Affinage

RAB29

Ras-related protein Rab-29 · UniProt O14966

Length
203 aa
Mass
23.2 kDa
Annotated
2026-04-28
32 papers in source corpus 22 papers cited in narrative 22 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RAB29 (also known as RAB7L1) is an atypical Rab GTPase that functions at the trans-Golgi network to regulate retrograde membrane trafficking, phagosome maturation, and innate immune signaling. It is constitutively membrane-associated due to geranylgeranylation and additional lipid-independent mechanisms, exhibits rapid intrinsic nucleotide exchange, lacks detectable GTPase activity, and is refractory to conventional GDP-dissociation inhibitors (PMID:9177482, PMID:36116551). RAB29 recruits LRRK2 to the TGN via the LRRK2 ankyrin domain and induces an asymmetric LRRK2 tetramer containing two kinase-active central protomers, thereby stimulating LRRK2-mediated phosphorylation of downstream Rab substrates (Rab8A, Rab10) and controlling TGN integrity, mannose-6-phosphate receptor retrograde trafficking, centrosomal homeostasis, immune synapse assembly, and ciliogenesis (PMID:29212815, PMID:38127736, PMID:24788816, PMID:26021297). RAB29 itself is phosphorylated by LRRK2 at Ser72 and by PKCα/δ at Ser185 under lysosomal stress, is proteolytically cleaved by the Salmonella effector GtgE, and is negatively regulated by the GAP TBC1D9 to control NF-κB–dependent IL-6 production and by mycobacterial PknG acting through RGDI-1 to block phagosome–lysosome fusion (PMID:29223392, PMID:37365944, PMID:22042847, PMID:41306588, PMID:30037848).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1997 Medium

    The first biochemical characterization of Rab29 revealed it to be an atypical Rab with rapid nucleotide exchange but undetectable intrinsic GTPase activity, establishing that its activation cycle differs fundamentally from canonical Rabs.

    Evidence Recombinant protein expression with radiolabeled GTP exchange and GTPase assays, including a C-terminal truncation splice variant

    PMID:9177482

    Open questions at the time
    • No GEF or GAP identified at this stage
    • Cellular function unknown
    • No mammalian cell-based validation of exchange properties
  2. 2011 High

    Identification of Rab29 as a host factor recruited to Salmonella-containing vacuoles and specifically cleaved by the broad-host effector GtgE established RAB29 as a restriction factor whose destruction promotes intracellular bacterial replication.

    Evidence Functional screen for typhoid toxin export factors, proteolytic cleavage assay with GtgE, engineered bacterial strains in human macrophages

    PMID:22042847

    Open questions at the time
    • Cleavage site on Rab29 not mapped
    • Whether Rab29 GTPase cycle status affects GtgE susceptibility unknown
    • Role in phagosome maturation not yet linked to GTP state
  3. 2013 High

    Genetic epistasis across rodent neurons and Drosophila dopamine neurons demonstrated that RAB29 and LRRK2 operate in a common pathway upstream of VPS35/retromer, connecting RAB29 to Parkinson's disease-associated neurodegeneration for the first time.

    Evidence Loss-of-function and overexpression rescue in primary rodent neurons and Drosophila, endolysosomal and Golgi phenotyping

    PMID:23395371

    Open questions at the time
    • Direct physical interaction between RAB29 and LRRK2 not shown
    • Molecular mechanism of pathway ordering unclear
    • VPS35 retromer connection mechanistically indirect
  4. 2014 Medium

    Demonstration that Rab29 is essential for TGN integrity and mannose-6-phosphate receptor retrograde trafficking defined its core vesicle trafficking function at the Golgi.

    Evidence Dominant-negative Rab29T21N expression and shRNA knockdown with M6PR retrograde trafficking and VSV-G anterograde trafficking assays

    PMID:24788816

    Open questions at the time
    • Effectors mediating TGN maintenance not identified
    • Mechanism linking Rab29 to coat/tether machinery unknown
    • Whether LRRK2 is involved in this trafficking step not tested
  5. 2015 Medium

    RAB29 was shown to coordinate Rab11+ endosome polarization via dynein recruitment at the TGN, linking it to immune synapse assembly (TCR recycling) and primary ciliogenesis — broadening its functional scope beyond conventional retrograde trafficking.

    Evidence Co-IP with Rab8/Rab11/IFT20, siRNA knockdown with TCR recycling and ciliogenesis assays in T cells and ciliated cells

    PMID:26021297

    Open questions at the time
    • Direct versus indirect interaction with dynein not resolved
    • Structural basis for Rab29–Rab11 coordination unknown
    • In vivo immune phenotype of Rab29 loss not tested
  6. 2016 High

    Genetic studies in C. elegans and mouse knockouts placed RAB29 and LRRK2 in an ordered pathway upstream of AP-3-dependent lysosomal trafficking and revealed age-dependent lysosomal pathology upon loss of either gene.

    Evidence C. elegans epistasis, mouse knockout models with kidney proximal tubule lysosomal phenotyping

    PMID:27424887

    Open questions at the time
    • Direct biochemical link between RAB29 and AP-3 not established
    • Brain-specific lysosomal phenotype not characterized
    • Mechanism of age-dependence unclear
  7. 2017 High

    Two independent studies established the direct physical and functional interaction between Rab29 and LRRK2: Rab29 recruits LRRK2 to the TGN via the ankyrin domain, stimulates LRRK2 kinase activity, and is itself phosphorylated by LRRK2 at Ser72, creating a feedforward signaling loop; C9ORF72 was also identified as a Rab29-interacting partner linked to TGN integrity.

    Evidence Reciprocal Co-IP, Rab29 KO cells with Rab10 phosphorylation readout, ankyrin domain mutagenesis, Phos-tag/32P labeling for Ser72, endogenous Co-IP of C9ORF72–Rab29

    PMID:28334866 PMID:29212815 PMID:29223392

    Open questions at the time
    • Whether Ser72 phosphorylation is activating or inhibitory in vivo unresolved
    • C9ORF72–Rab29 interaction domain not mapped
    • Stoichiometry of Rab29–LRRK2 complex unknown
  8. 2018 High

    Studies resolved that GTP-bound, membrane-associated Rab29 is the active species for LRRK2 recruitment and activation, while mycobacterial PknG was found to trap Rab29 in its GDP-bound form at the Golgi to block phagosome–lysosome fusion — revealing pathogen exploitation of Rab29's GTPase cycle.

    Evidence Membrane fractionation, GTP-binding requirement for LRRK2 interaction, PknG kinase-dead mutants, GTPase activity assays, Rab29 KD with intracellular mycobacterial survival

    PMID:29177506 PMID:30037848 PMID:30483055

    Open questions at the time
    • Specific GEF activating Rab29 not identified
    • Structural basis of PknG–Rab29 interaction unknown
    • Centrosomal phenotype not validated in neurons
  9. 2020 High

    A rigorous in vivo challenge showed that Rab29 knockout in mice does not reduce basal or stress-induced endogenous LRRK2 activity toward Rab10/Rab12, indicating that Rab29 is not the sole physiological activator of LRRK2 and that overexpression-based conclusions require reinterpretation.

    Evidence Rab29 KO and transgenic overexpression mouse models, LRRK2[R1441C] and VPS35[D620N] knock-in mice, lysosomal stressors, phospho-Rab10/Rab12 immunoblot

    PMID:33135724

    Open questions at the time
    • Whether Rab29 activates LRRK2 under specific tissue or stress contexts not excluded
    • Compensatory Rab mechanisms in KO mice not assessed
    • Discrepancy with cell-based overexpression data mechanistically unresolved
  10. 2022 Medium

    Biochemical characterization confirmed Rab29 is constitutively membrane-associated and refractory to GDI extraction, distinguishing it from typical Rabs, while macrophage studies revealed Rab29 controls TLR surface expression and downstream MAPK/NF-κB inflammatory signaling.

    Evidence Ultracentrifugation, GDI extraction assays, GDI/geranylgeranyltransferase KO cells; THP-1 shRNA knockdown with flow cytometry, phospho-ERK/p38, NF-κB translocation, cytokine ELISA

    PMID:36116551 PMID:36502628

    Open questions at the time
    • Non-geranylgeranylation membrane attachment mechanism not identified
    • Whether TLR surface phenotype is Golgi-trafficking-dependent not tested
    • In vivo immune phenotype not examined
  11. 2023 High

    Cryo-EM structures of Rab29-LRRK2 complexes revealed that Rab29 induces an asymmetric LRRK2 tetramer with two kinase-active and two kinase-inactive protomers, providing the first structural explanation for how membrane-associated Rab29 allosterically activates LRRK2.

    Evidence Cryo-EM at multiple oligomeric states, comparison with DNL201-trapped active conformation

    PMID:38127736

    Open questions at the time
    • Whether the tetramer forms on native TGN membranes unknown
    • Transition between oligomeric states not kinetically characterized
    • Impact of PD mutations on tetramer architecture not fully resolved
  12. 2023 Medium

    Identification of Ser185 as a lysosomal-stress-responsive phosphorylation site on Rab29, mediated by PKCα/δ rather than LRRK2, revealed a second regulatory input controlling Rab29 lysosomal localization and lysosomal size homeostasis.

    Evidence Mass spectrometry, phosphomimetic mutants, PKC inhibitors and knockdown, lysosomal morphometry

    PMID:37365944

    Open questions at the time
    • Interplay between Ser72 (LRRK2) and Ser185 (PKC) phosphorylation not characterized
    • Whether Ser185 affects Rab29–LRRK2 complex formation unknown
    • In vivo relevance not tested
  13. 2025 Medium

    RGDI-1 was identified as a functional GDI for Rab29, and mycobacterial PknG was shown to phosphorylate RGDI-1 using Rab29 as a scaffold, preventing RGDI-1 release and locking Rab29 in an inactive state — completing the mechanistic picture of how mycobacteria subvert Rab29 to block phagosome–lysosome fusion. Separately, TBC1D9 was identified as a GAP for Rab29 that controls NF-κB–dependent IL-6 production.

    Evidence Co-IP, in vitro kinase assay (PknG on RGDI-1), GTPase activity assay, RGDI-1 KO; GTP-dependent Co-IP of TBC1D9–Rab29, NF-κB reporter, IL-6 ELISA

    PMID:41306588 PMID:41439637

    Open questions at the time
    • RGDI-1 as Rab29 GDI conflicts with earlier reports that Rab29 does not bind GDIs — discrepancy not resolved
    • TBC1D9 GAP activity not reconstituted in vitro with purified proteins
    • Physiological GAP/GDI hierarchy for Rab29 unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • The identity of the primary GEF for Rab29, the structural basis of its constitutive membrane association beyond geranylgeranylation, and the reconciliation of overexpression-based LRRK2 activation with the negative in vivo KO results remain major unresolved questions.
  • No GEF identified for Rab29
  • Membrane attachment mechanism beyond lipid modification unknown
  • Physiological context in which Rab29 activates LRRK2 in vivo not defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0003924 GTPase activity 2
Localization
GO:0005794 Golgi apparatus 6 GO:0005764 lysosome 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 4 R-HSA-5653656 Vesicle-mediated transport 4
Partners
C9ORF72LRRK2RAB11RAB8ARGDI1TBC1D9VPS35

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 RAB7L1 (RAB29) deficiency in primary rodent neurons or Drosophila dopamine neurons recapitulated degeneration observed with familial PD mutant LRRK2, while RAB7L1 overexpression rescued LRRK2 mutant phenotypes; PD-associated defects in RAB7L1 or LRRK2 led to endolysosomal and Golgi apparatus sorting defects and deficiency of the VPS35 retromer component, placing RAB29 upstream of VPS35/retromer in a common pathway with LRRK2. Genetic epistasis in rodent primary neurons and Drosophila, loss-of-function and overexpression rescue experiments, cell biological assays Neuron High 23395371
2017 Rab29 recruits LRRK2 to the trans-Golgi network via conserved residues in the LRRK2 ankyrin domain and greatly stimulates LRRK2 kinase activity; pathogenic LRRK2 R1441G/C and Y1699C mutants are more readily recruited and activated by Rab29 than wild-type LRRK2; knockout of Rab29 in A549 cells reduces endogenous LRRK2-mediated phosphorylation of Rab10; Rab29 interaction with LRRK2 also controls LRRK2 biomarker phosphorylation at Ser910/935/955/973. Co-immunoprecipitation, LRRK2 kinase activity assays, Rab29 knockout cells, domain mutagenesis (ankyrin domain residues), phosphorylation assays The EMBO journal High 29212815
2018 GTP-bound and membrane-associated Rab7L1 (RAB29) interacts with LRRK2 and activates LRRK2 autophosphorylation at Ser1292 (required for LRRK2 toxicity); Rab7L1 controls the proportion of LRRK2 that is membrane-associated and mediates LRRK2 recruitment to the trans-Golgi network; PD mutations in LRRK2 enhance Rab7L1-mediated TGN recruitment and increase phosphorylation of Rab7L1 ~4-fold. In vitro phosphorylation assays, membrane/GTP-binding requirement studies, LRRK2 autophosphorylation assays, cell fractionation Human molecular genetics High 29177506
2014 Rab29 localizes to the trans-Golgi network and is essential for maintaining TGN integrity; inhibition or depletion of Rab29 causes TGN fragmentation; dominant-negative Rab29T21N or shRNA-Rab29 alters mannose-6-phosphate receptor (M6PR) distribution and disrupts retrograde trafficking of M6PR from endosomes to TGN, without affecting anterograde VSV-G trafficking. Dominant-negative expression (Rab29T21N), shRNA knockdown, immunofluorescence, CD8-tagged M6PR endocytosis assay, VSV-G trafficking assay PloS one Medium 24788816
2011 Rab29 is recruited to S. Typhi-containing vacuoles but not to broad-host Salmonella vacuoles; the type III secretion effector GtgE from broad-host Salmonella specifically cleaves Rab29 through proteolytic activity, and an S. Typhi strain engineered to express GtgE and cleave Rab29 exhibited increased intracellular replication in human macrophages, demonstrating Rab29 is required for typhoid toxin export. Screen for host factors required for typhoid toxin export, immunofluorescence localization, proteolytic cleavage assay with GtgE effector, genetic engineering of bacterial strains, intracellular replication assay Proceedings of the National Academy of Sciences of the United States of America High 22042847
2016 In C. elegans neurons, LRRK2 and RAB7L1 orthologs act in an ordered genetic pathway to regulate axonal elongation; the AP-3 complex acts as a downstream effector of LRRK2 and RAB7L1 in intracellular protein trafficking to the lysosome; in mice, deficiency of either RAB7L1 or LRRK2 leads to age-associated lysosomal defects in kidney proximal tubule cells. C. elegans genetic epistasis, mouse knockout models, cell-based trafficking assays Scientific reports High 27424887
2017 C9ORF72 interacts with RAB7L1 endogenously in SH-SY5Y neuroblastoma cells; C9orf72 haploinsufficiency leads to defective vesicle trafficking and dysfunctional trans-Golgi network phenotypes that are recapitulated by RAB7L1 knockout, and reversed by C9ORF72 overexpression or antisense oligonucleotide treatment. Co-immunoprecipitation of endogenous proteins, RAB7L1 genetic ablation, antisense oligonucleotides, patient-derived fibroblasts and iPSC-derived motor neurons Brain : a journal of neurology Medium 28334866
2017 LRRK2 phosphorylates Golgi-localized Rab7L1 at Ser72 as a major site (identified by Phos-tag, metabolic labeling, alanine-scan mutagenesis, and phospho-specific antibody); phosphorylation requires Golgi localization of Rab7L1; pathogenic LRRK2 mutants markedly enhance Ser72 phosphorylation; modulation of Ser72 phosphorylation alters trans-Golgi network morphology and distribution. Phos-tag electrophoresis, metabolic 32P labeling, alanine-scan mutagenesis of all Ser/Thr residues, phospho-specific antibody, in vitro kinase assay Biochemical and biophysical research communications High 29223392
2015 Rab29 colocalizes and interacts with Rab8, Rab11, and IFT20 at the trans-Golgi network in T cells; Rab29 depletion prevents TCR recycling to the immune synapse by blocking Rab11+ endosome polarization via defective recruitment of the dynein microtubule motor; Rab29 similarly promotes primary cilium growth and ciliary localization of Smoothened in ciliated cells. Co-immunoprecipitation, immunofluorescence colocalization, siRNA knockdown, TCR recycling assay, ciliogenesis assay Cell death and differentiation Medium 26021297
2018 RAB7L1 recruits LRRK2 to the Golgi complex, causing accumulation of phosphorylated RAB8A in a pericentrosomal/centrosomal location and centrosomal deficits; centrosomal alterations depend on Golgi integrity when wild-type LRRK2 is involved, and are at least partly mediated by aberrant LRRK2-mediated RAB8A phosphorylation (blocked by kinase inhibitors and RAB8A knockdown). Immunofluorescence, LRRK2 kinase inhibitors, RAB8A knockdown, RAB7L1 overexpression, centrosomal morphology assay Frontiers in molecular neuroscience Medium 30483055
2018 Mycobacterial PknG serine/threonine kinase interacts specifically with GDP-bound Rab7l1 at the Golgi complex, blocking the GDP-to-GTP transition of Rab7l1 in a kinase-activity-dependent manner, thereby preventing recruitment of active Rab7l1-GTP to bacilli-containing phagosomes and inhibiting phagosome-lysosome fusion; Rab7l1-GTP on phagosomes is required for subsequent recruitment of EEA1, Rab7, and LAMP2. Co-immunoprecipitation, immunofluorescence, GTPase activity assays, kinase-dead PknG mutant, Rab7l1 knockdown, intracellular survival assay Journal of immunology High 30037848
2020 Knockout of Rab29 does not influence endogenous LRRK2 activity (as measured by Rab10 and Rab12 phosphorylation) in wild-type, LRRK2[R1441C], or VPS35[D620N] knock-in mouse tissues and primary cell lines; transgenic Rab29 overexpression in mice is also insufficient to stimulate basal LRRK2 activity; lysosomal stress-induced (nigericin, monensin, chloroquine, LLOMe) LRRK2 activation is not blocked in Rab29-deficient cells. Rab29 knockout mouse tissues, knock-in mouse models, phospho-Rab10/Rab12 immunoblot, LRRK2 inhibitor controls, transgenic mouse overexpression The Biochemical journal High 33135724
2020 RAB29 knockdown does not recapitulate G2019S LRRK2-mediated EGFR trafficking defects (which are mediated by RAB10), but RAB29 overexpression rescues pathogenic LRRK2-mediated trafficking deficits independently of Golgi integrity, suggesting RAB29 positively modulates non-Golgi-related trafficking events. siRNA knockdown, EGFR trafficking assay, RAB10/RAB29 overexpression rescue, Golgi disruption experiments Cells Medium 32709066
2023 Cryo-electron microscopy structures of Rab29-LRRK2 complexes in three oligomeric states reveal that Rab29 induces an unexpected tetrameric assembly of LRRK2, comprising two kinase-active central protomers and two kinase-inactive peripheral protomers; the central protomers adopt an active-like conformation resembling that trapped by clinical kinase inhibitor DNL201. Cryo-electron microscopy structural determination, three oligomeric states captured Science High 38127736
2023 Rab29 is phosphorylated at Ser185 (not by LRRK2) under lysosomal overload stress, as identified by mass spectrometry; phosphomimetic Ser185 mutants counteract lysosomal enlargement; PKCα and PKCδ are involved in this phosphorylation and control lysosomal localization of Rab29 in concert with LRRK2. Mass spectrometry phosphorylation site identification, phosphomimetic mutant expression, PKC inhibitors/knockdown, lysosomal size assay, immunofluorescence Journal of cell science Medium 37365944
1997 Rat Rab29 encodes a Ras-related GTP-binding protein with rapid nucleotide exchange but lacking detectable intrinsic GTPase activity; the C-terminus harbors a structural element essential for nucleotide exchange, as shown by a splice variant (Rab29Δ37) lacking the C-terminus that is loaded with GTP during biosynthesis but shows almost no nucleotide exchange. Recombinant protein expression, radiolabeled GTP exchange assay, GTPase activity assay, cDNA cloning of splice variants Biochimica et biophysica acta Medium 9177482
2021 Rab29 does not bind GDI (GDP-dissociation inhibitor) in cytosol and has an unusually fast nucleotide exchange rate; conventional GTP-locked mutations do not have the expected activating effect; novel fast-exchange mutants (I64T and V156G) were characterized via fluorescence-based assay. Fluorescence-based nucleotide exchange assay, biochemical characterization of Rab29 mutants Methods in molecular biology Medium 34453707
2022 Unlike typical Rab proteins, Rab29 is predominantly membrane-associated (by ultracentrifugation fractionation), resistant to extraction from membranes by GDP-dissociation inhibitors in vitro, and fails to interact with GDIs; GDI knockout does not affect Rab29 membrane localization; geranylgeranyltransferase knockout decreases Rab29 hydrophobicity confirming geranylgeranylation, but additional mechanisms beyond geranylgeranylation contribute to membrane association. Ultracentrifugation fractionation, in vitro GDI extraction assay, GDI knockout cells, geranylgeranyltransferase knockout cells, hydrophobicity analysis The Journal of biological chemistry Medium 36116551
2022 Rab7l1 knockdown in THP-1 macrophages leads to higher surface expression of TLR2, TLR4, and CD14 (with lower intracellular levels), increased phospho-ERK1/2 and phospho-p38 MAPK, higher NF-κB nuclear translocation, and elevated TNF-α and IL-10 production upon LPS or Pam3CSK4 stimulation, indicating Rab7l1 regulates TLR surface expression and downstream MAPK/NF-κB signaling. shRNA knockdown, flow cytometry surface/intracellular receptor quantification, phospho-ERK/p38 immunoblot, NF-κB nuclear translocation assay, cytokine ELISA Biochemical and biophysical research communications Medium 36502628
2025 RGDI-1 (Rho GDP dissociation inhibitor-1) acts as a GDI for Rab7l1; mycobacterial PknG interacts with both Rab7l1-GDP and RGDI-1 (using Rab7l1 as a scaffold), phosphorylates RGDI-1, and prevents RGDI-1 dissociation from Rab7l1, thereby reducing Rab7l1 GTPase activity and blocking phagosome-lysosome fusion; when RGDI-1 is absent, PknG cannot inhibit P-L fusion. Co-immunoprecipitation, in vitro kinase assay (PknG phosphorylating RGDI-1), GTPase activity assay, RGDI-1 knockout/knockdown, intracellular mycobacterial survival assay ACS infectious diseases Medium 41439637
2025 TBC1D9, a Rab GTPase-activating protein (GAP), preferentially interacts with GTP-bound Rab29 (confirmed by co-immunoprecipitation) and co-localizes with Rab29 following stimulation; Rab29 overexpression inhibits NF-κB activation and IL-6 production, while Rab29 deficiency increases both, opposing TBC1D9's effect; thus TBC1D9 acts as a GAP for Rab29 to regulate homeostatic NF-κB signaling and selective IL-6 production. Co-immunoprecipitation (GTP-dependent interaction), depletion/overexpression assays, NF-κB reporter, proteomics, immunofluorescence co-localization, IL-6 ELISA Frontiers in cellular and infection microbiology Medium 41306588
2018 Rab29 specifically interacts with LRRK2 with higher affinity than Rac1; mutant Rab29 (but not Rac1) alters endosome-to-TGN retrograde trafficking of CI-M6PR and its stability; wild-type Rab29 (but not Rac1) rescues altered retrograde trafficking induced by pathogenic LRRK2G2019S. Co-immunoprecipitation, domain binding preference analysis, CI-M6PR retrograde trafficking assay, rescue experiments Journal of biomedical research Low 29336357

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 RAB7L1 interacts with LRRK2 to modify intraneuronal protein sorting and Parkinson's disease risk. Neuron 457 23395371
2017 Rab29 activation of the Parkinson's disease-associated LRRK2 kinase. The EMBO journal 217 29212815
2018 LRRK2 phosphorylates membrane-bound Rabs and is activated by GTP-bound Rab7L1 to promote recruitment to the trans-Golgi network. Human molecular genetics 200 29177506
2017 C9orf72 and RAB7L1 regulate vesicle trafficking in amyotrophic lateral sclerosis and frontotemporal dementia. Brain : a journal of neurology 128 28334866
2016 LRRK2 and RAB7L1 coordinately regulate axonal morphology and lysosome integrity in diverse cellular contexts. Scientific reports 105 27424887
2011 Proteolytic targeting of Rab29 by an effector protein distinguishes the intracellular compartments of human-adapted and broad-host Salmonella. Proceedings of the National Academy of Sciences of the United States of America 100 22042847
2014 A role of Rab29 in the integrity of the trans-Golgi network and retrograde trafficking of mannose-6-phosphate receptor. PloS one 72 24788816
2017 Parkinson's disease-associated mutant LRRK2 phosphorylates Rab7L1 and modifies trans-Golgi morphology. Biochemical and biophysical research communications 68 29223392
2018 Mycobacterial PknG Targets the Rab7l1 Signaling Pathway To Inhibit Phagosome-Lysosome Fusion. Journal of immunology (Baltimore, Md. : 1950) 59 30037848
2015 The small GTPase Rab29 is a common regulator of immune synapse assembly and ciliogenesis. Cell death and differentiation 56 26021297
2020 Endogenous Rab29 does not impact basal or stimulated LRRK2 pathway activity. The Biochemical journal 53 33135724
2023 Rab29-dependent asymmetrical activation of leucine-rich repeat kinase 2. Science (New York, N.Y.) 45 38127736
2018 RAB7L1-Mediated Relocalization of LRRK2 to the Golgi Complex Causes Centrosomal Deficits via RAB8A. Frontiers in molecular neuroscience 34 30483055
1997 Cloning and chromosome assignment to 1q32 of a human cDNA (RAB7L1) encoding a small GTP-binding protein, a member of the RAS superfamily. Cytogenetics and cell genetics 33 9284931
2020 Distinct Roles for RAB10 and RAB29 in Pathogenic LRRK2-Mediated Endolysosomal Trafficking Alterations. Cells 27 32709066
2011 Genetic variants in the RAB7L1 and SLC41A1 genes of the PARK16 locus in Chinese Parkinson's disease patients. The International journal of neuroscience 27 21812739
2014 An association analysis of the rs1572931 polymorphism of the RAB7L1 gene in Parkinson's disease, amyotrophic lateral sclerosis and multiple system atrophy in China. European journal of neurology 20 25040112
2018 Distinctive roles of Rac1 and Rab29 in LRRK2 mediated membrane trafficking and neurite outgrowth. Journal of biomedical research 12 29336357
2015 The rs1572931 polymorphism of the RAB7L1 gene promoter is associated with reduced risk of Parkinson's disease. Neurological research 12 26344175
2017 RAB7L1 promoter polymorphism and risk of Parkinson's disease; a case-control study. Neurological research 11 28245721
2023 Phosphorylation of Rab29 at Ser185 regulates its localization and role in the lysosomal stress response in concert with LRRK2. Journal of cell science 8 37365944
2021 Combined Knockout of Lrrk2 and Rab29 Does Not Result in Behavioral Abnormalities in vivo. Journal of Parkinson's disease 7 33523017
2019 Association of RIT2 and RAB7L1 with Parkinson's disease: a case-control study in a Taiwanese cohort and a meta-analysis in Asian populations. Neurobiology of aging 6 31818509
1997 Cloning of two splicing variants of the novel Ras-related GTPase Rab29 which is predominantly expressed in kidney. Biochimica et biophysica acta 6 9177482
2021 Rab29 Fast Exchange Mutants: Characterization of a Challenging Rab GTPase. Methods in molecular biology (Clifton, N.J.) 3 34453707
2020 RAB7L1 Participates in Secondary Brain Injury Induced by Experimental Intracerebral Hemorrhage in Rats. Journal of molecular neuroscience : MN 3 32691280
2022 The atypical Rab GTPase associated with Parkinson's disease, Rab29, is localized to membranes. The Journal of biological chemistry 2 36116551
2022 Rab7l1 plays a role in regulating surface expression of toll like receptors and downstream signaling in activated macrophages. Biochemical and biophysical research communications 1 36502628
2025 Association of the rs823144 variant of the RAB29 gene with the activity of lysosomal hydrolases in blood cells and risk of Parkinson's disease. Vavilovskii zhurnal genetiki i selektsii 0 41164274
2025 A TBC1D9-Rab29 axis controls homeostatic NF-κB signaling and selective IL-6 production in epithelial cells. Frontiers in cellular and infection microbiology 0 41306588
2025 PknG Protein of Mycobacterium tuberculosis Targets RGDI-1 to Regulate Rab7l1 GTPase Activity. ACS infectious diseases 0 41439637
2021 Expression of RAB7L1 in Patients with Pituitary Adenomas. Annals of clinical and laboratory science 0 33941558