| 2006 |
Rab35 localizes to the plasma membrane and endocytic compartments and controls a fast endocytic recycling pathway; inhibition of Rab35 leads to failed cytokinesis with accumulation of endocytic markers on cytoplasmic vacuoles, and Rab35 is required for intercellular bridge localization of PIP2 and septin SEPT2 during cytokinesis. |
Dominant-negative/GTP-locked mutant overexpression, fluorescence microscopy, endocytic marker trafficking assays in human cells |
Current biology : CB |
High |
16950109
|
| 2008 |
In C. elegans, RME-4 (a DENN domain protein) binds RAB-35 in its GDP-loaded conformation and is enriched on clathrin-coated pits; RME-4 recruits RAB-35 to coated pits/vesicles, and RAB-35 in turn promotes receptor recycling from early endosomes. Genetic epistasis shows RME-4 and RAB-35 function downstream of clathrin and upstream of RAB-7, acting synergistically with RAB-11 and RME-1. |
C. elegans genetic screens, yeast two-hybrid, GFP localization, epistasis analysis |
The EMBO journal |
High |
18354496
|
| 2008 |
Rab35 is recruited to the immunological synapse (IS) in T cells; EPI64C (TBC1D10C) functions as a Rab35-GAP both in vitro and in transfection assays. Dominant-negative Rab35 or EPI64C impair transferrin recycling in T cells and TCR enrichment at the IS, and conjugate formation is impaired by both Rab35-DN and EPI64C. |
In vitro GAP assay, transfection of DN constructs, co-localization microscopy, siRNA knockdown in Jurkat T cells |
The Journal of biological chemistry |
High |
18450757
|
| 2009 |
Rab35 directly associates with the actin-bundling protein fascin as an effector; active Rab35 recruits fascin to actin filaments and targeting Rab35 to the outer mitochondrial membrane triggers ectopic actin recruitment. Rab35 regulates actin filament assembly during Drosophila bristle development and filopodia formation in cultured cells. |
Direct binding assay (pulldown), ectopic mitochondrial targeting, Drosophila genetics, cell culture filopodia assay |
Science (New York, N.Y.) |
High |
19729655
|
| 2009 |
Rab35 colocalizes with Cdc42 and can activate Cdc42 both in vivo and in vitro; activated Rab35 stimulates neurite outgrowth in PC12 and N1E-115 cells via a Cdc42-dependent pathway, and siRNA knockdown of Rab35 abolishes neurite outgrowth. |
In vitro Cdc42 activation assay, siRNA knockdown, neurite outgrowth quantification, co-localization microscopy |
FEBS letters |
Medium |
19289122
|
| 2010 |
The DENN domain of connecdenn/DENND1A functions as a guanine nucleotide exchange factor (GEF) for Rab35; loss of Rab35 activity causes enlargement of early endosomes, inhibits MHC class I recycling, and prevents early endosomal recruitment of EHD1. |
In vitro GEF assay, siRNA knockdown, endosome morphology analysis, cargo recycling assay |
Molecular cell |
High |
20159556
|
| 2010 |
Connecdenn 2 (DENND1B) also functions as a Rab35 GEF through its DENN domain; all three connecdenns (DENND1A-C) function as Rab35 GEFs with different activity levels. The DENN domains of connecdenn 1 and 2 bind Rab35, whereas connecdenn 3 does not, showing that Rab35 binding and activation are separable functions. All three connecdenns bind clathrin and AP-2 through their C-termini. |
In vitro GEF assay, yeast two-hybrid, siRNA knockdown, endosome morphology |
The Journal of biological chemistry |
High |
20154091
|
| 2010 |
Rab35 mediates vesicle transport required for phagocytosis in Drosophila; Rab35-dependent recruitment of Cdc42 and Rac1 to sites of filopodium and lamellipodium formation occurs via microtubule tracks. |
Drosophila genetics, live-cell imaging, immunofluorescence in Drosophila S2 cells |
Molecular and cellular biology |
Medium |
20065041
|
| 2011 |
GTP-bound (active) Rab35 directly interacts with OCRL (a PtdIns(4,5)P2 5-phosphatase mutated in Lowe syndrome) and controls its localization at the intercellular bridge during cytokinesis; Rab35 or OCRL depletion inhibits cytokinesis abscission with local PtdIns(4,5)P2 and F-actin accumulation, and OCRL acts as an effector of Rab35 to remodel F-actin for abscission. |
Direct binding assay (GST pulldown), siRNA depletion, PtdIns(4,5)P2 imaging, F-actin quantification, cytokinesis assays in human cells and Lowe patient cell lines |
Nature cell biology |
High |
21706022
|
| 2011 |
MICAL-L1 is a Rab35-binding partner on tubular recycling endosomes; active Rab35 impairs MICAL-L1 recruitment to tubular recycling endosomes while Rab35 depletion promotes enhanced MICAL-L1 localization, indicating Rab35 is an upstream regulator of MICAL-L1. Arf6 also forms a complex with MICAL-L1 for recruitment to tubular endosomes. |
Co-immunoprecipitation, overexpression and depletion studies, fluorescence microscopy |
Traffic (Copenhagen, Denmark) |
Medium |
21951725
|
| 2011 |
Rab35 is required for the early stage of FcγR-mediated phagocytosis in macrophages; active Rab35 recruits ACAP2 (an ARF6 GAP) to the phagocytic cup, and this GTP-Rab35/ACAP2 interaction is required for actin-dependent pseudopod extension and phagosome formation. |
siRNA knockdown, live-cell imaging, expression of GTP/GDP-locked mutants, pulldown assay, co-localization microscopy in macrophages |
Journal of cell science |
High |
22045739
|
| 2011 |
Connecdenn 3 (DENND1C) directly binds actin via a unique C-terminal motif not found in connecdenn 1 or 2, coupling Rab35 activation to the actin cytoskeleton; connecdenn 3 co-localizes with fascin and actin filaments, identifying it as the relevant GEF for Rab35-mediated actin regulation and membrane protrusion formation. |
Direct actin-binding assay, GEF assay, co-localization microscopy, cell morphology analysis |
Molecular biology of the cell |
High |
22072793
|
| 2011 |
A genome-wide RUN domain screen identified RUSC2 as a GTP-Rab35-specific binding protein; the minimal Rab35-binding site of RUSC2 (residues 982-1199) was defined and used to develop RBD35, a GTP-Rab35 trapper that specifically pulls down active Rab35 and inhibits neurite outgrowth when overexpressed. |
Yeast two-hybrid genome-wide screen, in vitro pull-down, PC12 cell overexpression assay |
Cell structure and function |
Medium |
21737958
|
| 2012 |
ARF6 negatively regulates Rab35 activation via the Rab35 GAP EPI64B, which acts as an ARF6 effector; constitutively active ARF6 causes identical endocytic recycling and cytokinesis defects as GDP-Rab35. This ARF6/Rab35 GTPase cascade operates at clathrin-coated pits where activated ARF6 reduces Rab35 loading into the endocytic pathway. |
Constitutively active/inactive mutant expression, GAP activity assays, cytokinesis assays, endocytic recycling assays in human cells |
Current biology : CB |
High |
22226746
|
| 2012 |
Rab35 functions as a Rab35 effector and Arf6-GAP coupling mechanism through centaurin-β2 (ACAP2): Rab35 accumulates at Arf6-positive endosomes upon NGF stimulation and recruits centaurin-β2 in a Rab35-dependent manner; the Arf6-GAP activity of centaurin-β2 at these endosomes is indispensable for NGF-induced neurite outgrowth in PC12 cells. |
siRNA knockdown, rescue experiments, live-cell imaging, co-localization assays in PC12 cells |
Journal of cell science |
High |
22344257
|
| 2012 |
Rab35 suppresses Arf6 activity to downregulate Arf6-dependent recycling of β1-integrin and EGF receptors, while simultaneously maintaining cadherins at the cell surface; Rab35 knockdown promotes cell migration consistent with epithelial-mesenchymal transition by inverting this balance. |
siRNA knockdown, cell adhesion and migration assays, cargo recycling assays, co-immunoprecipitation |
Journal of cell science |
High |
23264734
|
| 2012 |
Rab35 regulates cadherin trafficking and stabilization at cell-cell contacts in myoblasts and HeLa cells; Rab35 is required for N- and M-cadherin recruitment to cell contacts, their association with p120 catenin, and for PIP5KIγ accumulation at contacts for PIP2 production. Rab35 knockdown impairs myoblast fusion. |
siRNA knockdown, dominant-negative expression, fluorescence microscopy, co-immunoprecipitation, myoblast fusion assay |
Molecular biology of the cell |
High |
23197472
|
| 2012 |
In Drosophila tracheal terminal cells, Rab35 and its apical membrane-localized GAP Whacked polarize seamless tube growth along the proximodistal axis; loss of Whacked (or constitutive Rab35 activation) leads to tube overgrowth at branch tips, while overexpression of Whacked or dominant-negative Rab35 causes ectopic tubes near the nucleus. |
Drosophila genetics (loss-of-function mutants), live imaging, epistasis analysis |
Nature cell biology |
High |
22407366
|
| 2012 |
TBC1D13 functions as a Rab35-specific GAP in vitro; overexpression of constitutively active Rab35 (but not Rab10) reverses the TBC1D13-dependent block in insulin-stimulated GLUT4 translocation in adipocytes, implicating Rab35 in the insulin-stimulated GLUT4 trafficking pathway. |
In vitro GAP activity screen, yeast two-hybrid, constitutively active mutant rescue, GLUT4 translocation assay in adipocytes |
Traffic (Copenhagen, Denmark) |
High |
22762500
|
| 2014 |
Rab35 promotes neurite outgrowth via MICAL-L1 as a scaffold: Rab35 determines the intracellular localization of MICAL-L1, which in turn recruits Rab8, Rab13, and Rab36 to Arf6-positive recycling endosomes. Each downstream Rab regulates neurite outgrowth non-redundantly downstream of Rab35 and MICAL-L1. |
Functional ablation (siRNA), rescue experiments, co-localization microscopy, neurite outgrowth quantification in PC12 cells |
Biology open |
High |
25086062
|
| 2014 |
Rab35 and its effector ACAP2 negatively regulate oligodendrocyte differentiation and myelination by inactivating Arf6; as differentiation initiates, Rab35 and ACAP2 activities decrease while Arf6 activity increases. Arf6 knockdown inhibits differentiation, placing Rab35/ACAP2 upstream of Arf6 in a GTPase switching mechanism. |
siRNA knockdown, GTPase activity assays, morphological differentiation scoring, myelination co-culture |
Molecular biology of the cell |
High |
24600047
|
| 2015 |
Rab35 is activated on newborn endosomes immediately after CCV scission via precise spatial-temporal loading: DENND1A is recruited first, then EPI64B disappears, allowing Rab35 activation; active Rab35 then directly recruits the OCRL phosphatase for post-scission PtdIns(4,5)P2 hydrolysis. Depletion of Rab35 or OCRL leads to retention of CI-MPR in peripheral clathrin-positive PtdIns(4,5)P2-rich endosomes. |
Live TIRF microscopy, siRNA depletion, cargo trafficking assays, direct binding assay, PtdIns(4,5)P2 imaging |
Current biology : CB |
High |
26725203
|
| 2015 |
Rab35 controls endosomal sorting of clathrin-independent endocytosis (CIE) cargo; Rab35 delivered via clathrin-mediated endocytosis inactivates Arf6 through ACAPs (Arf6 GAPs), maintaining tubular endosomal networks and preventing lysosomal degradation of CIE cargos (CD44, CD98, CD147). siRNA knockdown of Rab35 recreates the altered trafficking phenotype of CME inhibition. |
siRNA knockdown, CME inhibition, cargo trafficking assays, Arf6-GTP measurement, rescue by Rab35 or ACAPs expression |
Traffic (Copenhagen, Denmark) |
High |
25988331
|
| 2015 |
Two threonine residues (Thr-76 and Thr-81) in the switch II region of Rab35 are specifically required for binding ACAP2 (centaurin-β2) but dispensable for other Rab35 interactions; two asparagine residues (Asn-610 and Asn-691) in ACAP2 are key for Rab35 recognition. Binding-deficient mutants of either protein fail to support neurite outgrowth in PC12 cells. |
Deletion/point mutagenesis, pulldown assays, knockdown-rescue in PC12 cells |
The Journal of biological chemistry |
High |
25694427
|
| 2016 |
Rab35 directly couples cytokinesis with initiation of apico-basal polarity in 3D MDCK cyst cultures by tethering intracellular vesicles containing apical determinants (aPKC, Cdc42, Crumbs3, Podocalyxin) at the cleavage site through a direct interaction between Rab35 and the cytoplasmic tail of Podocalyxin. Rab35 inactivation leads to complete polarity inversion in 3D cysts. |
3D MDCK cyst cultures, dominant-negative expression, direct binding (pulldown), co-localization microscopy, polarity marker imaging |
Nature communications |
High |
27040773
|
| 2016 |
Neuronal activity drives Rab35 activation and binding to the ESCRT-0 protein Hrs, identified as a novel Rab35 effector; Rab35 activation and Hrs binding recruit downstream ESCRT machinery to synaptic vesicle pools to initiate activity-dependent SV protein degradation. |
Co-immunoprecipitation, siRNA knockdown, live-cell imaging, neuronal activity stimulation in rat hippocampal neurons |
The Journal of neuroscience : the official journal of the Society for Neuroscience |
High |
27535913
|
| 2016 |
Rab35 promotes axon elongation in primary neurons; PRPK (p53-related protein kinase) negatively regulates axonal elongation by targeting Rab35 for ubiquitin-proteasome degradation, and MAP1B interacts with PRPK to prevent this degradation. Rab35 also regulates Cdc42 activity in neurons. |
siRNA knockdown, ubiquitin-proteasome pathway assays, MAP1B KO neurons, rescue by Rab35 overexpression or PRPK inactivation, epistasis analysis |
The Journal of neuroscience : the official journal of the Society for Neuroscience |
High |
27383602
|
| 2016 |
Rab35 in Drosophila epithelium is dynamically planar-polarized, enriched at contractile interfaces of intercalating cells; disruption of Rab35 function allows oscillations but prevents ratchet-like stabilization of contractions, so interfaces fail to shorten. Rab35 compartment initiation does not require Myosin II but compartments fail to terminate without actomyosin. |
Drosophila genetics, live imaging, dominant-negative expression, Myosin II perturbation |
Nature communications |
High |
28883443
|
| 2017 |
GTP-bound Rab35 directly binds and recruits the autophagy receptor NDP52 to bacteria-containing endosomes and promotes NDP52 interaction with ubiquitin; TBC1D10A (GAP) inhibits this process while TBK1 (associated with NDP52) stimulates it. Rab35 also promotes NDP52 recruitment to damaged mitochondria and autophagosomes for mitophagy and autophagosome maturation. |
Direct binding assay, Co-IP, siRNA knockdown, bacterial infection model, mitophagy assay |
The EMBO journal |
High |
28848034
|
| 2017 |
Rab35 is required for evoked Weibel-Palade body (WPB) exocytosis in endothelial cells; TBC1D10A is its GAP in this context. Rab35 acts through ACAP2 as an effector, and ACAP2 negatively regulates WPB exocytosis, while Arf6 (downstream of ACAP2) supports exocytosis. |
Genome-wide RabGAP screen, RabGAP overexpression, pulldown, co-IP, siRNA knockdown, WPB exocytosis assay |
The Journal of biological chemistry |
High |
28566286
|
| 2018 |
LRRK2 kinase phosphorylates RAB35 to modulate α-synuclein propagation; the PD-linked G2019S mutation in LRRK2, which increases kinase activity, enhances α-synuclein propagation efficiency. Constitutive activation of RAB35 overrides reduced α-synuclein propagation in lrk-1 mutant C. elegans, placing RAB35 downstream of LRRK2 in this pathway. |
Cell culture, C. elegans genetics, rodent model, LRRK2 kinase inhibitor treatment, phosphorylation assays, epistasis |
Nature communications |
High |
30150626
|
| 2018 |
RAB35 is required for apoptotic cell recognition and phagosome maturation in C. elegans as a third, parallel pathway to CED-1 and CED-5; RAB-35 promotes the phagosomal PI(4,5)P2-to-PI(3)P shift and recruits RAB-5 to phagosomal surfaces. GEFs FLCN-1 and RME-4, and GAP TBC-10, regulate RAB-35 in this context. |
C. elegans genetic screen, epistasis analysis, phosphoinositide imaging, phagosome maturation assays |
PLoS genetics |
High |
30138370
|
| 2018 |
In C. elegans linker cell-type death (LCD), RAB-35 GTPase coordinates competitive phagocytosis onset and cell degradation; RAB-35 binds CNT-1, an ARF-6 GAP, and removes ARF-6 from phagosome membranes, facilitating PI(4,5)P2 removal and promoting phagolysosome maturation. |
Microfluidics-based long-term in vivo imaging, C. elegans genetics, phosphoinositide imaging, epistasis analysis |
Developmental cell |
High |
30220571
|
| 2018 |
RAB35 directly regulates p85/PI3K activity to control oscillatory circular dorsal ruffles (CDRs) required for chemotactic migration; RAB35 is necessary and sufficient for growth factor-induced CDR waves and essential for chemotactic migration and chemoinvasion. |
RNAi screen, live-cell imaging, PI3K activity assay, chemotaxis assay, CDR quantification |
Nature communications |
High |
29662076
|
| 2019 |
Rab35 controls cilium length, function, and membrane composition; Rab35 localizes to cilia along with its GEF (DENND1B) and GAP (TBC1D10A) regulators. Rab35 promotes ciliary targeting of Smoothened, limits ciliary accumulation of Arl13b and INPP5E, regulates ciliary PI(4,5)P2 levels, and interacts with Arl13b. Loss of Rab35 causes left-right asymmetry defects in zebrafish. |
siRNA knockdown, morpholinos (zebrafish), knockout, GFP localization, ciliary membrane composition analysis |
EMBO reports |
High |
31432619
|
| 2019 |
IL-17A induces recruitment of Rab35 and DENND1C (GEF) to the IL-17R/Act1 complex in airway smooth muscle cells, activating Rab35; Rab35 activation is required for PKCα activation and fascin phosphorylation at Ser39, allowing F-actin/myosin stress fiber formation and enhanced smooth muscle contraction. |
Co-IP, siRNA knockdown, PKCα inhibitor treatment, actin stress fiber imaging, muscle contraction assay |
Journal of immunology (Baltimore, Md. : 1950) |
High |
30683702
|
| 2020 |
Rab35 controls myelin growth by forming a complex with myotubularin-related PI 3-phosphatases MTMR13 and MTMR2; Rab35-dependent lipid turnover by myotubularins downregulates PI 3-phosphate levels and mTORC1 activity. Targeted disruption of Rab35 causes elevated PI 3-phosphates, hyperactivation of mTORC1, and focal hypermyelination in vivo, rescued by pharmacological inhibition of PI(3,5)P2 synthesis or mTORC1. |
Co-IP (complex formation), in vivo Rab35 knockout, PI phospholipid measurement, mTORC1 activity assay, pharmacological rescue |
Nature communications |
High |
32503983
|
| 2020 |
The C-terminal polybasic cluster (approximately 30 amino acids) of Rab35 is critical for its plasma membrane localization; reducing the number of basic amino acids in this region shifts Rab35 localization from the plasma membrane to the Golgi membrane. |
Rab35-Rab10 chimera constructs, confocal microscopy of EGFP-fused chimeras |
Acta histochemica et cytochemica |
Medium |
32873993
|
| 2020 |
Rab35 promotes tunneling nanotube (TNT) formation and TNT-mediated vesicle transfer in neuronal cells; Rab35-GTP, ACAP2, ARF6-GDP, and EHD1 act in a cascade to promote TNT formation, while MICAL-L1 (required for neurite outgrowth) is not required for TNTs, indicating distinct pathway branching. |
Overexpression of GTP/GDP-locked mutants, dominant-negative expression, TNT quantification, vesicle transfer assay |
Scientific reports |
Medium |
33033331
|
| 2021 |
BAG3 interacts with TBC1D10B (EPI64B, the Rab35 GAP) via a BAG3-HSP70-TBC1D10B complex that attenuates TBC1D10B's ability to inactivate RAB35; this supports RAB35 activation and HRS recruitment to initiate ESCRT-mediated endosomal tau clearance. BAG3-TBC1D10B colocalization is reduced in AD brains. |
Mass spectrometry (BAG3 interactome), Co-IP, live-cell imaging, BAG3 overexpression in P301S tau transgenic mice, IHC in human AD brains |
Biological psychiatry |
High |
35000752
|
| 2021 |
Rab35 negatively regulates Aβ production by sorting APP and BACE1 out of the endosomal network; Rab35 coordinates distinct trafficking steps for BACE1 and APP mediated by its effectors OCRL and ACAP2, respectively. Rab35 overexpression prevents amyloidogenic trafficking of APP and BACE1 induced by high glucocorticoid levels. |
Overexpression and knockdown, APP/BACE1 localization assays, Aβ production measurement, dominant-negative effector expression |
Cell death & disease |
High |
34876559
|
| 2021 |
Rab35 regulates insulin secretion in pancreatic β cells and interacts with phogrin (a marker of insulin granule exocytosis); Rab35 overexpression promotes insulin secretion and decreases phogrin expression, while Rab35 silencing inhibits insulin secretion and causes phogrin redistribution. The Rab35/phogrin interaction was confirmed by GST pulldown, co-IP, and co-localization. |
GST pulldown, co-IP, co-localization microscopy, insulin secretion assay in β-TC-6 cells |
Clinical and experimental pharmacology & physiology |
Medium |
34448213
|
| 2023 |
PI(4,5)P2 recruits Rab35 to migrasome formation sites by interacting with the C-terminal polybasic cluster of Rab35; active Rab35 then promotes migrasome formation by recruiting and concentrating integrin α5 at these sites, likely via direct Rab35-integrin α5 interaction. |
Live imaging, PI(4,5)P2 manipulation, Rab35 mutant expression, integrin α5 co-localization and pulldown |
Cell research |
High |
37142675
|
| 2023 |
DENND2B functions as a Rab35 GEF that recruits and activates Rab35 at the intercellular bridge (ICB) during cytokinesis; DENND2B's N-terminal region also interacts with active Rab35, making it both a GEF and effector. Knockdown of DENND2B delays abscission, causes multinucleation, F-actin accumulation at the ICB, impairs ESCRT-III recruitment, forms chromatin bridges, and activates the Aurora B NoCut/abscission checkpoint. |
GEF activity assay, Co-IP, siRNA knockdown, cytokinesis assays, ESCRT-III imaging, Aurora B activation measurement |
Cell reports |
High |
37454296
|
| 2023 |
The Chlamydia trachomatis effector CpoS interacts with Rab35 to suppress STING-dependent type I interferon responses; depletion of Rab35 phenocopies exacerbated interferon responses seen during CpoS-deficient infection, and CpoS mediates transport of sphingolipids to the inclusion via Rab GTPase interaction. |
Genetic complementation with CpoS variants, Rab35 siRNA knockdown, interferon response measurement, lipid transport assay |
mBio |
Medium |
37530528
|
| 2023 |
DENND1A and folliculin (FLCN) function as distinct Rab35 GEFs in different cellular contexts: in 3D MDCK cysts, only DENND1A knockout phenocopies Rab35 KO for podocalyxin (PODXL) mis-sorting, while FLCN knockdown phenocopies Rab35 KD in 2D cultures. The FLCN-Rab35-OCRL and DENND1A-Rab35-ACAP2 axes define two distinct functional cascades. |
siRNA knockdown, CRISPR knockout, PODXL trafficking assays in 2D and 3D MDCK cultures |
The Journal of biological chemistry |
High |
31992598
|
| 2023 |
USP32, a deubiquitylase, binds Rab35 and protects it from proteasomal degradation by reducing K48-ubiquitination; ETV1 transcription factor promotes USP32 expression in GISTs, and loss of Rab35 decreases exosome secretion and transmission of imatinib resistance. |
Co-IP, iTRAQ proteomics, ubiquitin assays, knockdown/overexpression, exosome quantification |
Oncogene |
High |
36725886
|
| 2024 |
A homozygous missense variant R27H in the GTPase fold of RAB35 causes a neurodevelopmental disorder; functional analysis shows R27H-Rab35 has enhanced interaction with its GEF DENND1A and decreased interaction with effector MICAL1, indicating an inactive conformation. R27H expression activates Arf6 (under negative Rab35 control), delays cytokinesis, and alters primary cilia length, number, and Arl13b composition. |
Exome sequencing, in vitro binding assays (GEF and effector interactions), Arf6 activation assay, cytokinesis assay, primary cilia analysis in patient variant |
The Journal of biological chemistry |
High |
38432637
|
| 2024 |
The Shigella effector IcsB post-translationally acylates Rab35 in its polybasic region (lysine Nε-fatty acylation), non-canonically entrapping Rab35 at the bacterial-containing vacuole (BCV); Rab35 and IcsB are required not for initial BCV breakage but for unwrapping damaged BCV remnants from Shigella after vacuolar rupture. |
STED super-resolution microscopy, bacterial genetics (IcsB mutants), post-translational modification analysis, infection assays |
Cell reports |
High |
38568808
|
| 2024 |
Congenital Rab35 knockout in mice causes embryonic lethality at E7.5; brain-specific Rab35 knockout causes severe defects in hippocampal lamination due to impaired pyramidal neuron distribution, and these mice show spatial memory and anxiety-related behavioral defects. Loss of RAB35 affects other RAB proteins associated with endocytic trafficking and cell adhesion molecules including contactin-2. |
Rab35 knockout mice (congenital and brain-specific), quantitative proteomics, behavioral testing, histology |
Communications biology |
High |
37085665
|
| 2024 |
Retromer directly associates with the RAB35 regulator TBC1D13 at the endosomal retrieval sub-domain, revealed by proximity proteomics and X-ray crystallography combined with biochemical validation, indicating Retromer is a hub for RAB35 GTPase cycle regulation at endosomes. |
Comparative proximity proteomics, X-ray crystallography, in silico predictions, biochemical validation |
bioRxivpreprint |
Medium |
bio_10.1101_2024.11.22.622898
|
| 2024 |
MICAL1, activated by Rab35 at HIV-1 budding sites, locally depolymerizes branched actin networks to promote HIV-1 budding and release; Rab35 is recruited at budding sites and functions in the same pathway as MICAL1, and both are required for viral release. MICAL1 controls timely ESCRT scission machinery recruitment during budding. |
Super-resolution microscopy, siRNA knockdown, Arp2/3 inhibition rescue, ESCRT recruitment imaging |
bioRxivpreprint |
Medium |
bio_10.1101_2024.10.07.616958
|