in macrophages. |
Immunofluorescence localization, siRNA knockdown, ELISA (TNF secretion), qRT-PCR (Tnf mRNA), intracellular flow cytometry (TNF protein), in vivo infection model |
Immunology and cell biology |
Medium |
34555867
|
| 2022 |
Double knockout of RAB6A/A' and RAB6B in radial glial (aRG) neural progenitors impairs apical localization of the polarity determinant CRB3 (Crumbs3) and induces retraction of the aRG apical process, leading to delamination and ectopic division. Live imaging showed RAB6+ post-Golgi vesicles move toward microtubule minus ends in a dynein-dependent manner. RAB6-dynein-LIS1 constitute a complex required for Golgi-to-apical-surface transport in aRG cells. |
In situ subcellular live imaging, RAB6A/A' and RAB6B double knockout (conditional KO mice/organoids), immunofluorescence for CRB3 apical localization, LIS1 knockout phenocopy, co-localization studies |
EMBO reports |
High |
35979738
|
| 2023 |
ELKS1 binds RAB6B through a C-terminal helical hairpin segment that engages RAB6B via a unique binding mode (co-crystal structure solved). Liquid-liquid phase separation (LLPS) of ELKS1 allows it to compete with other RAB6 effectors for RAB6B binding and accumulate RAB6B-coated liposomes into ELKS1 condensates. ELKS1 condensates recruit RAB6B-coated vesicles to vesicle-releasing sites and promote vesicle exocytosis. |
X-ray co-crystal structure of RAB6B–ELKS1 Rab6-binding domain complex, in vitro LLPS assay, liposome-condensate co-sedimentation, live cell vesicle exocytosis assay, mutagenesis |
The Journal of biological chemistry |
High |
37172719
|
| 2024 |
CNS-specific Rab6a/b double knockout (DKO) mice exhibit severe dysplasia of the neocortex and cerebellum. In Rab6 DKO neurons, synaptic vesicle precursors (SVPs) abnormally accumulate adjacent to the Golgi apparatus, causing defects in axonal extension and loss of axon-dendrite polarity. RAB6 DKO also causes significant lysosomal expansion in the soma. This establishes Rab6 (including Rab6b) as required for polarized anterograde transport of SVPs from the Golgi to the axon during neuronal polarity establishment. |
CNS-specific conditional Rab6a/b double KO mice (both sexes), in vitro primary neuron culture with Rab6a/b deletion, immunofluorescence for SVP markers and polarity markers, electron microscopy (lysosome expansion) |
The Journal of neuroscience |
High |
38830762
|
| 2023 |
Statin treatment (HMGCR inhibition) reduces RAB6B prenylation, which decreases RAB6B membrane association and affects integrin localization and downstream FAK signaling required for cell growth in PGC1α-suppressed BRAF-inhibitor-resistant melanoma cells. Combined re-expression of RAB6B and RAB27A reverses statin vulnerability in these cells. |
Pharmacological statin treatment, membrane fractionation (prenylation/membrane association), rescue by RAB6B+RAB27A re-expression, integrin localization immunofluorescence, FAK signaling western blot |
Nature communications |
Medium |
37277330
|
| 2019 |
RAB6B silencing in gastric cancer cells inhibits cell proliferation and G1/S transition through suppression of AKT/JNK signaling pathways, leading to reduced Cyclin D1 and CDK4 levels. miR-4268 directly targets RAB6B mRNA and phenocopies RAB6B silencing. |
siRNA-mediated RAB6B knockdown, luciferase reporter assay (miR-4268 targeting), cell cycle analysis, western blot (AKT/JNK/p38 pathway, Cyclin D1, CDK4), proliferation assays |
Cancer gene therapy |
Medium |
31303644
|
| 2023 |
miR-6216 directly targets and negatively regulates RAB6B expression in neural stem cells (NSCs). Overexpression of RAB6B promotes NSC proliferation, whereas forced overexpression of miR-6216 inhibits NSC proliferation. |
Luciferase reporter assay (miR-6216 targeting of RAB6B 3'UTR), RAB6B overexpression, miR-6216 overexpression, NSC proliferation assays |
Neuroscience research |
Medium |
37059126
|
| 2017 |
RAB6B was identified as a protein that co-immunoprecipitates with CEA (carcinoembryonic antigen) in LoVo colon cancer cells. RAB6B expression was down-regulated in LoVo cells in a radiation dose-dependent manner. |
Anti-CEA immunoprecipitation followed by LC-MS/MS mass spectrometry; western blot post-irradiation |
Radiation oncology journal |
Low |
28881503
|