Affinage

RAB39B

Ras-related protein Rab-39B · UniProt Q96DA2

Length
213 aa
Mass
24.6 kDa
Annotated
2026-06-10
100 papers in source corpus 16 papers cited in narrative 16 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RAB39B is a neuronal-enriched small RAB GTPase that operates at the endoplasmic reticulum/cis-Golgi interface and recycling endosomes to govern secretory trafficking critical for synaptic function (PMID:25784538, PMID:30987349, PMID:32762091). In its GTP-bound state it recruits PICK1 as a downstream effector to drive transport of the GluA2 AMPAR subunit from the ER to the Golgi and onto the neuronal surface, thereby setting AMPAR subunit composition; loss of RAB39B skews receptors toward GluA2-lacking Ca2+-permeable forms and alters synaptic activity (PMID:25784538). This trafficking function controls dendritic spine maturation, with RAB39B loss producing hypermobile, immature filopodia-like spines that are normalized by Ca2+-permeable AMPAR blockade, and is required for normal learning, memory, and social behavior (PMID:34035473, PMID:34761259). RAB39B also interacts with Class I PI3K components and restrains PI3K-AKT-mTOR signaling in neural progenitor cells; its deletion drives mTOR-dependent NPC overproliferation, macrocephaly, and ASD-like behaviors that are rescued by AKT inhibition (PMID:32115408). In dopaminergic neurons RAB39B sustains macroautophagy and α-synuclein homeostasis, and its loss-of-function impairs autophagic flux, causing α-synuclein accumulation, ER stress, mitochondrial dysfunction, and dopaminergic neuron death, effects reversible by rapamycin-induced autophagy activation (PMID:25434005, PMID:36715921, PMID:40473068). Disease-associated variants (T168K, G192R, W186X, nonstop p.*214) destabilize or mislocalize the protein and fail to support these functions, linking RAB39B to X-linked intellectual disability, autism, and early-onset Parkinson's disease (PMID:26399558, PMID:36715921, PMID:34761259).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2002 Low

    Established RAB39B as a distinct gene before any function was known, defining it as a novel RAB GTPase family member on Xq28.

    Evidence cDNA cloning from human fetal brain, genomic structure analysis, and northern blot tissue expression

    PMID:12438742

    Open questions at the time
    • No functional mechanism established beyond gene structure
    • Subcellular localization and effectors unknown
    • Neuronal role not yet addressed
  2. 2010 Medium

    First linked RAB39B to neuronal function by showing its Golgi localization and a requirement for synapse formation, answering whether the GTPase has a cell-biological role in neurons.

    Evidence shRNA knockdown in cultured neurons with immunofluorescence localization and growth-cone/presynaptic morphology analysis

    PMID:20159109

    Open questions at the time
    • No molecular effector or cargo identified
    • Mechanism connecting Golgi trafficking to synapse formation unresolved
  3. 2015 High

    Identified the molecular pathway by which RAB39B controls synapses—GTP-dependent recruitment of PICK1 to traffic GluA2 from ER to surface—establishing it as a determinant of AMPAR subunit composition.

    Evidence Co-IP and pulldown of GTP-bound RAB39B with PICK1, shRNA knockdown, GluA2 surface biotinylation, and electrophysiology in hippocampal neurons

    PMID:25784538

    Open questions at the time
    • GEF/GAP regulators of RAB39B nucleotide state not identified
    • Structural basis of PICK1 effector binding unresolved
  4. 2015 Low

    Tested how a PD-associated missense variant disrupts function, showing p.G192R mislocalizes the protein via its C-terminal targeting domain.

    Evidence Transfection of WT vs. mutant constructs in PC12 and SK-N-BE(2)C cells with immunofluorescence

    PMID:26399558

    Open questions at the time
    • Single localization experiment in transfected cells, single method
    • Functional consequence on trafficking not directly measured
  5. 2019 Medium

    Refined RAB39B localization to the ER/cis-Golgi secretory network distinct from RAB39A and assigned it a role in sphingolipid transport, clarifying the compartment in which it acts.

    Evidence Immunofluorescence co-localization, fluorescent lipid analog transport assays, and Chlamydia lipid-acquisition readout

    PMID:30987349

    Open questions at the time
    • Link between lipid transport and synaptic cargo trafficking unresolved
    • Effectors mediating lipid transport not identified
  6. 2020 High

    Connected RAB39B loss to neurodevelopmental overgrowth via a new interaction with Class I PI3K that normally restrains AKT-mTOR signaling in neural progenitors.

    Evidence Rab39b KO mice and human cerebral organoids, Co-IP with PI3K components, AKT-mTOR immunoblots, and AKT-inhibitor rescue with behavioral testing

    PMID:32115408

    Open questions at the time
    • Direct binding interface with PI3K not mapped
    • Whether the PI3K and PICK1/GluA2 roles are mechanistically connected unknown
  7. 2020 Medium

    Demonstrated that RAB39B maintains basal autophagic flux and postsynaptic NMDA receptor levels, linking its loss to memory deficits rescuable by autophagy activation.

    Evidence Rab39b KO mice, LC3/p62 autophagy immunoblots, synaptic fractionation, behavioral assays, and rapamycin rescue

    PMID:33364235

    Open questions at the time
    • Mechanism linking RAB39B to autophagosome biogenesis not defined
    • Relationship between autophagy and NMDA receptor regulation unclear
  8. 2020 Medium

    Mapped endogenous RAB39B expression across brain regions including dopaminergic neurons of the substantia nigra, providing the anatomical basis for both cognitive and parkinsonian phenotypes.

    Evidence In situ hybridization and immunohistochemistry with validated monoclonal antibodies and KO negative controls

    PMID:32228644

    Open questions at the time
    • Cell-type-specific function in dopaminergic vs. cortical neurons not dissected
  9. 2020 Medium

    Linked RAB39B to human synucleinopathy pathology, showing co-localization with Aβ plaques and Lewy bodies and reduced cytoplasmic RAB39B consistent with functional sequestration.

    Evidence Tissue microarray IHC, confocal co-localization, and subcellular fractionation on post-mortem DLB/AD brain

    PMID:32762091

    Open questions at the time
    • Causal direction between aggregate sequestration and RAB39B dysfunction not established
    • Correlative human tissue data
  10. 2021 High

    Established that RAB39B-driven GluA2 trafficking controls dendritic spine maturation in vivo, with Ca2+-permeable AMPAR blockade restoring spine stability.

    Evidence Rab39b KO mice, live two-photon spine FRAP/motility imaging, AMPAR surface assays, and NASPM pharmacological rescue

    PMID:34035473

    Open questions at the time
    • How spine maturation defects produce specific cognitive phenotypes unresolved
  11. 2022 Medium

    Extended the loss-of-function model to a nonstop variant, showing protein instability drives the same Ca2+-permeable AMPAR shift, immature spine phenotype, and behavioral deficits.

    Evidence Heterologous expression protein-stability assay, Rab39b KD mouse, AMPAR surface assays, spine morphology, and behavioral testing

    PMID:34761259

    Open questions at the time
    • Degradation pathway of unstable mutant not defined
  12. 2023 Medium

    Demonstrated that RAB39B deficiency impairs macroautophagy in dopaminergic cells, driving α-synuclein accumulation, ER stress, and mitochondrial apoptosis, with PD mutants failing to rescue.

    Evidence shRNA knockdown in SH-SY5Y cells, autophagy and α-synuclein immunoblots, mitochondrial potential and ROS assays, and WT vs. mutant rescue

    PMID:36715921

    Open questions at the time
    • Step in autophagy machinery directly regulated by RAB39B not identified
    • Cell-line model, not primary dopaminergic neurons
  13. 2023 Medium

    Showed that RAB39B dosage must be balanced—overexpression also impairs memory, synaptic transmission, and autophagy with autism-like behavior—indicating a tightly controlled level.

    Evidence AAV-mediated RAB39B overexpression in mice, behavioral testing, neuronal morphology, electrophysiology, and synaptic/autophagy immunoblots

    PMID:36977207

    Open questions at the time
    • Mechanism by which excess RAB39B disrupts trafficking not defined
  14. 2024 Low

    Modeled the PD-associated T168K variant in vivo, implicating impaired dopamine vesicular transmission as a contributor to dopaminergic dysfunction.

    Evidence C. elegans transgenic dopaminergic neurons expressing human RAB39B T168K, confocal imaging, motor and dopamine pharmacology assays

    PMID:38444482

    Open questions at the time
    • Indirect inference about dopamine vesicular transport mechanism
    • Single lab, invertebrate model
  15. 2025 Medium

    Consolidated the in vivo parkinsonian mechanism, showing RAB39B loss reduces ATG machinery and triggers α-synuclein accumulation, inflammasome activation, necroptosis, and dopaminergic neuron loss reversible by rapamycin.

    Evidence Rab39b KO male mice, autophagy/α-synuclein immunoblots, mitochondrial and ROS assays, TH+ neuron IHC, NLRP3/necroptosis markers, and rapamycin rescue

    PMID:40473068

    Open questions at the time
    • Direct molecular target of RAB39B in autophagy induction unresolved
    • Single lab in vivo study

Open questions

Synthesis pass · forward-looking unresolved questions
  • How RAB39B nucleotide cycling is regulated and whether its distinct roles in AMPAR trafficking, PI3K-mTOR signaling, and autophagy share a unifying molecular mechanism remain unresolved.
  • No GEF/GAP identified for RAB39B
  • No structural model of effector recognition
  • Mechanistic link between secretory trafficking and autophagy regulation undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003924 GTPase activity 2 GO:0060089 molecular transducer activity 2
Localization
GO:0005783 endoplasmic reticulum 3 GO:0005794 Golgi apparatus 3 GO:0005768 endosome 1
Pathway
R-HSA-9612973 Autophagy 3 R-HSA-112316 Neuronal System 2 R-HSA-5653656 Vesicle-mediated transport 2 R-HSA-162582 Signal Transduction 1
Partners
GLUA2/GRIA2PICK1PIK3 (CLASS I PI3K)

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 RAB39B is a neuronal-specific protein localized to the Golgi compartment. shRNA-mediated downregulation of RAB39B in neurons leads to alteration in the number and morphology of neurite growth cones and a significant reduction in presynaptic buttons, indicating a role in synapse formation and maintenance. shRNA knockdown in cultured neurons, immunofluorescence localization, morphological analysis American journal of human genetics Medium 20159109
2014 Loss of RAB39B (complete deletion or destabilizing missense mutation p.Thr168Lys) results in reduced steady-state levels of α-synuclein and reduced density of α-synuclein immunoreactive puncta in dendritic processes. shRNA knockdown of Rab39b in cultured neurons and multiple cell models confirmed that RAB39B regulates α-synuclein homeostasis. shRNA knockdown in cultured neurons, immunofluorescence, western blot in multiple cell models, in vitro protein stability assay for p.T168K mutant American journal of human genetics Medium 25434005
2015 RAB39B p.G192R mutation causes mislocalization of the mutant protein in PC12 and SK-N-BE(2)C cells, likely by altering the structure of the hypervariable C-terminal domain that mediates intracellular targeting. Transfection of wild-type and mutant RAB39B constructs in PC12 and SK-N-BE(2)C cells, immunofluorescence localization Molecular neurodegeneration Low 26399558
2015 GTP-bound RAB39B interacts with PICK1 (protein interacting with C-kinase 1) as a downstream effector. The RAB39B–PICK1 complex controls trafficking of GluA2 from the endoplasmic reticulum to the Golgi and hence surface expression of the GluA2 AMPAR subunit. RAB39B downregulation in mouse hippocampal neurons skews AMPAR composition toward non-GluA2-containing Ca2+-permeable forms, altering synaptic activity. Co-immunoprecipitation, pulldown assays (GTP-bound RAB39B with PICK1), shRNA knockdown, electrophysiology, surface biotinylation of GluA2 Nature communications High 25784538
2019 RAB39B localizes to the secretory network at the endoplasmic reticulum/cis-Golgi interface (distinct from RAB39A which localizes to late endosomes/multivesicular bodies). RAB39B controls transport of sphingolipids biosynthesized at the ER-Golgi factory, while RAB39A controls trafficking of lipids at multivesicular bodies. Immunofluorescence co-localization, lipid transport assays using fluorescent lipid analogs, Chlamydia trachomatis lipid-acquisition assay as trafficking readout International journal of molecular sciences Medium 30987349
2020 RAB39B interacts with PI3K components (Class I PI3K), and its deletion promotes PI3K-AKT-mTOR signaling in neural progenitor cells (NPCs) in mouse cortex and human cerebral organoids. Hyperactivated mTOR signaling in RAB39B-null NPCs (including outer radial glia) drives overproliferation and impaired differentiation, leading to macrocephaly and ASD-like behaviors. AKT inhibition rescued enlarged organoid size and NPC overproliferation. Rab39b knockout mice, human cerebral organoids with RAB39B mutation, co-immunoprecipitation (RAB39B with PI3K components), western blot for AKT-mTOR pathway, AKT inhibitor rescue experiment, behavioral testing Genes & development High 32115408
2020 RAB39B deficiency in Rab39b KO mice impairs autophagic flux at basal level and reduces NMDA receptor levels in the postsynaptic density, leading to impaired learning and memory. Rapamycin-induced autophagy activation partially rescued impaired memory and synaptic plasticity. Rab39b knockout mice, LC3/p62 western blot for autophagic flux, synaptic fractionation with NMDA receptor immunoblot, behavioral assays (Morris water maze, novel object recognition), rapamycin rescue Frontiers in cell and developmental biology Medium 33364235
2020 RAB39B is localized throughout the cortex, hippocampus, and substantia nigra of mice, with high levels in MAP2-positive cortical and hippocampal neurons and TH-positive dopaminergic neurons in the substantia nigra pars compacta. In situ hybridization, immunohistochemistry with novel monoclonal antibodies against RAB39B, western blot on brain lysates, Rab39b knockout mouse validation Molecular brain Medium 32228644
2021 Lack of RAB39B in Rab39b KO mice affects neuronal dendritic spine refinement, increasing spine hypermobility and producing an immature filopodia-like spine arrangement with increased Ca2+-permeable (GluA2-lacking) AMPAR composition. The Ca2+-permeable AMPAR antagonist NASPM restored spine hypermobility, confirming that RAB39B-driven GluA2 trafficking controls spine maturation. Rab39b KO mouse model, live two-photon spine imaging (FRAP/motility), AMPAR subunit surface expression assay, NASPM pharmacological rescue, behavioral assays Molecular psychiatry High 34035473
2023 RAB39B deficiency impairs macroautophagy in SH-SY5Y dopaminergic cells, leading to increased α-synuclein and phospho-α-synuclein(Ser129) in the ER and mitochondria. This triggers ER stress, unfolded protein response, ER stress-induced pro-apoptotic cascade, mitochondrial membrane potential loss, and mitochondrial superoxide increase, ultimately activating mitochondrial apoptosis. PD mutants (T168K, W186X, G192R) of RAB39B failed to prevent these effects, unlike wild-type RAB39B. shRNA knockdown in SH-SY5Y cells, western blot for autophagy markers and α-synuclein, mitochondrial membrane potential assay, ROS measurement, apoptosis assays, rescue with wild-type vs. mutant RAB39B constructs Molecular neurobiology Medium 36715921
2022 A RAB39B nonstop mutation (c.640T>C; p.*214Glnext*21) causes RAB39B protein instability and increased degradation. Rab39b knockdown in a murine model increased GluA2-lacking Ca2+-permeable AMPAR composition at the hippocampal neuronal surface and increased dendritic spine density in an immature filopodia-like state, impairing social and memory behaviors. Heterologous cell expression of mutant RAB39B (western blot for protein stability), Rab39b KD mouse model, AMPAR subunit surface expression assay, dendritic spine morphology analysis, behavioral testing Human molecular genetics Medium 34761259
2025 RAB39B deficiency in Rab39b knockout male mice causes macroautophagy impairment (reduced Atg3, Atg5, Atg7, Atg12, Atg16L1 in substantia nigra), upregulation of α-synuclein and α-synuclein oligomers in dopaminergic neurons, ER stress-triggered apoptosis, mitochondrial dysfunction, NLRP3 inflammasome activation, and necroptosis (RIPK1-RIPK3-MLKL pathway). Rapamycin reversed autophagy dysfunction, reduced α-synuclein, and rescued motor deficits and dopaminergic neuron loss. Rab39b KO male mice, western blot for autophagy proteins and α-synuclein, mitochondrial membrane potential, ROS assay, immunohistochemistry for TH+ neurons and Lewy bodies, NLRP3/cytokine measurements, rapamycin rescue Life sciences Medium 40473068
2023 RAB39B overexpression in mouse brain (via neonatal AAV injection) impairs recognition and working memory, causes autism-like behaviors, decreases dendritic arborization of primary neurons in vitro, reduces synaptic transmission, and alters autophagy, without affecting synaptic protein levels or PSD distribution. AAV-mediated RAB39B overexpression in mice, behavioral testing, in vitro neuronal morphology assay, electrophysiology, western blot for synaptic/autophagy markers Journal of cellular and molecular medicine Medium 36977207
2024 Expression of the RAB39B T168K variant in C. elegans dopaminergic neurons leads to disrupted dendrites, blunt neuronal cells, motor dysfunction, and abnormal dopamine secretion (basal slowing response). Dopamine synthesis and recycling were normal, suggesting the mutation impairs dopamine vesicular transmission from the presynaptic membrane. C. elegans transgenic model expressing human RAB39B T168K, confocal microscopy of dopaminergic neurons, behavioral (motor) assays, dopamine pharmacology assays Heliyon Low 38444482
2020 RAB39B co-localizes with Aβ plaques in post-mortem human brain tissue from DLB and AD cases, and is present in a subpopulation of Lewy bodies in DLB. In DLB, cytoplasmic RAB39B is reduced (by subcellular fractionation) without change in total protein, consistent with sequestration in aggregates impairing RAB39B function. Physiologically, RAB39B is localized to Golgi vesicles and recycling endosomes. Tissue microarray immunohistochemistry, confocal co-localization with Aβ/α-synuclein markers, subcellular fractionation + western blot, post-mortem human brain tissue Brain pathology (Zurich, Switzerland) Medium 32762091
2002 RAB39B is expressed in a variety of human tissues and is located on chromosome Xq28, consisting of two exons. The protein shows 74.2% amino acid identity with RAB39A, establishing it as a novel member of the RAB GTPase family. cDNA cloning from human fetal brain library, sequencing, genomic structure analysis, northern blot for tissue expression Cytogenetic and genome research Low 12438742

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Mutations in RAB39B cause X-linked intellectual disability and early-onset Parkinson disease with α-synuclein pathology. American journal of human genetics 204 25434005
2010 Mutations in the small GTPase gene RAB39B are responsible for X-linked mental retardation associated with autism, epilepsy, and macrocephaly. American journal of human genetics 200 20159109
1993 Glycosylation of neuraminidase determines the neurovirulence of influenza A/WSN/33 virus. Journal of virology 131 8411368
2020 Cerebral organoid and mouse models reveal a RAB39b-PI3K-mTOR pathway-dependent dysregulation of cortical development leading to macrocephaly/autism phenotypes. Genes & development 124 32115408
1975 Temperature-sensitive mutants of influenza WSN virus defective in virus-specific RNA synthesis. Journal of virology 114 1165595
1990 Function of two discrete regions is required for nuclear localization of polymerase basic protein 1 of A/WSN/33 influenza virus (H1 N1). Molecular and cellular biology 113 2196448
1991 Two signals mediate nuclear localization of influenza virus (A/WSN/33) polymerase basic protein 2. Journal of virology 111 1985200
2015 The RAB39B p.G192R mutation causes X-linked dominant Parkinson's disease. Molecular neurodegeneration 88 26399558
2015 The intellectual disability protein RAB39B selectively regulates GluA2 trafficking to determine synaptic AMPAR composition. Nature communications 78 25784538
2015 Loss-of-function mutations in RAB39B are associated with typical early-onset Parkinson disease. Neurology. Genetics 77 27066548
1982 Complete nucleotide sequence of the neuraminidase gene of human influenza virus A/WSN/33. Journal of virology 75 7077751
2002 Persistence of viral RNA in the brain of offspring to mice infected with influenza A/WSN/33 virus during pregnancy. Journal of neurovirology 57 12161820
2003 Invasion and persistence of the neuroadapted influenza virus A/WSN/33 in the mouse olfactory system. Viral immunology 49 14583155
1992 Nuclear retention of M1 protein in a temperature-sensitive mutant of influenza (A/WSN/33) virus does not affect nuclear export of viral ribonucleoproteins. Journal of virology 44 1527844
2016 A novel RAB39B gene mutation in X-linked juvenile parkinsonism with basal ganglia calcification. Movement disorders : official journal of the Movement Disorder Society 42 27943471
2014 Activation of A1-adenosine receptors promotes leukocyte recruitment to the lung and attenuates acute lung injury in mice infected with influenza A/WSN/33 (H1N1) virus. Journal of virology 42 24965449
2019 Metabolomic Analysis of Influenza A Virus A/WSN/1933 (H1N1) Infected A549 Cells during First Cycle of Viral Replication. Viruses 41 31683654
1994 Abortive replication of influenza virus A/WSN/33 in HeLa229 cells: defective viral entry and budding processes. Virology 40 7941316
2017 Mutations in RAB39B in individuals with intellectual disability, autism spectrum disorder, and macrocephaly. Molecular autism 35 29152164
2015 Genetic analysis of the RAB39B gene in Chinese Han patients with Parkinson's disease. Neurobiology of aging 35 26163985
1983 The sequence of RNA segment 1 of influenza virus A/NT/60/68 and its comparison with the corresponding segment of strains A/PR/8/34 and A/WSN/33. Nucleic acids research 35 6828387
1982 Complete nucleotide sequence of the polymerase 3 gene of human influenza virus A/WSN/33. Journal of virology 35 7045393
1982 Sequence analysis of the polymerase 1 gene and the secondary structure prediction of polymerase 1 protein of human influenza virus A/WSN/33. Journal of virology 35 7143569
1985 Influenza viral (A/WSN/33) hemagglutinin is expressed and glycosylated in the yeast Saccharomyces cerevisiae. Proceedings of the National Academy of Sciences of the United States of America 34 2580304
1998 A novel spliced transcript of influenza A/WSN/33 virus. Virus genes 33 9857991
2002 Isolation and characterization of a human novel RAB (RAB39B) gene. Cytogenetic and genome research 32 12438742
1994 Analysis of the signals for polarized transport of influenza virus (A/WSN/33) neuraminidase and human transferrin receptor, type II transmembrane proteins. Journal of virology 32 8107243
2020 RAB39B Deficiency Impairs Learning and Memory Partially Through Compromising Autophagy. Frontiers in cell and developmental biology 30 33364235
2017 X-linked Parkinsonism with Intellectual Disability caused by novel mutations and somatic mosaicism in RAB39B gene. Parkinsonism & related disorders 29 28851564
1995 Characterization of putative defective interfering (DI) A/WSN RNAs isolated from the lungs of mice protected from an otherwise lethal respiratory infection with influenza virus A/WSN (H1N1): a subset of the inoculum DI RNAs. Virology 29 7793084
1988 Nucleotide sequence of RNA segment 7 and the predicted amino sequence of M1 and M2 proteins of FPV/Weybridge (H7N7) and WSN (H1N1) influenza viruses. Virus research 27 3414185
2015 Infection of mice with influenza A/WSN/33 (H1N1) virus alters alveolar type II cell phenotype. American journal of physiology. Lung cellular and molecular physiology 26 25595651
2008 The human H5N1 influenza A virus polymerase complex is active in vitro over a broad range of temperatures, in contrast to the WSN complex, and this property can be attributed to the PB2 subunit. The Journal of general virology 26 19008377
2019 Rab39a and Rab39b Display Different Intracellular Distribution and Function in Sphingolipids and Phospholipids Transport. International journal of molecular sciences 25 30987349
2001 Persistence of the influenza A/WSN/33 virus RNA at midbrain levels of immunodefective mice. Journal of neurovirology 25 11517384
1982 Proteolytic activation of influenza WSN virus in cultured cells is performed by homologous plasma enzymes. The Journal of general virology 25 6218257
1977 Characterization of cytoplasmic inclusions formed during influenza/WSN virus infection of chick embryo fibroblast cells. Intervirology 23 885697
2014 The temperature-sensitive and attenuation phenotypes conferred by mutations in the influenza virus PB2, PB1, and NP genes are influenced by the species of origin of the PB2 gene in reassortant viruses derived from influenza A/California/07/2009 and A/WSN/33 viruses. Journal of virology 22 25122786
2020 RAB39B's role in membrane traffic, autophagy, and associated neuropathology. Journal of cellular physiology 21 32761840
1980 Construction and characterization of a bacterial clone containing the hemagglutinin gene of the WSN strain (HON1) of influenza virus. Gene 21 6254839
2021 Dysfunction of RAB39B-Mediated Vesicular Trafficking in Lewy Body Diseases. Movement disorders : official journal of the Movement Disorder Society 20 33939203
2020 Clinical and Neuropathological Features Associated With Loss of RAB39B. Movement disorders : official journal of the Movement Disorder Society 20 31951675
2016 RAB39B gene mutations are not a common cause of Parkinson's disease or dementia with Lewy bodies. Neurobiology of aging 20 27459931
2004 Introduction of a temperature-sensitive phenotype into influenza A/WSN/33 virus by altering the basic amino acid domain of influenza virus matrix protein. Journal of virology 19 15331690
1993 Persistence of viral genes in a variant of MDBK cell after productive replication of a mutant of influenza virus A/WSN. Archives of virology 19 8418792
2005 Attenuating mutations of the matrix gene of influenza A/WSN/33 virus. Journal of virology 18 15650216
1989 Effects of cell differentiation on replication of A/WS/33, WSN, and A/PR/8/34 influenza viruses in mouse brain cell cultures: biological and immunological characterization of products. Journal of virology 18 2648025
2021 RAB39B-mediated trafficking of the GluA2-AMPAR subunit controls dendritic spine maturation and intellectual disability-related behaviour. Molecular psychiatry 17 34035473
1986 Identification of the defects in the hemagglutinin gene of two temperature-sensitive mutants of A/WSN/33 influenza virus. Virology 17 3765394
2015 The C terminus of NS1 protein of influenza A/WSN/1933(H1N1) virus modulates antiviral responses in infected human macrophages and mice. The Journal of general virology 16 25934792
2010 Prophylactic activity of intramuscular peramivir in mice infected with a recombinant influenza A/WSN/33 (H1N1) virus containing the H274Y neuraminidase mutation. Antimicrobial agents and chemotherapy 16 20404128
1990 Characterization of a temperature-sensitive mutant in the RNA polymerase PB2 subunit gene of influenza A/WSN/33 virus. Archives of virology 15 2222191
2020 RAB39B is redistributed in dementia with Lewy bodies and is sequestered within aβ plaques and Lewy bodies. Brain pathology (Zurich, Switzerland) 14 32762091
2012 Therapeutic activity of intramuscular peramivir in mice infected with a recombinant influenza A/WSN/33 (H1N1) virus containing the H275Y neuraminidase mutation. Antimicrobial agents and chemotherapy 14 22664977
1989 Role of hemagglutinin cleavage and expression of M1 protein in replication of A/WS/33, A/PR/8/34, and WSN influenza viruses in mouse brain. Journal of virology 14 2648024
1988 Transient expression and sequence of the matrix (M1) gene of WSN influenza A virus in a vaccinia vector. Virology 14 3354209
1986 Identification of defects in the neuraminidase gene of four temperature-sensitive mutants of A/WSN/33 influenza virus. Virology 14 3750846
1990 Inhibition of influenza virus A/WSN replication by a trypsin inhibitor, 6-amidino-2-naphthyl p-guanidinobenzoate. Biochemical and biophysical research communications 13 2350338
1984 Mechanism of interference between influenza A/WSN and B/Kanagawa viruses. The Journal of general virology 13 6747607
1976 Temperature-sensitive virion transcriptase activity in mutants of WSN influenza virus. Archives of virology 13 999515
2023 Deficiency of RAB39B Activates ER Stress-Induced Pro-apoptotic Pathway and Causes Mitochondrial Dysfunction and Oxidative Stress in Dopaminergic Neurons by Impairing Autophagy and Upregulating α-Synuclein. Molecular neurobiology 12 36715921
2016 RAB39B gene mutations are not linked to familial Parkinson's disease in China. Scientific reports 11 27694831
2000 Mapping to distal Xq28 of nonspecific X-linked mental retardation MRX72: linkage analysis and clinical findings in a three-generation Sardinian family. American journal of medical genetics 11 11050621
1993 MDBK cells which survived infection with a mutant of influenza virus A/WSN and subsequently received many passages contained viral M and NS genes in full length in the absence of virus production. Archives of virology 11 8517796
2020 Distribution of Parkinson's disease associated RAB39B in mouse brain tissue. Molecular brain 10 32228644
2020 Genetic Analysis of RAB39B in an Early-Onset Parkinson's Disease Cohort. Frontiers in neurology 10 32670181
2019 MDCK-B4GalNT2 cells disclose a α2,3-sialic acid requirement for the 2009 pandemic H1N1 A/California/04/2009 and NA aid entry of A/WSN/33. Emerging microbes & infections 10 31560252
2022 Research on Coverage Optimization in a WSN Based on an Improved COOT Bird Algorithm. Sensors (Basel, Switzerland) 9 35591071
2020 A novel RAB39B mutation and concurrent de novo NF1 mutation in a boy with neurofibromatosis type 1, intellectual disability, and autism: a case report. BMC neurology 9 32873259
2016 Lack of RAB39B mutations in early-onset and familial Parkinson's disease in a Taiwanese cohort. Neurobiology of aging 9 27838047
2012 The compensatory G88R change is essential in restoring the normal functions of influenza A/WSN/33 virus matrix protein 1 with a disrupted nuclear localization signal. Journal of virology 9 23077315
2022 RAB39B as a Chemosensitivity-Related Biomarker for Diffuse Large B-Cell Lymphoma. Frontiers in pharmacology 8 35910358
2018 An Effective Hybrid Routing Algorithm in WSN: Ant Colony Optimization in combination with Hop Count Minimization. Sensors (Basel, Switzerland) 8 29596336
2017 Generation of induced pluripotent stem cell line (ZZUi005-A) from a 21-year-old patient with a novel RAB39B gene mutation in X-linked juvenile parkinsonism. Stem cell research 8 29128816
1995 Non-sialate inhibitor of influenza A/WSN/33 neuraminidase. Biochemistry 8 7539292
1994 Use of competitive PCR to estimate the level of NS gene persisting in MDCK cells which survived productive replication of a mutant of influenza virus A/WSN. Journal of virological methods 8 7868652
2023 Increased level of RAB39B leads to neuronal dysfunction and behavioural changes in mice. Journal of cellular and molecular medicine 7 36977207
2018 Generation of RAB39B knockout isogenic human embryonic stem cell lines to model RAB39B-mediated Parkinson's disease. Stem cell research 7 29499499
2013 An Influenza Virus M2 Protein Specific Chimeric Antigen Receptor Modulates Influenza A/WSN/33 H1N1 Infection In Vivo. The open virology journal 7 23493233
2022 Clinical characterization of a novel RAB39B nonstop mutation in a family with ASD and severe ID causing RAB39B downregulation and study of a Rab39b knock down mouse model. Human molecular genetics 6 34761259
2025 Absence of Rab39b-induced macroautophagy impairment increases neurotoxic α-synuclein and causes degeneration of substantia nigra dopaminergic neurons in mouse model of X-linked Parkinson's disease. Life sciences 4 40473068
2023 Loss of RAB39B does not alter MPTP-induced Parkinson's disease-like phenotypes in mice. Frontiers in aging neuroscience 4 36761179
2015 [Inhibition of replication and transcription of WSN influenza A virus by IFIT family genes]. Sheng wu gong cheng xue bao = Chinese journal of biotechnology 4 26021086
2024 Novel RAB39B loss-of-function mutation in patient with typical early-onset Parkinson's disease. Parkinsonism & related disorders 3 38503262
2024 Energy efficient cluster-based routing protocol for WSN using multi-strategy fusion snake optimizer and minimum spanning tree. Scientific reports 3 39039083
2022 Multimodal imaging of a patient with RAB39B mutation. Neuroradiology 3 35088096
2022 Knockdown of FLT4, Nup98, and Nup205 Cellular Genes Effectively Suppresses the Reproduction of Influenza Virus Strain A/WSN/1933 (H1N1) In vitro. Infectious disorders drug targets 3 35339191
2020 Filamentous versus Spherical Morphology: A Case Study of the Recombinant A/WSN/33 (H1N1) Virus. Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada 3 32036809
2025 Two case reports of RAB39B deletion displaying highly variable parkinsonism. Parkinsonism & related disorders 2 40245817
2024 Expression of human Ras-related protein Rab39B variant T168K in Caenorhabditis elegans leads to motor dysfunction and dopaminergic neuron degeneration. Heliyon 2 38444482
2023 Novel RAB39B variant associated intellectual disability and levodopa-responsive young-onset parkinsonism. Parkinsonism & related disorders 2 37844350
2021 Generation of induced pluripotent stem cell line (ZZUi027-A) derived from skin fibroblasts from a Parkinson's disease patient with RAB39B gene mutation. Stem cell research 2 34247111
2019 LCSS-Based Algorithm for Computing Multivariate Data Set Similarity: A Case Study of Real-Time WSN Data. Sensors (Basel, Switzerland) 2 30621241
2018 Pre-exposure with influenza A virus A/WSN/1933(H1N1) resulted in viral shedding reduction from pigs challenged with either swine H1N1 or H3N2 virus. Veterinary microbiology 2 30593376
2014 Based on regular expression matching of evaluation of the task performance in WSN: a queue theory approach. TheScientificWorldJournal 2 25401151
2023 Influenza A virus strain PR/8/34, but neither HAM/2009 nor WSN/33, is transiently inhibited by the PB2-targeting drug paliperidone. Archives of virology 1 36637551
2022 Prenatal diagnosis of de novo int22h1/int22h2-mediated Xq28 duplication syndrome involving RAB39B following a previous ambiguous genitalia pregnancy. Taiwanese journal of obstetrics & gynecology 1 35595445
1988 Selective inhibition of WSN influenza virus haemolysis by pea lectin. The Journal of general virology 1 2832534
1975 Morphology of A/WSN influenza virus-infected chick embryo cells. Acta virologica 1 239562
2025 RAB39B: A novel biomarker for acute myeloid leukemia identified via multi-omics and functional validation. Open medicine (Warsaw, Poland) 0 40177653

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