| 1999 |
RAB11A localizes to an apical pericentriolar endosomal compartment (apical recycling endosome) in polarized MDCK epithelial cells, and this compartment is accessible to membrane markers internalized from either apical or basolateral poles, functionally defining it as the apical recycling endosome; integrity of this compartment depends on intact microtubules. |
Immunofluorescence, antibody labeling, nocodazole treatment, dimeric IgA trafficking assay in MDCK cells |
Molecular biology of the cell |
High |
9880326
|
| 2000 |
A dominant-negative GTP-binding-deficient RAB11A mutant (Rab11aS25N) inhibits both apical recycling and basolateral-to-apical transcytosis of IgA but does not inhibit basolateral recycling of transferrin in polarized MDCK cells, placing RAB11A specifically in the apical recycling/transcytotic pathway. |
Inducible expression of wild-type, dominant-negative (S25N), and constitutively active (S20V) RAB11A mutants; IgA and transferrin trafficking assays in MDCK cells |
The Journal of biological chemistry |
High |
10869360
|
| 1999 |
RAB11A is the predominant GTPase associated with H+/K+-ATPase-enriched gastric microsomes (stoichiometry ~1 Rab11a per 6 H+/K+-ATPase), and expression of dominant-negative Rab11a N124I in parietal cells blocks histamine-stimulated recruitment of H+/K+-ATPase to the apical plasma membrane. |
Mass spectrometry identification; adenoviral expression of dominant-negative Rab11a N124I; aminopyrine uptake assay; immunocytochemistry in primary rabbit parietal cell cultures |
The American journal of physiology |
High |
10484323
|
| 1998 |
RAB11A remains associated with H+/K+-ATPase-containing tubulovesicle membranes during fusion with the secretory canaliculus upon histamine stimulation and redistributes to apical canalicular membranes without cycling off into the soluble fraction, indicating RAB11A stays membrane-bound during recycling vesicle fusion. |
Subcellular fractionation, immunofluorescence, Western blot of resting and stimulated rabbit parietal cells |
The American journal of physiology |
Medium |
9688847
|
| 2005 |
RAB11A and myosin Vb are required for bile canalicular formation in hepatic WIF-B9 cells; knockdown of Rab11a or expression of GDP-locked Rab11a, or overexpression of a motorless myosin Vb tail domain, each prevents canalicular formation and blocks delivery of apical ABC transporters to the plasma membrane. |
shRNA knockdown, dominant-negative overexpression, immunofluorescence, live-cell imaging in WIF-B9 hepatic epithelial cells |
Proceedings of the National Academy of Sciences of the United States of America |
High |
16214890
|
| 2002 |
RAB11A and its effector myosin Vb regulate recycling of the M4 muscarinic acetylcholine receptor; dominant-negative Rab11aS25N blocks M4 trafficking to recycling endosomes, and expression of the myosin Vb C-terminal tail enhances M4 accumulation in perinuclear endosomes and impairs M4 recycling to the cell surface. |
Dominant-negative RAB11A and myosin Vb tail overexpression; receptor trafficking assays; colocalization with transferrin receptor and Rab11a markers in cell culture |
The Journal of neuroscience |
High |
12427833
|
| 2006 |
RAB11A directly and specifically interacts with the GDP-bound form of itself to bind the carboxyl terminus of epithelial Ca2+ channels TRPV5 and TRPV6; coexpression of GDP-locked RAB11A with TRPV5 or TRPV6 reduces channel plasma membrane abundance and Ca2+ uptake, demonstrating RAB11A traffics these channels to the apical membrane via direct cargo interaction in the GDP-bound state. |
Co-immunoprecipitation, colocalization, dominant-negative GDP-locked RAB11A expression, Ca2+ uptake assay in epithelial cells |
Molecular and cellular biology |
High |
16354700
|
| 2007 |
RAB11A regulates CFTR recycling in Rab11a-specific apical recycling endosomes in polarized human airway epithelial cells; endogenous CFTR forms a complex with endogenous myosin Vb and Rab11a, and silencing myosin Vb or expressing a myosin Vb tail fragment (whose dominant-negative effect requires the ability to interact with RAB11A) decreases apical CFTR and Cl- secretion. |
Co-immunoprecipitation of endogenous proteins, RNAi knockdown, dominant-negative myosin Vb tail fragment, CFTR Cl- secretion assay in polarized airway epithelial cells |
The Journal of biological chemistry |
High |
17462998
|
| 2009 |
RAB11A and heat shock protein HSP90 interact; rab11a regulates resecretion of extracellular alpha-synuclein in neurons (recycling endosome-mediated pathway), and HSP90 inhibitor geldanamycin prevents resecretion and attenuates neurotoxicity. |
Quantitative proteomic analysis, co-immunoprecipitation of Rab11a and HSP90, pharmacological inhibition of HSP90, resecretion assay in neurons |
The Journal of neuroscience |
Medium |
19193894
|
| 2010 |
RAB11A controls trafficking of TLR4 from the endocytic recycling compartment (ERC) to E. coli phagosomes; RAB11A silencing reduces TLR4 on phagosomes, inhibits IRF3 signaling pathway (interferon-β induction) induced by E. coli, and reduces TRAM on phagosomes, without affecting NF-κB activation. |
siRNA knockdown of Rab11a; confocal colocalization; TLR4/TRAM phagosome recruitment assay; IRF3 activation and IFN-β reporter assays in macrophages |
Immunity |
High |
20933442
|
| 2011 |
RAB11A is indispensable for transport of influenza A virus vRNPs to the plasma membrane; RAB11A associates with vRNPs throughout cytoplasmic transport and forms a complex with vRNPs biochemically; siRNA depletion or dominant-negative/constitutively active RAB11A expression causes aberrant vRNP accumulation in the perinuclear region and prevents plasma membrane delivery. |
siRNA knockdown, dominant-negative and constitutively active RAB11A overexpression, immunofluorescence, co-immunoprecipitation of RAB11A with vRNPs |
Journal of virology |
High |
21525351
|
| 2018 |
RAB11A-positive recycling endosome membranes serve as the primary platform for autophagosome assembly; WIPI2 localizes to autophagosome precursors by binding RAB11A in concert with PI3P formed on RAB11A-positive membranes upon starvation; loss of RAB11A impairs recruitment of autophagic machinery and autophagy of the transferrin receptor and damaged mitochondria. |
RAB11A knockout/knockdown, WIPI2-RAB11A co-localization and binding assays, PI3P detection on RAB11A membranes, autophagy flux assays (transferrin receptor, mitophagy), live imaging |
Developmental cell |
High |
29634932
|
| 2014 |
TBC1D9B functions as a GTPase-activating protein (GAP) for RAB11A in polarized MDCK cells; TBC1D9B interacts with RAB11A in a nucleotide-dependent manner, specifically stimulates GTP hydrolysis by RAB11A (not Rab11b or Rab4a at physiological Mg2+), colocalizes with Rab11a-positive recycling endosomes, and its overexpression (but not inactive mutant) decreases basolateral-to-apical IgA transcytosis while shRNA depletion increases this Rab11a-dependent pathway. |
GTPase activity assay (in vitro with purified proteins), co-immunoprecipitation, shRNA knockdown, overexpression of WT and catalytically inactive TBC1D9B, IgA transcytosis assay, active Rab11a pull-down |
Molecular biology of the cell |
High |
25232007
|
| 2009 |
RAB11A forms a tripartite complex with myosin Vb and Rab11-FIP2; the myosin Vb·RAB11A·Rab11-FIP2 complex is required for cholesterol-regulated translocation of NPC1L1 from the endocytic recycling compartment to the plasma membrane; dominant-negative mutants of any component inhibit NPC1L1 export and decrease cellular cholesterol uptake. |
Dominant-negative mutant expression, RNAi, co-immunoprecipitation, cholesterol uptake assay, NPC1L1 surface trafficking assay |
The Journal of biological chemistry |
High |
19542231
|
| 2014 |
RAB11A deficiency in intestinal epithelial cells causes accumulation of apical proteins in cytoplasm and mislocalisation to basolateral membranes, shortened microvilli and microvillus inclusion bodies; RAB8A is mislocalised in Rab11a-KO mice and vice versa, demonstrating a functional interdependence between RAB11A, RAB8A, and myosin Vb in intestinal apical polarity. |
Conditional intestinal Rab11a-knockout mice; immunofluorescence; electron microscopy; complementary analysis of Rab8a-KO mice and myosin Vb mutant patient tissue |
Biology open |
High |
25527643
|
| 2013 |
RAB11A directly interacts with Reggie-1/Flotillin-2 at the tubulovesicular recycling compartment; knockdown of reggie-1 reduces association of Rab11a with tubular structures and impairs transferrin receptor recycling and E-cadherin recycling; these defects are rescued by constitutively active Rab11a, placing Reggie-1 as a regulator of the RAB11A-dependent recycling pathway. |
Co-immunoprecipitation (direct interaction of Reggie-1 with Rab11a), shRNA knockdown, constitutively active Rab11a rescue, calcium-switch E-cadherin recycling assay, transferrin recycling assay |
Molecular biology of the cell |
High |
23825023
|
| 2014 |
RAB11A and myosin Vb regulate phosphorylation of ezrin at T567 in enterocytes; dominant-negative Rab11a or myosin Vb depletion prevents subapical enrichment of Rab11a, co-distributing ezrin kinases, and inhibits ezrin phosphorylation and microvilli development, suggesting RAB11A-positive recycling endosomes serve as signaling platforms for ezrin activation. |
Dominant-negative Rab11a expression, myosin Vb RNAi, immunofluorescence, phospho-ezrin (T567) detection in enterocyte models and microvillus inclusion disease patient samples |
Journal of cell science |
High |
24413175
|
| 2014 |
MYO5B uncoupling from RAB11A (but not RAB8A) induces formation of microvillus inclusions; the RAB11A-MYO5B interaction is required for preventing microvillus inclusion formation in enterocytes, while the RAB8A-MYO5B interaction is required for microvilli establishment. |
Stable MYO5B knockdown in CaCo2-BBE cells; expression of MVID-associated MYO5B-P660L mutant; surface biotinylation; dual immunofluorescence; expression of RAB-binding domain mutants |
The Journal of clinical investigation |
High |
24892806
|
| 2014 |
Global Rab11a knockout in mice causes peri-implantation lethality; Rab11a vesicular trafficking is required for secretion of multiple soluble matrix metalloproteinases (MMPs) from embryonic fibroblasts. |
Global Rab11a-null mice; multiple cargo trafficking assays including MMP secretion assays; complementation analysis in Rab11a-null MEFs |
The Journal of biological chemistry |
High |
25271168
|
| 2014 |
RAB11A-positive endosome trafficking is controlled by LMTK1 in neurons; LMTK1 knockout increases prevalence, velocity, and run length of anterograde Rab11A-positive endosomes, promoting dendrite growth; a non-phosphorylatable LMTK1 mutant (Ser34Ala, a Cdk5 phosphorylation site) dramatically promotes dendritic formation, indicating a Cdk5-LMTK1-RAB11A pathway regulates dendritic development. |
LMTK1 knockout neurons; live imaging of RAB11A-positive endosome dynamics; LMTK1 Ser34Ala mutant expression; in vivo and in vitro dendrite morphometry |
Molecular biology of the cell |
High |
24672056
|
| 2019 |
TBC1D9B, a RAB11A GAP, is a LMTK1-binding protein; LMTK1 controls the GAP activity of TBC1D9B on RAB11A; TBC1D9B mediates LMTK1 activity on RAB11A to regulate dendritic spine formation, defining a Cdk5-LMTK1-TBC1D9B-RAB11A cascade. |
Yeast two-hybrid, co-immunoprecipitation; TBC1D9B knockdown in primary neurons; spine density morphometry; in vitro kinase assays |
The Journal of neuroscience |
High |
31628178
|
| 2015 |
RAB11A mediates VE-cadherin recycling and controls endothelial barrier function; VE-cadherin directly interacts with Rab11-FIP2 (at aa 453-484) forming a ternary complex with RAB11A; silencing RAB11A or Rab11-FIP2 prevents VE-cadherin recycling and its plasma membrane expression, blocks junctional reannealing after inflammation, and in vivo RAB11A knockdown in pulmonary microvessels increases vascular leakage. |
Yeast two-hybrid, co-immunoprecipitation, calcium-switch assay, cell surface biotinylation, flow cytometry, RNAi, in vivo Rab11a knockdown in mouse lung |
Arteriosclerosis, thrombosis, and vascular biology |
High |
26663395
|
| 2015 |
RAB11A regulates apical localization of syntaxin 3 in enterocytes; Rab11a deficiency (conditional KO or stable KD in CaCo2-BBE cells) alters syntaxin 3 apical localization, shortens microvillar length, and causes lateral membrane microvilli formation. |
Conditional intestinal Rab11a-KO mice, stable Rab11a-KD CaCo2-BBE cells, immunofluorescence for syntaxin 3 and apical markers |
Journal of cell science |
High |
25673875
|
| 2015 |
Huntingtin (HTT) forms a complex with PAR3, aPKC, and RAB11A and ensures microtubule-dependent apical vesicular transport of PAR3-aPKC through RAB11A, establishing epithelial polarity during mammary morphogenesis. |
Co-immunoprecipitation (HTT with PAR3, aPKC, RAB11A), conditional HTT depletion in mammary epithelium in vivo, live imaging of vesicular transport, dominant-negative RAB11A rescue experiments |
PLoS biology |
High |
25942483
|
| 2017 |
Endothelin-1 stimulates PKC-mediated phosphorylation of RAB11A at serine 177, which inhibits RAB11A activity and reduces RAB11A-dependent surface trafficking of BK channel β1 subunits in arterial smooth muscle cells, leading to BK channel inhibition and vasoconstriction; expression of phosphorylation-incapable Rab11A S177A blocks the ET-1 effect. |
PKC inhibitors, phosphorylation-incapable (S177A) and phosphomimetic RAB11A mutants, surface protein quantification, single BK channel recordings, myography for vasoconstriction in cerebral arteries |
Circulation research |
High |
28696251
|
| 2020 |
The C9ORF72-SMCR8-WDR41 complex functions as a GTPase-activating protein (GAP) for RAB8A and RAB11A; cryo-EM structure at 3.2 Å reveals that Arg147 of SMCR8 is the arginine finger critical for stimulating GTP hydrolysis by Rab8a and Rab11a. |
Cryo-EM structure determination (3.2 Å); biochemical GTPase activity assays; site-directed mutagenesis of Arg147; structural comparison with FLCN-FNIP2 GAP complex |
Proceedings of the National Academy of Sciences of the United States of America |
High |
32303654
|
| 2008 |
RAB11A directly interacts with the carboxyl-terminal tail of the human prostacyclin receptor (hIP); this interaction was mapped to Val299-Gln320 of the hIP C-tail and is augmented by agonist stimulation; overexpression of RAB11A increases hIP recycling to the plasma membrane, while dominant-negative Rab11a S25N impairs it. |
Yeast two-hybrid screen, co-immunoprecipitation in HEK293 and endothelial cells, dominant-negative/wild-type overexpression, receptor recycling assay |
Cellular signalling |
High |
18832025
|
| 2007 |
RAB11A controls the biogenesis of Birbeck granules (BGs) by regulating Langerin recycling and stability; dominant-negative Rab11A or Rab11A depletion missorts Langerin to lysosomes and blocks BG formation; loss of RCP (a Rab11A effector) also modestly affects Langerin stability and BG biogenesis, indicating a RAB11A-RCP complex mediates these events. |
Dominant-negative Rab11A overexpression, Rab11A siRNA knockdown, RCP knockdown, immunofluorescence tracking of Langerin, electron microscopy for BG biogenesis |
Molecular biology of the cell |
High |
17538027
|
| 2008 |
RAB11A undergoes agonist-dependent regulated exocytosis of discoidal/fusiform vesicles (DFVs) in bladder umbrella cells; constitutively active Rab11a stimulates increased apical surface area without stretch, while dominant-negative Rab11a inhibits stretch-induced exocytosis; secretory cargo (hGH) is packaged into Rab11a-positive DFVs and its release depends on Rab11a activity. |
Adenoviral delivery of dominant-active and dominant-negative Rab11a mutants in situ; apical surface area measurements; hGH secretion assay; fluid and membrane endocytosis tracers |
Proceedings of the National Academy of Sciences of the United States of America |
High |
18843107
|
| 2013 |
RAB11A acts upstream of RAB8A to promote stretch-induced exocytosis of DFVs in bladder umbrella cells; Rabin8 (a Rab11A effector and GEF for Rab8) stimulates exocytosis independently of its catalytic activity; myosin 5B works with the Rab8a-Rab11a module to promote DFV transit through the subapical actin cytoskeleton before fusion. |
Dominant-negative and constitutively active Rab GTPase expression, catalytically inactive Rabin8 expression, dominant-negative myosin 5B tail, exocytosis quantification in umbrella cells |
Molecular biology of the cell |
High |
23389633
|
| 2008 |
Gβγ subunits interact with RAB11A and colocalize at recycling endosomes in response to LPA receptor activation; this Gβγ-RAB11A interaction recruits PI3K and promotes AKT phosphorylation at endosomal compartments; dominant-negative RAB11A or wortmannin (PI3K inhibitor) attenuates LPA-induced AKT activation and cell survival/proliferation. |
Co-immunoprecipitation (Gβγ with Rab11a), confocal colocalization, dominant-negative Rab11a expression, wortmannin treatment, AKT phosphorylation assay, RNAi depletion of Rab11a |
Molecular biology of the cell |
High |
18701709
|
| 2006 |
RAB11A regulates EGFR recycling; transfection of RAB11A accelerates EGFR recycling while dominant-negative Rab11aS25N postpones EGFR recycling in MCF10A breast cells; dominant-negative RAB11A inhibits EGF-stimulated proliferation and anchorage-dependent colonization but increases cell motility toward EGFR ligands. |
Iodinated ligand:receptor recycling assay, dominant-negative RAB11A transfection, proliferation and motility assays, ERK1/2 and AKT signaling assays |
Breast cancer research and treatment |
Medium |
16791477
|
| 2009 |
RAB11A-positive recycling endosomes regulate apoptotic cell death signaling by diverting recycling endosome trafficking to the Golgi apparatus via a pathway involving Src-family kinases, Cdc42, and Rab11a; inhibition of this pathway blocks Golgi fragmentation and caspase-independent cell death progression. |
E4orf4 model, pharmacological inhibition of SFKs and Cdc42, dominant-negative Rab11a, live-cell imaging of Golgi dynamics, cell death assays |
Molecular biology of the cell |
Medium |
19641023
|
| 2006 |
Insulin stimulates transient GTP-loading of RAB11A in cardiomyocytes in a PI3-kinase- and Akt-dependent manner (2.3-fold activation peaking at 4 min), identifying RAB11A as a direct element of the insulin-regulated GLUT4 trafficking machinery. |
Biotinylated GTP-analog incorporation assay in H9c2-hIR cells expressing HA-tagged Rab11a, PI3K inhibitor treatment, Akt RNAi knockdown |
Cellular signalling |
Medium |
17158030
|
| 2014 |
The RAB11A tripartite complex with Rab11-FIP2 and MYO5B requires specific residues (S229 and G233 in FIP2) for FIP2-MYO5B interaction; mutation of these residues or Rab11-FIP2 knockdown increases speed and track length of RAB11A-containing vesicle movement, consistent with impaired MYO5B tethering at the cytoskeleton. |
Random mutagenesis of Rab11-FIP2, yeast two-hybrid, co-immunoprecipitation, live-cell imaging of Rab11a vesicle movement in HeLa and MDCK cells |
Traffic (Copenhagen, Denmark) |
High |
24372966
|
| 2012 |
The MYO5B/RAB11A/Rab11-FIP2 complex platform operates at two distinct spatial sites in live cells: first at the ERC sorting site where transport vesicles form, and subsequently at the docking/tethering/fusion stage at the plasma membrane, as demonstrated for langerin cargo trafficking. |
Live-FRET, fast FRAP video, fast confocal, and TIRF microscopy of MYO5B/Rab11A/Rab11-FIP2 complex dynamics in live cells with langerin as cargo |
Traffic (Copenhagen, Denmark) |
High |
22420646
|
| 2019 |
RAB11A binding to the globular tail domain (GTD) of Myosin-5b abolishes the head-GTD autoinhibitory interaction of Myo5b, thereby activating its motor function; FIP2 bridges Myo5b and membrane-bound RAB11A (with higher affinity for FIP2 than for Myo5b), with FIP2 binding not affecting Myo5b motor activity. |
In vitro binding and ATPase assays with purified proteins; affinity measurements for Rab11a-FIP2 and Rab11a-Myo5b interactions |
Bioscience reports |
High |
30545898
|
| 2016 |
RAB11A is essential for lamellar body biogenesis in the human epidermis; Rab11a silencing in 3D reconstructed human epidermis reduces lamellar body density and secretion, misdirects lamellar body cargoes to the lysosomal degradation pathway, and causes an epidermal barrier defect. |
Rab11a siRNA in 3D reconstructed human epidermis, electron microscopy, immunofluorescence, barrier function assay, lipid quantification in stratum corneum |
The Journal of investigative dermatology |
High |
26872604
|
| 2017 |
RAB11A inactivation in macrophages facilitates efferocytosis of apoptotic neutrophils by increasing surface CD36; Rab11a knockdown increases surface CD36 and decreases surface ADAM17, while overexpression of wild-type Rab11a inhibits efferocytosis; ADAM17 depletion rescues the decreased CD36 in cells overexpressing wild-type Rab11a, placing RAB11A upstream of ADAM17-mediated surface expression of CD36. |
siRNA knockdown, wild-type and dominant-negative Rab11a overexpression, ADAM17 depletion, CD36 surface flow cytometry, efferocytosis assays, in vivo intratracheal Rab11a-KD macrophage instillation |
Journal of immunology |
High |
28053235
|
| 2018 |
RAB11A-Rab8a acts in a cascade to regulate formation of tunneling nanotubes (TNTs); overexpression of Rab11a and Rab8a increases TNT-connected cells and vesicle propagation between cells; RAB11A activates Rab8a independently of the GEF Rabin8; VAMP3 acts downstream of Rab8a in TNT formation. |
Dominant-negative and constitutively active Rab GTPase expression, RNAi knockdown, live-cell imaging of vesicle transfer, epistasis analysis with catalytically inactive Rabin8 |
Journal of cell science |
High |
30209134
|
| 2017 |
RAB11A controls disruption of Rab8a and Rab11a double-KO mice causes basolateral microvillus formation; inducible Rab11a deletion from neonatal enterocytes alone is sufficient to induce basolateral microvilli within 3 days; distinct apical cargoes require either individual or both Rab8a and Rab11a for apical transport. |
Enterocyte-specific Rab8a/Rab11a double and single conditional KO mice; inducible Rab11a deletion; immunofluorescence; electron microscopy |
Journal of cell science |
High |
28596241
|
| 2021 |
RAB11A-positive vesicles serve as hubs for congregation of influenza A virus vRNP complexes enabling specific genome assembly through vRNP:vRNP interactions; in Rab11a-deficient cells, vRNP bundles are smaller with less co-localization between distinct vRNA segments and more non-infectious particles are produced, indicating RAB11A promotes selective packaging of all 8 genome segments. |
Rab11a-deficient cells (CRISPR/siRNA), fluorescence microscopy with tetracysteine-tagged NP vRNP reporter, vRNA FISH, PFU/genome ratio measurements |
PLoS pathogens |
High |
33970958
|
| 2022 |
The C-terminal domains of the PB2 polymerase subunit of influenza A virus directly interact with RAB11A in solution at 1:1 stoichiometry, mediating vRNP association with RAB11A; the switch I region of RAB11A important for Rab11-FIP binding is also required for PB2-C binding, suggesting IAV polymerase and Rab11-FIPs compete for the same RAB11A binding site. |
Pulldown assays from infected cell lysates, in vitro direct binding assays, SAXS structural analysis of PB2-C/RAB11A complex, site-directed mutagenesis of RAB11A switch I region |
Journal of virology |
High |
35019720
|
| 2021 |
RAB11A controls YAP localization to adherens and tight junctions in intestinal epithelial cells; RAB11A controls biochemical associations of YAP with α-catenin, β-catenin, and Merlin; loss of RAB11A leads to nuclear accumulation of YAP and enhanced YAP-β-catenin complex formation, and RAB11A-deficient mice show reduced epithelial integrity after chemical injury. |
Conditional RAB11A-KO mice; co-immunoprecipitation of YAP with junctional components; immunofluorescence; chemical injury colitis model |
The Journal of biological chemistry |
High |
34058200
|
| 2023 |
RAB11A and RAB11B redundantly control mitotic spindle function in intestinal progenitor cells; double (but not single) KO of Rab11a and Rab11b causes mitotic arrest and apoptosis with abnormal mitotic spindle formation; proteomic profiling of Rab11a/Rab11b immunoprecipitates reveals a shared interactome of mitotic spindle microtubule regulators; disrupting Rab11 impairs kinesin KIF11 function and bipolar spindle formation. |
Single and double conditional KO mice; ex vivo enteroids; untargeted proteomics of RAB11A/B immunoprecipitates; mitotic spindle immunofluorescence; kinesin KIF11 functional assays |
EMBO reports |
High |
37424454
|
| 2013 |
FLCN (Birt-Hogg-Dubé protein) binds to RAB11A through its C-terminal DENN-like domain and promotes loading of the amino acid transporter PAT1 onto RAB11A vesicles for plasma membrane targeting; suppression of either RAB11A or FLCN re-routes PAT1 to lysosomes and down-regulates mTORC1. |
Co-immunoprecipitation, FLCN and Rab11a siRNA knockdown, in vitro GEF activity assay (FLCN does not act as GEF for Rab11a), cargo trafficking assay for PAT1, mTORC1 activity measurement |
Journal of cell science |
Medium |
30446510
|
| 2023 |
Accessory ESCRT-III proteins (CHMP1A, CHMP1B, CHMP5, IST1) are selectively required for formation of ILVs in RAB11A-positive recycling endosomes (Rab11a-exosomes) but are not involved in degradation of ubiquitinylated proteins in late endosomes; CHMP5 knockdown in human HCT116 cells selectively inhibits RAB11A-exosome production. |
Comparative proteomics of human small EVs, Drosophila secondary cell genetics, CHMP5 knockdown in HCT116 cells, EVsecretion assay, ubiquitin-protein degradation assay |
Journal of extracellular vesicles |
High |
36872252
|