| 1994 |
Rab6 controls intra-Golgi transport, specifically between cis/medial and late Golgi compartments. Overexpression of GTP-bound (Q72L) or wild-type Rab6 blocked transport between alpha-mannosidase II-positive and sialyl-transferase-positive Golgi compartments without affecting ER-to-cis/medial Golgi or TGN-to-plasma membrane steps. |
Transient overexpression of wild-type, GTP-bound (Q72L), and GDP-bound (T27N) Rab6 mutants in mouse L cells and HeLa cells; intracellular transport assays using secreted alkaline phosphatase (SEAP) and influenza hemagglutinin (HA) as markers |
The Journal of cell biology |
High |
7798313
|
| 1994 |
Golgi apparatus localization of Rab6 requires geranylgeranylation (not farnesylation) and sequences in the N-terminal 71 amino acids including the effector domain. The C-terminal hypervariable domain is required to prevent prenylated/palmitoylated Rab6 from mislocalizing to the plasma membrane. |
Chimeric Ras-Rab proteins and Rab6 mutants with altered C-terminal lipid modifications expressed in mammalian cells; complementation of yeast ypt6 null mutants |
Molecular and cellular biology |
High |
8264642
|
| 1994 |
Rab6 interaction with RabGDI requires the effector domain, loop3/beta3, and the hypervariable region; geranylgeranylation on CXC or CC motifs supports significantly better membrane extraction by RabGDI than farnesylation or palmitoylation. The effector domain is required for RabGDI binding but not for efficient processing by RabGGTase. |
In vitro membrane extraction assays with Rab6 mutants bearing various C-terminal lipid modifications; binding studies with recombinant proteins |
The Journal of biological chemistry |
High |
8175798
|
| 1995 |
The nucleotide-bound conformation of Rab6 determines its posttranslational geranylgeranylation: only the GDP-bound form is isoprenylated and becomes membrane-bound in insect cells, whereas the GTP-bound form is not modified. |
Expression of GDP- and GTP-conformation point mutants of Rab6 in insect cells; Triton X-114 partitioning and cell fractionation to assess membrane association |
FEBS letters |
Medium |
8521955
|
| 1995 |
Rab6 interacts with GDI beta (GDP-dissociation inhibitor beta isoform) in a GDP-dependent manner; GDI beta removes Rab6 from membranes. Rab6 also interacts with a novel, unidentified protein in its two-hybrid screen. |
Yeast two-hybrid screen using Rab6 as bait against mouse brain cDNA library; in vitro membrane extraction assay with recombinant GDI beta |
The Journal of biological chemistry |
Medium |
7782346
|
| 1996 |
Rab6 is required for transport between cis and medial Golgi cisternae in a reconstituted cell-free Golgi transport assay. Anti-Rab6 antibodies and Fab fragments, as well as dominant-negative Rab6(N126I), inhibit transport and membrane fusion at the cisternal level. |
Cell-free reconstituted Golgi transport assay; inhibition with polyclonal antibodies, Fab fragments, and dominant-negative Rab6 mutant protein |
The Journal of biological chemistry |
High |
8663167
|
| 1997 |
GTP-bound forms of Rab6 (wild-type and Q72L mutant) cause redistribution of Golgi resident proteins (e.g., beta-1,4-galactosyltransferase) into the ER and allow sialylated O-glycan addition to an ER-retained protein, phenocopying brefeldin A. This effect requires intact microtubules. GDP-bound Rab6 (T27N) does not cause redistribution but inhibits basal O-glycosylation. |
Overexpression of Rab6 mutants in HeLa cells; immunofluorescence, subcellular fractionation, glycosylation assays; microtubule depolymerization with nocodazole |
Proceedings of the National Academy of Sciences of the United States of America |
High |
9050864
|
| 1998 |
Rab6 interacts in its GTP-bound form with Rabkinesin-6, a kinesin-like protein localized to the Golgi apparatus. The C-terminal domain of Rabkinesin-6 contains the Rab6-interacting domain. Overexpression of this C-terminal domain inhibits Rab6-GTP-dependent intracellular transport effects, identifying a molecular motor as an effector of Rab6. |
Yeast two-hybrid screen; co-immunoprecipitation; pulldown with GST-fusion proteins; dominant-negative overexpression assays in cells |
Science (New York, N.Y.) |
High |
9438855
|
| 1999 |
Rab6 regulates a COPI-independent Golgi-to-ER retrograde transport pathway. FP-Rab6-positive transport carriers specifically accumulate Shiga toxin B-fragment (STB) during Golgi-to-ER transport. Overexpression of GDP-bound Rab6(T27N) inhibits Shiga holotoxin toxicity without affecting STB transport to the Golgi or Golgi morphology. Rab6/STB transport carriers are excluded from COPI-dependent recycling markers. |
Live-cell fluorescence microscopy of FP-Rab6 fusion; microinjection of COPI-blocking antibodies; T7 vaccinia-driven overexpression of Rab6 T27N; toxicity assays |
The Journal of cell biology |
High |
10562278
|
| 1999 |
GAPCenA is a GTPase-activating protein (GAP) specifically active on Rab6 in vitro (and to lesser extent on Rab4 and Rab2). A minor pool of GAPCenA associates with the centrosome and forms complexes with cytosolic gamma-tubulin, suggesting a role in coordinating microtubule nucleation with Golgi dynamics. |
Identification by two-hybrid screen; in vitro GAP assay with recombinant proteins; immunofluorescence; cell fractionation; gamma-tubulin co-immunoprecipitation |
The EMBO journal |
High |
10202141
|
| 1999 |
Golgins golgin-230/245/256 and golgin-97 target to the Golgi through a conserved C-terminal domain that preferentially binds Rab6. Mutations abolishing Golgi targeting also abrogate Rab6 binding. This domain defines a conserved family of Rab6-interacting coiled-coil proteins (golgins) likely involved in Rab6-regulated membrane tethering. |
Protein blot binding assay; mutagenesis; Golgi targeting assays in cells; sequence analysis across species |
Current biology : CB |
Medium |
10209123
|
| 2000 |
Rab6A and Rab6A' are generated by alternative splicing of the RAB6A gene, differing in only three amino acids flanking the PM3 GTP-binding domain. Rab6A Q72L overexpression induces redistribution of Golgi proteins to the ER (retrograde), but Rab6A' Q72L does not. Rab6A' does not interact with Rabkinesin-6 but does interact with GAPCenA; one amino acid at position 87 (T vs A) underlies these functional differences. |
Gene structure analysis; GTP-binding assays; HeLa cell overexpression; immunofluorescence; yeast two-hybrid interaction assays for effector binding |
Molecular biology of the cell |
High |
11071909
|
| 2000 |
Rab6-KIFL (Rab6-binding kinesin) was identified as a Rab6-interacting protein. Endogenous Rab6-KIFL localizes to the spindle midzone during anaphase and to the cleavage furrow/midbody during telophase. Microinjection of anti-Rab6-KIFL antibodies results in binucleate cells due to defective cleavage furrow formation, demonstrating a role for this Rab6 effector in cytokinesis. |
Yeast two-hybrid identification; immunofluorescence; microinjection of inhibitory antibodies; time-lapse microscopy |
The EMBO journal |
High |
11060022
|
| 2001 |
Retrograde transport from early/recycling endosomes to the TGN requires the Rab6A' isoform (not Rab6A) along with specific SNARE complexes (syntaxin 6, syntaxin 16, Vti1a with VAMP3/cellubrevin and VAMP4). Rab6A has been previously implicated in Golgi-to-ER transport instead. |
Novel permeabilized cell transport assay; protein interaction studies; dominant-negative and antibody inhibition approaches |
The Journal of cell biology |
High |
11839770
|
| 2002 |
Rab6 recruits the dynactin complex to Golgi membranes in a GTP-dependent and Rab6-specific manner. Other Golgi Rabs (tested) do not bind dynactin and cannot support its membrane recruitment, establishing Rab6 as a specificity factor for dynactin recruitment. |
Pulldown and co-immunoprecipitation assays with recombinant Rab proteins; Golgi membrane recruitment assays; comparison with other Golgi Rabs |
Current biology : CB |
High |
12401177
|
| 2002 |
Two novel Rab6-interacting proteins, Rab6IP2A and Rab6IP2B (splice variants), are recruited to Golgi membranes in a Rab6:GTP-dependent manner. Overexpression of the Rab6-binding domain of Rab6IP2 partly inhibits retrograde transport of Shiga toxin B-subunit from plasma membrane to Golgi. |
Yeast two-hybrid screen; co-immunoprecipitation; Golgi recruitment assays; Shiga toxin transport assays with Rab6-binding domain overexpression |
Traffic (Copenhagen, Denmark) |
Medium |
11929610
|
| 2003 |
Rab6 is in its GTP-bound conformation on the Golgi apparatus and on transport intermediates as demonstrated by GFP-tagged conformation-specific recombinant antibodies expressed intracellularly. The geometry of transport intermediates is modulated by Rab6 activity. |
Antibody phage display to generate GTP-conformation-specific Rab6 antibodies; GFP-tagging and intracellular expression for live-cell imaging; fixed-cell immunostaining |
Science (New York, N.Y.) |
High |
12738866
|
| 2004 |
Both Rab6A and Rab6A' GTP-restricted mutants promote microtubule-dependent recycling of Golgi resident glycosylation enzymes to the ER with similar efficiency. Rab6-directed Golgi-to-ER recycling requires functional dynactin (inhibited by p50/dynamitin overexpression or C-terminal Bicaudal-D fragment). Reduced Rab6 via siRNA perturbs Golgi organization and delays Golgi-to-ER recycling. |
siRNA knockdown of individual Rab6 isoforms; overexpression of GTP-restricted mutants; p50/dynamitin dominant-negative overexpression; immunofluorescence |
Molecular biology of the cell |
High |
15483056
|
| 2004 |
TMF/ARA160 is a Rab6-binding golgin that binds all three known Rab6 isoforms. Depletion of TMF by RNAi causes modest dispersal of Golgi membranes, suggesting a role in Golgi organization. |
Pulldown and binding assays between TMF and Rab6 isoforms; RNAi depletion with immunofluorescence analysis of Golgi morphology |
BMC cell biology |
Medium |
15128430
|
| 2006 |
siRNA knockdown reveals that Rab6A' (but not Rab6A) is the major isoform regulating retrograde Shiga toxin transport and Golgi-associated protein recycling through the ER. Rab6A' is also required for cell cycle progression through mitosis; cells with impaired Rab6A' are blocked in metaphase with activated Mad2-spindle checkpoint. Ile62 is a key residue uncoupling Rab6A' functions in mitosis and retrograde trafficking. |
isoform-specific siRNA knockdown; Shiga toxin B-subunit transport assay; cell cycle analysis; mutagenesis of Ile62 |
Traffic (Copenhagen, Denmark) |
High |
16536738
|
| 2006 |
Rab6A' GTPase activity at kinetochores regulates inactivation of the Mad2-spindle checkpoint. Impaired Rab6A' function (by dominant-negative expression or GAPCenA depletion) blocks cells in metaphase with activated Mad2 checkpoint and retains p150(Glued) (dynactin subunit) at kinetochores, suggesting Rab6A' regulates dynein/dynactin dynamics at kinetochores during mitosis. |
Dominant-negative Rab6A' expression; GAPCenA siRNA depletion; immunofluorescence for Mad2 and p150(Glued) at kinetochores; cell cycle analysis |
The EMBO journal |
High |
16395330
|
| 2007 |
Rab6 marks exocytotic vesicles and, together with kinesin-1, drives processive microtubule-based transport to the cell periphery. Rab6 directs targeting of secretory vesicles to plasma membrane sites enriched in the cortical protein ELKS. Although Rab6 is not essential for secretion, it controls the spatial organization of exocytosis. |
Live-cell imaging of GFP-Rab6; siRNA knockdown of Rab6 and kinesin-1; co-localization of vesicles with ELKS-positive cortical sites; secretion assays |
Developmental cell |
High |
17681140
|
| 2007 |
R6IP1 (Rab6-interacting protein 1) links Rab6 and Rab11 function: R6IP1 binds both Rab6 (targeting it to Golgi) and Rab11A (GTP-bound). Overexpression of R6IP1 promotes Rab11A-Rab6 interaction (FRET/FLIM) and causes pericentriolar accumulation of Rab11-positive recycling endosomes. R6IP1 function is also required during metaphase and cytokinesis. |
Yeast two-hybrid; co-immunoprecipitation; FRET/FLIM live-cell imaging; siRNA depletion; immunofluorescence; cell cycle analysis |
Traffic (Copenhagen, Denmark) |
High |
17725553
|
| 2007 |
Rab6 depletion suppresses Golgi ribbon fragmentation/dispersal induced by ZW10/RINT-1 or COG complex inactivation (epistatic relationship). Dominant-negative Rab6 and C-terminal Bicaudal-D fragment (which interferes with dynactin/dynein) both suppress ZW10-knockdown-induced Golgi disruption. Rab6 therefore acts upstream in two separate retrograde tether-dependent Golgi trafficking pathways (ZW10/RINT-1 and COG). |
siRNA epistasis experiments; dominant-negative Rab6 expression; dominant-negative Bicaudal-D fragment; immunofluorescence; multiple Rab depletion combinations |
Molecular biology of the cell |
High |
17699596
|
| 2007 |
TMF/ARA160 is functionally involved in two Rab6-dependent retrograde pathways: retrograde transport of Shiga toxin from endosomes to TGN, and retention of specific Golgi enzymes (GalNAc-T2 but not GalT) at the Golgi. TMF localizes to cisternal tips/budding structures at the Golgi as shown by immunoelectron microscopy. |
siRNA knockdown of TMF and Rab6; Shiga toxin transport assay; immunofluorescence; immunoelectron microscopy; chimeric protein domain swap experiments |
Experimental cell research |
High |
17698061
|
| 2008 |
SCYL1BP1 (GORAB) localizes to the Golgi apparatus and interacts with Rab6, functioning as a golgin. Loss-of-function mutations in SCYL1BP1 cause gerodermia osteodysplastica, associating Rab6-dependent secretory pathway defects with age-related connective tissue changes. |
Identification of disease-causing mutations; subcellular localization studies; interaction assays between GORAB and Rab6 |
Nature genetics |
Medium |
18997784
|
| 2008 |
DYNLRB1 (dynein light chain) specifically interacts with all three Rab6 isoforms and co-localizes at the Golgi. DYNLRB1 shows preferred association with GTP-bound Rab6A but GDP-bound Rab6A' and Rab6B, representing the first direct interaction identified between Rab6 and the dynein complex. |
Yeast two-hybrid; co-immunoprecipitation; pulldown with GTP/GDP-loaded Rab6 isoforms; immunofluorescence co-localization |
Cell motility and the cytoskeleton |
Medium |
18044744
|
| 2008 |
Three Rab6a effectors (PIST, BicaudalD2, p150(Glued)) bind activated Rab6a through >15-kDa coiled-coil domains with Kd values in the high-nanomolar to low-micromolar range. BicaudalD2 and p150 binding moderately inhibits intrinsic Rab6a GTPase activity; PIST binding does not. Effectors bind in an apparent single-step reaction with relatively rapid on- and off-rates. |
In vitro biophysical binding assays (SPR, fluorescence); identification of minimal binding domains; GTPase activity assays with bound effectors |
The Journal of biological chemistry |
High |
19019823
|
| 2009 |
Crystal structure of Rab6a(GTP) in complex with a 378-residue fragment of Rab6IP1 (containing RUN and PLAT domains) solved at 3.2 Å. The first and last alpha-helices of the RUN domain mediate binding to switch I, switch II, and the interswitch region of Rab6. Comparison with Rab6-GCC185 complex reveals conformational flexibility in the conserved hydrophobic triad of Rab6 that enables recognition of compositionally distinct effectors. |
X-ray crystallography; structure determination at 3.2 Å resolution; structural comparison with Rab6-GCC185 complex |
Structure (London, England : 1993) |
High |
19141279
|
| 2010 |
BICDR-1 (Bicaudal-D-related protein 1) is a Rab6 effector that interacts with kinesin Kif1C and the dynein/dynactin complex, and accumulates Rab6 secretory vesicles in the pericentrosomal region of young neurons, restricting anterograde secretory transport and inhibiting neuritogenesis. BICDR-1 expression declines during development, permitting later anterograde transport required for neurite outgrowth. |
Co-immunoprecipitation; live-cell imaging; siRNA knockdown; zebrafish morpholino neural development assay; vesicle motility measurements |
The EMBO journal |
High |
20360680
|
| 2010 |
Rab33B and Rab6 act sequentially in an intra-Golgi retrograde trafficking Rab cascade: Rab6 acts downstream of Rab33B (overexpression of GTP-Rab33B induces dissociation of Rab6 from Golgi membranes). Efficient GTP-Rab6-induced relocation of Golgi enzymes to the ER is Rab33B-dependent, but not vice versa. |
siRNA epistasis experiments; overexpression of GTP-restricted Rab mutants; immunofluorescence; Golgi morphology analysis; Shiga toxin transport assay |
Traffic (Copenhagen, Denmark) |
High |
20163571
|
| 2011 |
Rab8A associates with exocytotic vesicles in a Rab6-dependent manner. Rab8A is required for docking and fusion (but not budding or motility) of exocytotic carriers. MICAL3 links Rab8A and ELKS at the cell cortex; MICAL3 monooxygenase activity is required for vesicle-docking complex remodeling and fusion. Rab6 and Rab8 thus cooperate sequentially in constitutive exocytosis. |
Live-cell imaging; siRNA knockdown of Rab6 and Rab8; co-immunoprecipitation; MICAL3 catalytic mutant expression; vesicle docking/fusion quantification |
Current biology : CB |
High |
21596566
|
| 2012 |
The Ric1-Rgp1 complex is the guanine nucleotide exchange factor (GEF) for Rab6A in human cells. Both Ric1 and Rgp1 are required to catalyze nucleotide exchange on Rab6A and preferentially bind its GDP-bound form. Loss of Ric1 or Rgp1 destabilizes Rab6 and blocks retrograde transport of mannose-6-phosphate receptors to the Golgi. Rab33B-GTP binds the C-terminus of Ric1, establishing a Rab33B→Ric1/Rgp1→Rab6A cascade. |
In vitro nucleotide exchange assay with recombinant proteins; co-immunoprecipitation; siRNA knockdown; retrograde transport assay for mannose-6-phosphate receptors; domain-binding studies |
The Journal of biological chemistry |
High |
23091056
|
| 2012 |
Rab6 depletion causes accumulation of trans-Golgi clathrin-coated and COPI-coated vesicles and an increase of >50% in Golgi cisternae number. Rab6 is essential for trafficking of these two morphological classes of coated vesicles at the trans-Golgi. |
siRNA knockdown of Rab6; electron microscopy and electron tomography; quantitative morphometric analysis |
Traffic (Copenhagen, Denmark) |
High |
22335553
|
| 2013 |
Rab6A/A' are required for post-Golgi trafficking of TNF from TGN-derived tubular carriers to the cell surface in LPS-activated macrophages. Rab6 localizes to p230-positive TGN tubular carriers, and its depletion reduces carrier egress and partially reduces p230 membrane association. Both Rab6 isoforms are needed for macrophage Golgi organization and efficient post-Golgi TNF transport. |
siRNA and shRNA depletion; dominant-negative mutants; live-cell imaging of Rab6-GFP on TGN tubular carriers; secretion assays; electron microscopy |
PloS one |
High |
23437303
|
| 2014 |
COH1 (VPS13B) Golgi localization depends on RAB6: RAB6A/A' knockdown prevents COH1 localization to the Golgi, constitutively inactive RAB6_T27N increases solubilization of COH1 from membranes, and constitutively active RAB6_Q72L preferentially co-immunoprecipitates with COH1. COH1 depletion in primary neurons impairs neurite outgrowth. |
siRNA knockdown; co-immunoprecipitation with RAB6 mutants; lipid membrane fractionation; neurite outgrowth assay in primary neurons |
The Journal of biological chemistry |
High |
25492866
|
| 2015 |
KIF1C transports Rab6A vesicles and influences Golgi organization by binding Rab6A directly at both its motor domain and C-terminus. Rab6A binding to the KIF1C motor domain inhibits microtubule interaction in vitro and in cells. KIF1C depletion slows protein delivery to the cell surface, impairs vesicle motility, and causes Golgi fragmentation. KIF1C can protect Golgi from fragmentation independently of motor function when both Rab6A-binding sites are intact. |
In vitro microtubule interaction assay; pulldown; co-immunoprecipitation; siRNA knockdown; live-cell imaging; cargo delivery assay |
eLife |
High |
25821985
|
| 2015 |
BICD2 stabilizes GTP-bound Rab6A on Golgi membranes: BICD2 knockdown reduces active Rab6A levels at the Golgi, and overexpression of C-terminal BICD2 decreases GFP-Rab6A exchange rate at Golgi (by FRAP). Rab6A and BICD2 jointly mediate COPI-independent Golgi-to-ER retrograde transport (Golgi tubule fusion with ER in BFA-treated cells). |
Golgi-targeting reconstitution in permeabilized cells; immunofluorescence; FRAP; siRNA knockdown; BFA-induced Golgi-to-ER transport assay |
Biochimica et biophysica acta |
High |
25962623
|
| 2015 |
GORAB missense mutations (p.Ala220Pro and p.Ser175Phe) in the IGRAB domain disrupt RAB6 binding and Golgi targeting of GORAB. ARF5 (GTP-bound) also binds the same IGRAB domain, and the p.Ala220Pro mutation abrogates both RAB6 and ARF5 binding while p.Ser175Phe selectively impairs ARF5 binding. |
Yeast two-hybrid screening; immunofluorescence; Brefeldin A treatment; mutagenesis; protein interaction assays |
The Journal of investigative dermatology |
Medium |
26000619
|
| 2015 |
RAB6A knockout mouse embryonic fibroblasts (MEFs) show altered Golgi morphology, decreased Golgi-associated levels of Rab6 effectors (Bicaudal-D and myosin II), delayed VSV-G secretion, and protection against ricin toxicity. RAB6A homozygous null mice die at early embryonic development, establishing RAB6A as an essential gene. |
Conditional RAB6A knockout using Cre-loxP/tamoxifen system; Western blot; immunofluorescence; secretion assays; ricin toxicity assays |
Biology of the cell |
High |
26304202
|
| 2017 |
In melanocytes, the RAB6/ELKS-dependent secretory pathway directly transports and docks Golgi-derived carriers (carrying MART-1 and TYRP2/DCT) to melanosomes, controlling melanosome formation, maturation, and pigment synthesis. RAB6 KO mice display pigmentation defects. |
Live-cell imaging; siRNA knockdown; RAB6 KO mouse model; cargo tracking; melanosome maturation assays |
Nature communications |
High |
28607494
|
| 2018 |
Rab6-dependent retrograde transport of LAT (linker for activation of T cells) through the Golgi-TGN is required for its polarized delivery to the immune synapse and for TCR-mediated T lymphocyte activation. This retrograde traffic also depends on Syntaxin-16. Rab6 KO CD4+ T lymphocytes show impaired TCR stimulation in vivo. |
siRNA knockdown of Rab6 and Syntaxin-16 in human cells; Rab6 KO mouse CD4+ T cells; LAT trafficking assays; immune synapse formation assays; TCR stimulation assays |
The Journal of experimental medicine |
High |
29440364
|
| 2019 |
RAB6 and microtubules restrict protein secretion to focal-adhesion-juxtaposed hotspots at the cell surface. Most post-Golgi carriers are RAB6-positive regardless of cargo, and RAB6 inactivation leads to broad reduction of protein secretion. |
Synchronized secretion assay (RUSH system); live-cell imaging; siRNA/dominant-negative Rab6 inactivation; colocalization with focal adhesion markers |
The Journal of cell biology |
High |
31142554
|
| 2019 |
Rab6 negatively regulates cell migration by interacting with Cdc42 and Trio (a GEF for Cdc42), thereby suppressing Cdc42 activity. Loss of Rab6 promotes actin protrusion formation and upregulates Cdc42 activity while downregulating myosin II phosphorylation. |
Rab6 KO/knockdown; Cdc42 GTPase activity assay; co-immunoprecipitation of Rab6 with Cdc42 and Trio; actin protrusion quantification; cell migration assays in vitro and in vivo |
Cellular and molecular life sciences : CMLS |
Medium |
30830239
|
| 2020 |
ELKS1 captures Rab6-positive Golgi-derived vesicular cargo at presynaptic nerve terminals via Golgin-like mechanisms. Knockout and rescue experiments establish that ELKS1 captures Rab6 cargo; the capturing mechanism can be transferred to mitochondria by mistargeting ELKS1 or Rab6. |
ELKS1 and Rab6 knockout and rescue experiments; live-cell imaging; mitochondria mistargeting experiments; presynaptic vesicle assays in neurons |
Cell reports |
High |
32521280
|
| 2021 |
Newly synthesized TrkB receptors traffic through the secretory pathway in Rab6-positive carriers and are directly delivered into the axon. The combined activity of kinesin-1 and kinesin-3 drives formation and anterograde transport of these TrkB/Rab6-positive secretory carriers beyond the proximal axon. |
Microfluidic compartmental devices; inducible secretion assay; live-cell imaging; siRNA/knockout of kinesin-1 and kinesin-3; Rab6 co-localization assays |
Developmental cell |
High |
33571451
|
| 2022 |
Post-Golgi transport of RAB6+ vesicles in apical radial glia (aRG) cells occurs toward microtubule minus ends and depends on dynein and LIS1 (dynein activator). Double knockout of RAB6A/A' and RAB6B impairs apical localization of the apical determinant Crumbs3 (CRB3) and induces retraction of the apical process, leading to aRG delamination and ectopic division. These defects are phenocopied by LIS1 knockout. |
In situ subcellular live imaging; conditional RAB6 double knockout; LIS1 knockout; CRB3 localization assays; neuroepithelial integrity analysis |
EMBO reports |
High |
35979738
|
| 1993 |
A cytosolic complex of p62 and Rab6 associates with TGN38/41 and is required for budding of exocytic vesicles from the TGN. Immunodepletion or competing peptides targeting p62, Rab6, or TGN38/41 cytoplasmic domains completely inhibit vesicle budding in a cell-free system. |
Co-immunoprecipitation from cell extracts; cell-free vesicle budding assay; immunodepletion; competing peptide inhibition; sizing column and velocity sedimentation |
The Journal of cell biology |
High |
8349729
|
| 1999 |
Rab6 in Drosophila photoreceptors controls rhodopsin anterograde transport through the Golgi; GTPase-defective Rab6(Q71L) prevents maturation of rhodopsin beyond an immature 40-kDa form, depletes Rh1 and Rh3 levels, and causes retinal degeneration. |
Transgenic overexpression in Drosophila photoreceptors; Western blot analysis of rhodopsin forms; histological analysis; heat-shock rhodopsin pulse-chase |
The Journal of biological chemistry |
High |
9685396
|
| 2000 |
In platelets, Rab6 is phosphorylated by protein kinase C (PKC) in a thrombin-stimulated manner. PKC phosphorylation of Rab6 increases GTP affinity ~3-fold, does not alter GTPase activity, and causes translocation of Rab6 from platelet particulate fractions to the cytosol. |
Metabolic [32P] labeling; PKC inhibitor (Ro-31-8220); cell fractionation; in vitro PKC phosphorylation of recombinant Rab6C; nucleotide binding affinity measurements |
The Biochemical journal |
High |
10455022
|