Affinage

ARL1

ADP-ribosylation factor-like protein 1 · UniProt P40616

Length
181 aa
Mass
20.4 kDa
Annotated
2026-06-09
44 papers in source corpus 26 papers cited in narrative 26 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ARL1 is a myristoylated Ras-superfamily small GTPase that operates as a master organizer of the trans-Golgi network (TGN), cycling between GDP- and GTP-bound states to control the recruitment of tethering and coat machinery that drives membrane traffic (PMID:8834805, PMID:11792819). Its Golgi association requires N-terminal myristoylation, and the GTP-bound form is the active species: a GDP-restricted mutant collapses Golgi structure while a GTP-restricted mutant expands the Golgi, stabilizes COPI/AP-1 coats, and arrests cargo transport (PMID:11792819). In its active state ARL1 recruits a defined set of effectors to the trans-Golgi, including GRIP-domain golgins (golgin-245, golgin-97, and the yeast/plant ortholog Imh1) (PMID:11303027, PMID:16830178, PMID:24610947) and the BAR-domain arfaptins, which compete with the golgins for ARL1 binding and act in membrane deformation and as negative regulators of retrograde transport (PMID:21239483, PMID:25789876). ARL1 also directs trans-Golgi-specific targeting of the Arf1 GEFs BIG1/BIG2 (binding directly via Sec71 in Drosophila), thereby coupling ARL1 activation to local Arf1 activation and downstream AP-1/secretory granule biogenesis (PMID:22291037, PMID:24610947). Functionally, ARL1 is required for retrograde endosome-to-TGN transport — including Shiga toxin delivery via a Vti1a/syntaxin-6/syntaxin-16 SNARE complex — distinct from the anterograde role of its upstream activator ARFRP1 (PMID:19224922, PMID:31575603). ARL1 membrane recruitment depends on the GTP-bound master regulator ARFRP1, which bifurcates to activate ARL1 (golgin recruitment) and ARL5 (GARP recruitment) (PMID:17127620, PMID:31575603); its activity is negatively regulated by the GAP Gcs1 and by MON2 in yeast (PMID:21562219, PMID:22594927). Across yeast, trypanosomes, Leishmania, plants, and flies, ARL1 is essential for Golgi integrity, secretion, endocytic trafficking, and starvation-induced autophagy via Atg9/GARP trafficking (PMID:12210899, PMID:16042563, PMID:18286177, PMID:27462928, PMID:28627726), and oxidative stress triggers proteolytic degradation of ARL1, dissociating GRIP golgins and disrupting the trans-Golgi (PMID:32583744). Cryo-EM of the Arl1-Gea2 complex shows ARL1 binds the outer DCB-domain surface of the GEF dimer through a conserved aromatic triad, an interface required for golgin Golgi association (PMID:38431634).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1996 Medium

    Established ARL1 as a bona fide Golgi-localized Ras-like GTPase, defining the organelle and the biochemical activity that all subsequent work would build on.

    Evidence Immunofluorescence co-localization, GST-pulldown GTP-binding assay, and BFA perturbation of rat Arl1

    PMID:8834805

    Open questions at the time
    • No effectors identified
    • Myristoylation requirement inferred from BFA kinetics, not directly demonstrated
    • No functional transport role established
  2. 2001 High

    Showed that the GTP/GDP cycle of ARL1 governs Golgi architecture and coat recruitment, and identified the first specific effectors, establishing ARL1 as an active regulator rather than a passive marker.

    Evidence Dominant-negative/constitutively active mutant overexpression, transport assays, and co-IP in mammalian cells; yeast two-hybrid identifying SCOCO and golgin-245

    PMID:11303027 PMID:11792819

    Open questions at the time
    • Upstream GEF unidentified (only inferred BFA-sensitive exchange factor)
    • Mechanism linking ARL1 to coat stabilization unresolved
    • GAP not identified
  3. 2002 Medium

    Demonstrated in yeast that ARL1 loss disrupts secretion, vacuolar sorting, endocytosis, and vacuole biogenesis, and connected it to ion homeostasis, establishing conserved trafficking functions and pleiotropy.

    Evidence Gene deletion with secretion/CPY-sorting/lucifer-yellow assays, morphological EM, and genetic suppression in S. cerevisiae

    PMID:11840166 PMID:12210899 PMID:15126631

    Open questions at the time
    • Molecular basis linking ARL1 to K+ influx via HAL4/HAL5 unresolved
    • Whether trafficking and ion phenotypes share a mechanism unclear at this stage
    • Direct effectors in yeast not yet defined
  4. 2006 High

    Placed ARL1 within a GTPase cascade by showing its Golgi recruitment requires the upstream GTPase ARFRP1, and established the conserved GTP-dependent ARL1-GRIP golgin interaction.

    Evidence ARFRP1 dominant-negative/RNAi/knockout-embryo analysis in mammalian cells; site-directed mutagenesis of ARL1 and GRIP domain with live imaging in plant cells

    PMID:16830178 PMID:17127620

    Open questions at the time
    • GEF directly acting on ARL1 still unidentified
    • How ARFRP1 controls ARL1 nucleotide state mechanistically unresolved
    • Cargo consequences of golgin recruitment not yet mapped
  5. 2009 High

    Resolved the division of labor between ARL1 and ARFRP1, assigning ARL1 specifically to retrograde endosome-to-TGN transport through a defined SNARE complex.

    Evidence siRNA knockdown with Shiga toxin retrograde and VSVG anterograde transport assays plus SNARE complex analysis in mammalian cells

    PMID:19224922

    Open questions at the time
    • Whether all golgin effectors contribute equally to retrograde transport unresolved
    • GCC185 recruitment shown independent of ARL1, complicating the tethering model (#11)
  6. 2011 High

    Defined arfaptins as ARL1-specific BAR-domain effectors that compete with golgins, and identified the GAP Gcs1 as a negative regulator, establishing distinct ARL1 effector complexes and the deactivation arm of its cycle.

    Evidence Co-IP, siRNA, live imaging, and domain mapping in mammalian cells; in vitro GAP assay and genetic epistasis in yeast

    PMID:21239483 PMID:21562219

    Open questions at the time
    • Spatial segregation of arfaptin- vs golgin-bound ARL1 microdomains not directly visualized at this point
    • Mammalian GAP equivalent not defined
  7. 2012 High

    Established the mechanistic link from ARL1 activation to Arf1 activation by showing ARL1 directly recruits the Arf1 GEFs BIG1/BIG2 to the trans-Golgi, and uncovered conformation-specific separation of trafficking and ion functions plus MON2 as a regulator.

    Evidence Liposome affinity purification and direct binding (Drosophila Sec71) with siRNA in mammalian cells; allele-specific complementation in yeast

    PMID:22291037 PMID:22594927

    Open questions at the time
    • How a single GTPase adopts distinct functional conformations structurally unresolved at this stage
    • MON2 mechanism of negative regulation unclear
    • Ion-homeostasis effector still unknown
  8. 2014 High

    Demonstrated tissue-specific requirement of ARL1 for golgin recruitment, AP-1 localization, and secretory granule biogenesis, linking ARL1-driven Arf1 activation to a developmental secretory program.

    Evidence Loss-of-function clonal analysis and salivary gland secretion/morphology assays in Drosophila

    PMID:24610947

    Open questions at the time
    • Why granule biogenesis is especially ARL1-dependent in specific tissues unresolved
    • Quantitative contribution of each golgin to granule formation not dissected
  9. 2016 Medium

    Extended ARL1 function to autophagy, showing it (with Ypt6/Arl3 and the COG complex) controls Atg9 and GARP trafficking required for autophagosome formation under stress.

    Evidence Deletion mutants and autophagy assays (GFP-Atg8, Pho8Δ60, ApeI maturation, Atg9 localization) in S. cerevisiae

    PMID:27462928 PMID:28627726

    Open questions at the time
    • Whether the autophagy role is conserved in mammals not established here
    • Direct effector linking ARL1 to Atg9 trafficking unidentified
  10. 2019 High

    Consolidated the ARFRP1-master-regulator model with bifurcated ARL1→golgin and ARL5→GARP cascades, and showed ARL1/Imh1 can bypass Ypt6 to restore GARP-dependent retrograde transport.

    Evidence siRNA epistasis and retrograde cargo assays in mammalian cells; overexpression rescue and domain mapping in yeast

    PMID:30726160 PMID:31575603

    Open questions at the time
    • How ARFRP1 coordinately times ARL1 vs ARL5 activation unresolved
    • Functional overlap between Imh1/golgin and Ypt6 tethering pathways not fully separated
  11. 2020 Medium

    Identified oxidative stress as a physiological input that controls ARL1 levels via proteolytic degradation, coupling redox state to Golgi integrity and transport.

    Evidence H2O2 treatment with protease-inhibitor and ROS-scavenger rescue, immunofluorescence, and EM in HeLa cells

    PMID:32583744

    Open questions at the time
    • Identity of the protease degrading ARL1 unknown
    • Whether degradation is regulated/signal-specific or bulk unresolved
  12. 2024 High

    Provided structural mechanism for ARL1 effector engagement, showing how ARL1 docks onto the GEF dimer outer surface via a conserved aromatic triad to enable golgin Golgi association.

    Evidence Cryo-EM of full-length Gea2 and the Arl1-Gea2 complex with interface mutagenesis and Imh1 Golgi localization assay

    PMID:38431634

    Open questions at the time
    • Structures of ARL1 bound to GRIP golgins or arfaptins not resolved
    • Structural basis of conformational switching between functional states unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular effector that mediates ARL1's non-trafficking roles (K+ homeostasis) and the identity of the mammalian ARL1 GAP/protease remain undefined.
  • No effector links ARL1 to Trk1/Trk2-mediated K+ influx beyond the HAL4/HAL5 genetic placement
  • Mammalian GAP not identified
  • Protease degrading ARL1 under oxidative stress not identified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0003924 GTPase activity 3 GO:0060089 molecular transducer activity 3
Localization
GO:0005794 Golgi apparatus 3
Pathway
R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-9609507 Protein localization 3 R-HSA-9612973 Autophagy 2

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 Rat Arl1 (rArl1) is a 22 kDa Ras-like small GTPase that localizes to the Golgi complex, co-localizing with mannosidase II and p28. Its Golgi association requires N-terminal myristoylation (inferred from BFA redistribution kinetics distinct from ARF/beta-COP). Recombinant GST-rArl1 binds GTP-γ-S in a dose-dependent manner, confirming GTP-binding activity. Immunofluorescence co-localization, GST-pulldown GTP-binding assay, BFA treatment, subcellular fractionation Journal of cell science Medium 8834805
2001 ARL1 enriches at the trans-Golgi (AP-1-marked side). Golgi association requires N-terminal myristoylation. Dominant-negative ARL1(T31N) (GDP-restricted) causes disappearance of Golgi structure, while constitutively active ARL1(Q71L) (GTP-restricted) expands the Golgi into a vesicle-tubule network, stably recruits COPI and AP-1 coats, and arrests VSV-G transport. GTP-bound Arl1 interacts with arfaptin-2/POR1 but not GGA1. Dominant-negative/constitutively active mutant overexpression, immunofluorescence, subcellular fractionation, co-immunoprecipitation Journal of cell science High 11792819
2001 ARL1 shares effectors with ARFs: MKLP1 and arfaptin2/POR1 bind ARL1 but not ARL2 or ARL3. Two-hybrid screens identified specific ARL1-binding proteins SCOCO and Golgin-245. SCOCO Golgi membrane binding is reversed by brefeldin A, suggesting a BFA-sensitive ARL1 exchange factor exists. Expression of [Q71L]ARL1 alters Golgi structure similarly to [Q71L]ARF1. Yeast two-hybrid, co-immunoprecipitation, brefeldin A treatment, overexpression in mammalian cells The Journal of biological chemistry High 11303027
2002 In S. cerevisiae, loss of ARL1 causes defects in membrane traffic: reduced protein secretion, missorting of carboxypeptidase Y (CPY) to the vacuole, and reduced fluid-phase endocytosis (lucifer yellow uptake). Temperature-sensitive growth of arl1Δ ssd1 is suppressed by YPT1 (yeast Rab1a homolog), indicating partially overlapping functions. Gene deletion, radiolabeled secretion assay, vacuolar protein sorting assay, lucifer yellow uptake, genetic epistasis/suppression Yeast High 12210899
2002 A point mutation in ARL1 (dlp2 allele) in S. cerevisiae causes defects in central vacuole formation due to aberrant membrane trafficking (many small vesicles instead of large central vacuoles), without affecting protein sorting to vacuoles. This ARL1 mutation also inhibits progression of autophagic cell death and Bax-induced apoptotic cell death. Genetic mapping, morphological analysis (electron microscopy), biochemical assays of vacuole function, Bax overexpression Cell death and differentiation Medium 11840166
2004 Yeast ARL1 controls K+ influx: arl1 mutants show reduced 86Rb+ uptake (~30-40% less) and increased 14C-methylammonium internalization (consistent with plasma membrane hyperpolarization), while K+ and H+ efflux are normal. Overexpression suppressors include HAL4 and HAL5 (Ser/Thr kinases regulating K+-influx mediators Trk1p/Trk2p), placing ARL1 upstream of HAL4/HAL5 in K+ homeostasis. Radiolabeled ion uptake assays (86Rb+, 14C-methylammonium), high-copy suppressor screen, genetic analysis Journal of cell science Medium 15126631
2005 T. brucei ARL1 is expressed only in the mammalian bloodstream form, localizes to the Golgi apparatus, and is essential for viability. RNAi depletion of TbARL1 causes Golgi disintegration and delay in exocytosis of GPI-anchored VSG to the parasite surface. RNAi knockdown, immunofluorescence localization, VSG exocytosis assay Biochemical Society transactions Medium 16042563
2006 ARFRP1 (GTP-bound form) controls Golgi targeting of ARL1 and its effector Golgin-245. ARFRP1-T31N (dominant-negative) or RNAi depletion of ARFRP1 displaces ARL1 and Golgin-245 from the Golgi and alters syntaxin 6 distribution, while GM130 and giantin targeting are unaffected. In Arfrp1-/- embryos, ARL1 dislocates from Golgi membranes. Dominant-negative/constitutively active mutant overexpression, RNAi, immunofluorescence, mouse knockout embryo analysis Molecular membrane biology High 17127620
2006 In plant (Arabidopsis/tobacco) cells, ARL1 GTP-bound form is required for recruitment of a GRIP-domain golgin to the Golgi. Site-directed mutagenesis of conserved residues in the GRIP domain of golgin and in ARL1 abolishes ARL1-GRIP interaction and redistributes GRIP to the cytosol, confirming direct ARL1–GRIP interaction is required for Golgi localization of the golgin. Live cell imaging, site-directed mutagenesis, GFP localization in plant cells Plant molecular biology Medium 16830178
2008 Leishmania ARL-1 localizes to the TGN via N-terminal myristoylation (essential for localization). The dominant-negative empty-form mutant LdARL-1/T34N inhibits endocytosis and intracellular trafficking from TGN to the lysosome/multivesicular tubule and to acidocalcisomes, likely through mislocalisation of GRIP-domain vesicle tethering factors. Expression of GTP/GDP-locked and nucleotide-free mutants, fluorescence localization, endocytosis assays PloS one Medium 18286177
2009 ARL1 and ARFRP1 have differential roles in TGN trafficking in mammalian cells: ARL1 knockdown specifically impairs retrograde transport of Shiga toxin to the TGN (via a SNARE complex containing Vti1a, syntaxin 6, and syntaxin 16), while ARFRP1 knockdown impairs anterograde transport of VSVG from the TGN. siRNA knockdown, Shiga toxin retrograde transport assay, VSVG anterograde transport assay, SNARE complex analysis The Journal of biological chemistry High 19224922
2009 Endogenous GCC185 Golgi recruitment does not require Rab6A/A' or Arl1 in mammalian cells. Depletion of both Rab6A/A' and Arl1 had no effect on localization of endogenous GCC185 or its isolated GRIP domain. Knockdown by siRNA, immunofluorescence of endogenous proteins, yeast two-hybrid Cell Medium 19703403
2011 Arfaptins (arfaptin-1 and arfaptin-2) associate with trans-Golgi membranes through interaction with Arl1 (not Arfs) via their BAR domain-containing region. Arfaptins compete with golgin-97 and golgin-245 for Arl1 binding. Time-lapse imaging shows arfaptins, but not golgin-97, are incorporated into vesicular/tubular structures emanating from the Golgi, suggesting Arl1 recruits arfaptins to the trans-Golgi for membrane deformation. Co-immunoprecipitation, siRNA knockdown, live cell time-lapse imaging, domain mapping The Journal of biological chemistry High 21239483
2011 In yeast, the GAP Gcs1 acts on Arl1; loss of Gcs1 causes cold-sensitive growth and impaired endosomal transport through dysregulated (hyperactive) Arl1. Deletions in the Arl1 or Ypt6 vesicle-tethering pathways restore growth and trafficking in gcs1Δ by preventing Arl1 activation. Increased abundance of the Arl1 effector Imh1 also restores growth through Arl1 binding, suggesting excess active Arl1 sequesters proteins at the trans-Golgi membrane. Genetic epistasis, gene deletion, in vitro GAP assay, overexpression studies Molecular biology of the cell Medium 21562219
2012 The small G protein Arl1 directs trans-Golgi-specific targeting of Arf1 exchange factors BIG1 and BIG2 (but not GBF1) in mammalian cells. Using Drosophila, Arl1 was found to bind directly to Sec71 (BIG1/2 ortholog) via an N-terminal region of Sec71. This establishes a pathway in which Arl1 recruits BIG1/BIG2 specifically to the trans-Golgi, thereby activating Arf1 at the trans-side. Liposome-based affinity purification, direct binding assay, siRNA knockdown in mammalian cells, immunofluorescence The Journal of cell biology High 22291037
2012 In yeast, Arl1 has at least three functional conformations in vivo. The GTP-restricted allele ARL1[Q72L] complements membrane traffic (CPY secretion) but not K+ homeostasis, while the XTP-restricted allele ARL1[D130N] complements ion phenotypes but not membrane traffic. ARL1[F52G] and ARL1[Y82G] mutations (predicted to disrupt Imh1 GRIP domain binding) fail to complement both phenotypes. MON2 functions as a negative regulator of the GTP-restricted form of Arl1. Site-directed mutagenesis, allele-specific complementation, CPY secretion assay, ion sensitivity assays, genetic interaction analysis FEMS yeast research Medium 22594927
2014 In Drosophila, Arl1 is essential for recruitment of three of four GRIP-domain golgins to the Golgi. Loss of Arl1 causes dispersal of AP-1 (a clathrin adaptor requiring Arf1 for membrane recruitment) at the trans-Golgi and complete failure of secretory granule biogenesis in larval salivary glands, establishing Arl1 as required to enhance Arf1 activation at the trans-Golgi in specific tissues. Loss-of-function clonal analysis, immunofluorescence, salivary gland morphology/secretion assay Journal of cell science High 24610947
2015 Arfaptin-1 acts as a negative regulator of Arl1-mediated retrograde transport. Knockdown of arfaptin-1 accelerates retrograde transport of Shiga toxin B from endosomes to the Golgi, while overexpression inhibits it; an Arl1-binding-defective mutant (arfaptin-1b-F317A) fails to inhibit transport. Arfaptin-1 and golgin-97/golgin-245 do not interfere with each other's TGN localization, suggesting distinct Arl1-containing complexes in separate microdomains. siRNA knockdown, Shiga toxin transport assay, overexpression of wild-type and binding-defective mutants, immunofluorescence PloS one Medium 25789876
2015 In Drosophila, Arl1 and its guanine nucleotide exchange factor Gartenzwerg (Garz) function in the same pathway as Arfaptin to control synapse growth. Genetic epistasis and biochemical data demonstrate that Arl1 and Garz are required for Arfaptin function at the Golgi during presynaptic nerve terminal growth. Genetic epistasis, biochemical interaction assays, overexpression in Drosophila motor neurons Biology open Medium 26116655
2016 In S. cerevisiae, Arl1 (along with Ypt6) is required for starvation-induced autophagy specifically under high-temperature stress. Both proteins are required for proper trafficking of Atg9 to the phagophore assembly site (PAS); their absence prevents autophagosome construction at restrictive temperature. Arl1 and Ypt6 participate in autophagy by targeting the GARP complex to the PAS to regulate anterograde trafficking of Atg9. Deletion mutants, autophagy-specific assays (GFP-Atg8, Pho8Δ60), Atg9 localization, degron-inducible double mutant construction Autophagy Medium 27462928
2017 In yeast, the Arl3-Arl1 GTPase cascade cooperates with the COG complex subunit Cog8 to regulate selective autophagy (Cvt pathway) via Atg9 trafficking. arl3Δcog8Δ and arl1Δcog8Δ double mutants show profound defects in aminopeptidase I maturation. Atg9 accumulates at the late Golgi in these double mutants under normal (but not starvation) conditions, placing Arl1 upstream of Atg9 trafficking at the Golgi. Double-deletion genetics, aminopeptidase I maturation assay, Atg9 localization by fluorescence microscopy Traffic Medium 28627726
2019 ARFRP1 functions as a master regulator upstream of both ARL1 and ARL5 to coordinate tethering factor recruitment to the TGN: ARFRP1 activates ARL1 (which recruits golgins) and ARL5 (which recruits GARP), and this bifurcated GTPase cascade is essential for delivery of retrograde cargos to the TGN. siRNA knockdown, epistasis analysis, retrograde cargo transport assays, immunofluorescence The Journal of cell biology High 31575603
2019 In yeast, Arl1 and its effector golgin Imh1 can suppress Ypt6 dysfunction in retrograde endosome-to-TGN transport. Overexpression of Arl1 or Imh1 restores GARP complex localization to the TGN in ypt6Δ cells. The N-terminal domain of Imh1 is critical for restoring GARP localization and endosome-to-TGN transport in the absence of Ypt6. Overexpression rescue genetics, GARP localization assay, retrograde transport assay, domain deletion analysis Molecular biology of the cell Medium 30726160
2020 H2O2-induced oxidative stress causes protease-dependent degradation of Arl1 in HeLa cells, leading to dissociation of GRIP-domain proteins Golgin-97 and Golgin-245 from the trans-Golgi, loss of trans-Golgi cisternae, and inhibition of both anterograde and retrograde protein transport. ROS scavenger N-acetyl cysteine or protease inhibitors rescue Arl1 levels and Golgi function. H2O2 treatment, immunofluorescence, protease inhibitor rescue, ROS scavenger rescue, electron microscopy Molecular biology of the cell Medium 32583744
2021 ARG2 interacts with ARL1 (identified by yeast two-hybrid assay). ARL1 knockdown inhibits autophagy while ARL1 overexpression promotes it in dermal fibroblasts, placing ARL1 downstream of ARG2 in autophagy regulation. Yeast two-hybrid, siRNA knockdown, overexpression, autophagy assays in fibroblasts Antioxidants Low 34943028
2024 Cryo-EM structures of full-length Gea2 and the Arl1-Gea2 complex reveal that: (1) Gea2 forms a stable dimer via DCB and HUS domain interfaces; (2) Arl1 binds to the outer surface of the Gea2 DCB domain (not the dimerization surface), leaving the Gea2 dimer intact; (3) the interaction involves the classic FWY aromatic residue triad and two Arl1-specific residues; (4) mutations disrupting the Arl1-Gea2 interface abolish Imh1 Golgi association. Cryo-EM structure determination, mutagenesis, Imh1 Golgi localization assay Nature communications High 38431634

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 ARL1, a LOB-domain protein required for adventitious root formation in rice. The Plant journal : for cell and molecular biology 291 15960615
2001 ADP-ribosylation factors (ARFs) and ARF-like 1 (ARL1) have both specific and shared effectors: characterizing ARL1-binding proteins. The Journal of biological chemistry 129 11303027
2001 Regulation of Golgi structure and function by ARF-like protein 1 (Arl1). Journal of cell science 115 11792819
1996 The mammalian ARF-like protein 1 (Arl1) is associated with the Golgi complex. Journal of cell science 80 8834805
2012 The small G protein Arl1 directs the trans-Golgi-specific targeting of the Arf1 exchange factors BIG1 and BIG2. The Journal of cell biology 57 22291037
2002 ARL1 and membrane traffic in Saccharomyces cerevisiae. Yeast (Chichester, England) 45 12210899
2011 Arfaptins are localized to the trans-Golgi by interaction with Arl1, but not Arfs. The Journal of biological chemistry 44 21239483
2005 The Arf-like GTPase Arl1 and its role in membrane traffic. Biochemical Society transactions 44 16042553
2016 Autophagy in Saccharomyces cerevisiae requires the monomeric GTP-binding proteins, Arl1 and Ypt6. Autophagy 39 27462928
2009 The localization of the Golgin GCC185 is independent of Rab6A/A' and Arl1. Cell 38 19703403
2006 Knockout of Arfrp1 leads to disruption of ARF-like1 (ARL1) targeting to the trans-Golgi in mouse embryos and HeLa cells. Molecular membrane biology 38 17127620
2002 An ARL1 mutation affected autophagic cell death in yeast, causing a defect in central vacuole formation. Cell death and differentiation 38 11840166
2014 The Arf family G protein Arl1 is required for secretory granule biogenesis in Drosophila. Journal of cell science 36 24610947
2019 ARFRP1 functions upstream of ARL1 and ARL5 to coordinate recruitment of distinct tethering factors to the trans-Golgi network. The Journal of cell biology 32 31575603
2017 Multiple activities of Arl1 GTPase in the trans-Golgi network. Journal of cell science 32 28468990
2009 Differential effects of depletion of ARL1 and ARFRP1 on membrane trafficking between the trans-Golgi network and endosomes. The Journal of biological chemistry 32 19224922
2004 Yeast ARL1 encodes a regulator of K+ influx. Journal of cell science 31 15126631
2008 The leishmania ARL-1 and Golgi traffic. PloS one 30 18286177
2006 ARL1 plays a role in the binding of the GRIP domain of a peripheral matrix protein to the Golgi apparatus in plant cells. Plant molecular biology 29 16830178
2020 Hydrogen peroxide induces Arl1 degradation and impairs Golgi-mediated trafficking. Molecular biology of the cell 20 32583744
2019 Role of Arf-like proteins (Arl1 and Arl2) of Mucor circinelloides in virulence and antifungal susceptibility. Fungal genetics and biology : FG & B 19 31014992
2017 The Arl3 and Arl1 GTPases co-operate with Cog8 to regulate selective autophagy via Atg9 trafficking. Traffic (Copenhagen, Denmark) 18 28627726
2021 Resolvin D1 Suppresses H2O2-Induced Senescence in Fibroblasts by Inducing Autophagy through the miR-1299/ARG2/ARL1 Axis. Antioxidants (Basel, Switzerland) 17 34943028
2019 Action of Arl1 GTPase and golgin Imh1 in Ypt6-independent retrograde transport from endosomes to the trans-Golgi network. Molecular biology of the cell 17 30726160
2011 Dysregulated Arl1, a regulator of post-Golgi vesicle tethering, can inhibit endosomal transport and cell proliferation in yeast. Molecular biology of the cell 17 21562219
2005 Functional analysis of Arl1 and golgin-97 in endosome-to-TGN transport using recombinant Shiga toxin B fragment. Methods in enzymology 16 16413290
2012 Comparison of the influence of small GTPases Arl1 and Ypt6 on yeast cells' tolerance to various stress factors. FEMS yeast research 14 22188384
2004 ARL1 participates with ATC1/LIC4 to regulate responses of yeast cells to ions. Biochemical and biophysical research communications 12 14975746
2022 Case Report: Dramatic Response to Crizotinib in a Patient With Non-Small Cell Lung Cancer Positive for a Novel ARL1-MET Fusion. Frontiers in oncology 10 35237515
2005 Interaction of Arl1 GTPase with the GRIP domain of Golgin-245 as assessed by GST (glutathione-S-transferase) pull-down experiments. Methods in enzymology 10 16413289
2020 Estimation of Hg(II) in Soil Samples by Bioluminescent Bacterial Bioreporter E. coli ARL1, and the Effect of Humic Acids and Metal Ions on the Biosensor Performance. Sensors (Basel, Switzerland) 9 32498220
2020 Arf-like proteins (Arl1 and Arl2) are involved in mitochondrial homeostasis in Mucor circinelloides. Fungal biology 9 32540185
2005 ARL1 has an essential role in Trypanosoma brucei. Biochemical Society transactions 9 16042563
2015 Arfaptin-1 negatively regulates Arl1-mediated retrograde transport. PloS one 8 25789876
2004 The yeast genes, ARL1 and CCZ1, interact to control membrane traffic and ion homeostasis. Biochemical and biophysical research communications 7 15184059
2015 Preconcentration and detection of mercury with bioluminescent bioreporter E. coli ARL1. Applied microbiology and biotechnology 5 26099333
2012 Mon2 is a negative regulator of the monomeric G protein, Arl1. FEMS yeast research 5 22594927
2015 The guanine exchange factor Gartenzwerg and the small GTPase Arl1 function in the same pathway with Arfaptin during synapse growth. Biology open 4 26116655
2003 [Screening of the drug resistance-associated gene in HepG2 cell line transfected with aldose reductase like gene-1 (ARL-1)]. Ai zheng = Aizheng = Chinese journal of cancer 4 14693054
2025 Identification of the arl1 locus controlling leaf rolling and its application in maize breeding. Molecular breeding : new strategies in plant improvement 3 39763573
2003 Preparation and characterization of polyclonal antibodies against ARL-1 protein. World journal of gastroenterology 3 12854140
2024 Structural insight into an Arl1-ArfGEF complex involved in Golgi recruitment of a GRIP-domain golgin. Nature communications 2 38431634
2005 [Preparation and characterization of monoclonal antibody against ARL-1 protein]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 0 15629086
2000 [The construction of PQE-ARL-1 recombinant expression plasmid and the preparation and purification of ARL-1 protein]. Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 0 11135699

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