| 1993 |
Rab17 is the first identified epithelial cell-specific small GTPase, expressed in kidney, liver, and intestine but absent in non-epithelial organs and fibroblasts; it is induced upon mesenchymal-to-epithelial differentiation in the developing kidney and localizes to the basolateral plasma membrane and apical tubules by immunofluorescence and immunoelectron microscopy. |
Northern blot, in situ hybridization, immunofluorescence, immunoelectron microscopy |
The Journal of cell biology |
High |
8486736
|
| 1998 |
Rab17 localizes to the perinuclear recycling endosome in non-polarized BHK-21 cells and to the apical recycling endosome in polarized Eph4 epithelial cells; dominant-negative (GTP-binding defective) and constitutively active (GTPase-defective) Rab17 mutants both specifically increase basolateral-to-apical transcytosis of transferrin receptor and FcLR 5-27 chimeric receptor, and stimulate apical recycling, establishing Rab17 as a regulator of apical recycling endosome traffic. |
Confocal immunofluorescence, expression of GTP-binding and GTPase-defective mutants, transcytosis assays in polarized Eph4 cells |
The Journal of cell biology |
High |
9490718
|
| 1998 |
In polarized MDCK cells co-expressing Rab17 and the polymeric immunoglobulin receptor (pIgR), Rab17 localizes to apical vesicles/tubules accessible to dimeric IgA internalized from both apical and basolateral surfaces; overexpression of Rab17 impairs basolateral-to-apical transcytosis of dimeric IgA, demonstrating a role for Rab17 in regulating transcellular traffic through apical recycling endosomes. |
Stable MDCK cell lines, immunofluorescence morphology, biochemical transcytosis assay with dimeric IgA |
The Journal of biological chemistry |
High |
9624171
|
| 1999 |
In mouse enterocytes, Rab17 colocalizes with IgA primarily along the basolateral plasma membrane and in basolateral endosomes/vesicles, and also in the apical cytoplasm, supporting Rab17 involvement in IgA transcytosis through a glycolipid raft-containing compartment. |
Immunogold electron microscopy, colocalization analysis in intestinal explants |
Gastroenterology |
Medium |
10029620
|
| 2011 |
Rab17 localizes to recycling endosomes and melanosomes in melanocytic cells; siRNA knockdown of Rab17 increases melanosome accumulation at the cell periphery, inhibits filopodia formation (without affecting melanosome maturation or movement), and causes intracellular melanin retention, placing Rab17 downstream of Rab27a in melanosome release via filopodia. |
GFP-Rab17 localization, siRNA knockdown, double knockdown epistasis with Rab27a, quantitative melanin assays, live imaging |
Traffic |
High |
21291502
|
| 2012 |
Rab17 is specifically localized at dendritic growth cones, shafts, filopodia, and mature spines (but not axons) in mouse hippocampal neurons; shRNA knockdown of Rab17 reduces dendrite growth and branching and dramatically decreases dendritic spine number due to impaired filopodia formation, without affecting axon growth. |
shRNA knockdown, immunofluorescence, live imaging in mouse hippocampal neurons |
The Journal of biological chemistry |
High |
22291024
|
| 2012 |
ERK2 (but not ERK1) suppresses expression of Rab17; knockdown of ERK2 increases Rab17 and liprin-β2 expression and inhibits invasive migration of MDA-MB-231 cells, and knockdown of Rab17 rescues invasiveness of ERK2-depleted cells, demonstrating that ERK2 drives invasion by transcriptionally suppressing Rab17. |
ERK1/2 siRNA, re-expression of ERK1 vs ERK2, gene expression arrays, Rab17 siRNA rescue in 3D invasion assays |
Journal of cell science |
High |
22328529
|
| 2013 |
Rabex-5 (a Rab5-GEF) physically interacts with GDP-locked Rab17 (identified by yeast two-hybrid), acts as a GEF for Rab17, and promotes translocation of Rab17 from the cell body to dendrites; shRNA knockdown of Rabex-5 reduces dendritic Rab17 signals and inhibits dendrite morphogenesis, whereas Rab5 knockdown affects both axon and dendrite morphogenesis. |
Yeast two-hybrid with GDP-locked Rab17 mutant, GEF activity assay, shRNA knockdown, immunofluorescence in hippocampal neurons |
The Journal of biological chemistry |
High |
23430262
|
| 2014 |
Rab17 knockdown reduces surface expression of the kainate receptor subunit GluK2 but not AMPA receptor subunit GluA1; Rab17 colocalizes with Syntaxin-4 in dendrites; Rab17 knockdown redistributes Syntaxin-4 from dendrites to axons; constitutively active Rab17 promotes dendritic surface expression of GluK2 by enhancing Syntaxin-4 translocation to dendrites, establishing a Rab17→Syntaxin-4→GluK2 trafficking pathway. |
shRNA knockdown, constitutively active Rab17 overexpression, surface biotinylation, immunofluorescence colocalization in hippocampal neurons |
The Journal of biological chemistry |
High |
24895134
|
| 2014 |
Rab17 is recruited to Group A Streptococcus-containing autophagosome-like vacuoles (GcAVs) from recycling endosomes; dominant-negative Rab17 (N132I) reduces GcAV formation efficiency; overexpression of Rab17 increases transferrin receptor-positive GcAV content; knockdown of upstream activator Rabex-5 similarly reduces GcAV formation, establishing Rab17-mediated recycling endosome membrane supply to autophagosomes during antibacterial autophagy. |
Colocalization microscopy, dominant-negative/overexpression constructs, Rabex-5 knockdown, GcAV formation efficiency quantification |
Cellular microbiology |
Medium |
25052408
|
| 2016 |
Mass spectrometry and immunofluorescence of efferosomes and phagosomes in macrophages showed that efferosomes recruit Rab17, whereas phagosomes do not; Rab17 mediates trafficking of efferocytosed cargo from the phagolysosome to recycling endosomes, bypassing the MHC class II loading compartment and preventing antigen presentation of apoptotic cell-derived antigens. |
Mass spectrometry of isolated vesicles, immunofluorescence colocalization, functional antigen presentation assay |
Cell death & disease |
High |
28005073
|
| 2016 |
Rab17 undergoes monosumoylation (shifting its apparent mass from 25 kDa to 40 kDa), which requires prior prenylation; sumoylated, GTP-bound Rab17 selectively interacts with Syntaxin 2 (but not Syntaxins 3 or 4) in polarized hepatic WIF-B cells; a sumoylation-deficient K68R mutant causes redistribution of Syntaxin 2 and 5'-nucleotidase from the apical membrane to subapical puncta without affecting MRP2 distribution, implicating sumoylated Rab17 in transcytotic vesicle fusion at the apical surface. |
Recombinant adenovirus expression, immunoblotting, sumoylation mutant (K68R), co-immunoprecipitation with syntaxins, immunofluorescence in WIF-B cells |
The Journal of biological chemistry |
High |
26957544
|
| 2018 |
Using polarized hepatic WIF-B cells expressing wild-type, GTP-bound (constitutively active), GDP-bound (dominant-negative), or K68R (sumoylation-deficient) Rab17, rab17 was confirmed to regulate basolateral-to-apical transcytotic vesicle docking and fusion at the apical surface; GTP hydrolysis is required for vesicle delivery; and rab17 acts as a general component of the transcytotic machinery for multiple classes of newly synthesized apical residents. |
Adenoviral expression of rab17 mutants in WIF-B cells, transcytosis assays, vesicle docking/fusion morphology |
Molecular biology of the cell |
High |
30256711
|
| 2019 |
Influenza A virus HA and NA partially colocalize with Rab17-positive apical recycling endosome compartments post-TGN; dominant-negative Rab17 significantly delays HA transport to the plasma membrane; NA moves rapidly with Rab17 in a cholesterol-dependent manner; co-immunoprecipitation showed HA associates with Rab17 in lipid raft fractions, indicating Rab17 mediates apical trafficking of viral envelope proteins via lipid rafts. |
Confocal colocalization, dominant-negative Rab17 expression, live-cell imaging, co-immunoprecipitation, cholesterol depletion (methyl-β-cyclodextrin) |
Frontiers in microbiology |
Medium |
31456775
|
| 2020 |
ALS2 physically interacts with Rab17 but lacks GEF activity toward it; RABGEF1 (Rabex-5) functions as the GEF for Rab17; ALS2 acts downstream of RABGEF1 and regulates maturation of Rab17-residing nascent endosomes (arising via clathrin-independent endocytosis) to EEA1-positive early endosomes; Rab17 localization to recycling endosomes is dependent on Rab11 expression; upon Rac1 activation, Rab17 and ALS2 are recruited to membrane ruffles and early endosomes. |
Yeast two-hybrid, GEF activity assay, knockdown experiments, immunofluorescence, Rac1 activation assay |
Biochemical and biophysical research communications |
Medium |
31959474
|
| 2024 |
RAB17 inhibits ferroptosis in endometrial cancer cells by promoting ubiquitin-proteasome-dependent degradation of transferrin receptor (TFRC); RAB17 expression is upregulated under low-glucose conditions, and the RAB17-TFRC axis limits ferroptosis to promote cancer cell survival during glucose deprivation. |
Overexpression/knockdown, Western blot, ubiquitin-proteasome inhibitor treatment, in vitro and in vivo ferroptosis assays |
Cell death & disease |
Medium |
39242574
|
| 2025 |
In hepatoma-derived Clone 9 cells, rab17 expression induces actin- and cholesterol-dependent lateral membrane protrusions in a GTP-dependent manner; rab17 selectively redistributes invadopodia proteins to protrusion tips, decreasing matrix degradation; rab17 interacts with MAL2 in a GTP-dependent manner; rab17 redirects newly synthesized membrane protein trafficking from Golgi to induced protrusions in a GTP-dependent fashion. |
Adenoviral expression of WT and mutant rab17, actin/cholesterol inhibitors, immunofluorescence, matrix degradation assay, co-immunoprecipitation with MAL2 |
Molecular biology of the cell |
Medium |
39813085
|
| 2025 |
LMO4 promotes ubiquitin-proteasome-dependent degradation of RAB17 in oral squamous cell carcinoma cells; restoration of RAB17 expression reduces LMO4-driven proliferation, migration, and ferroptosis resistance, placing RAB17 downstream of LMO4 as a tumor suppressor subject to post-translational regulation. |
LMO4 knockdown/overexpression, RAB17 rescue experiments, proteasome inhibitor treatment, xenograft model, Western blot |
Cell death & disease |
Medium |
41213908
|