Affinage

PI4KB

Phosphatidylinositol 4-kinase beta · UniProt Q9UBF8

Length
816 aa
Mass
91.4 kDa
Annotated
2026-06-10
42 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PI4KB (PI4KIIIβ) is a type III phosphatidylinositol 4-kinase that phosphorylates phosphatidylinositol to generate PI4P, and the Golgi/trans-Golgi PI4P pools it produces control membrane trafficking, secretion, lipid transport, antiviral signaling, autophagy, and myelination (PMID:11277933, PMID:39580461, PMID:33106410). Catalytically, PI4KB is a high-Km type III kinase whose activity is tuned both by membrane recruitment and by phosphorylation at a defined cluster of sites (S294 increasing kinase activity, with additional sites including S496/T504 governing localization) (PMID:16606619, PMID:11277933). Its function depends on recruitment to specific membranes by a panel of adaptors: ACBD3 binds PI4KB and, upon membrane recruitment, stimulates its lipid kinase activity to support Golgi function (PMID:27009356, PMID:27989622), while ARL5A/B GTPases and their effector ARMH3/C10orf76 define a SYS1–ARFRP1–ARL5–ARMH3 axis that generates the main TGN PI4P pool driving GOLPH3 recruitment, glycosylation, and secretion (PMID:31829496, PMID:35844135, PMID:39580461); RAB30 and SCAMP5 provide additional recruitment routes (PMID:30290718, PMID:40958389). PI4KB partitions into distinct subcellular PI4P pools, with the C10orf76/ARMH3-recruited pool at distal Golgi feeding CERT-mediated ceramide transport, separate from the ACBD3-associated proximal pool (PMID:37195633). PI4KB is regulated post-translationally by phosphorylation-dependent 14-3-3 binding, which forms a 2:2 complex that protects PI4KB from proteolysis without altering its catalytic activity or blocking ACBD3-mediated recruitment (PMID:28864297, PMID:30679637). Beyond constitutive trafficking, PI4KB-generated PI4P directs cGAMP-triggered STING Golgi-to-endosome transport via ARMH3 (PMID:36921576), drives non-canonical autophagosome formation downstream of a P38–ULK1 cascade that phosphorylates PI4KB at S256/T263 in oncogenic KRAS contexts (PMID:40055523), and is required for myelination in Schwann cells through Golgi lipid metabolism and protein glycosylation (PMID:33106410). PI4KB is broadly hijacked by RNA viruses, which redirect it to replication organelles through viral proteins that co-opt ACBD3 or other partners to locally synthesize PI4P (PMID:27009356, PMID:30755512, PMID:31747597).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2001 High

    Established PI4KB's core biochemical identity by showing recombinant enzyme produces PI4P with type III kinase kinetics and mapping its phosphorylation-site cluster, framing how the enzyme would later be found to be regulated.

    Evidence Recombinant protein expression, in vitro lipid kinase assay, MALDI-MS and LC-MS/MS phosphosite mapping

    PMID:11277933

    Open questions at the time
    • Did not assign functional consequences to individual phosphosites
    • No information on physiological kinases responsible
  2. 2006 Medium

    Resolved that distinct phosphorylation states partition PI4KB between compartments and tune its activity, linking S294 phosphorylation to Golgi localization/activation and S496/T504 to nuclear speckles and cell viability.

    Evidence Anti-phosphopeptide antibodies, immunofluorescence, microinjection, lipid kinase assay

    PMID:16606619

    Open questions at the time
    • Upstream kinases not identified
    • Nuclear speckle function of PI4KB mechanistically unexplained
  3. 2011 High

    Defined how PI4KB is spatially targeted by identifying ACBD3 as the Golgi adaptor that recruits it, and revealed this axis is hijacked by viruses to build PI4P-rich replication sites.

    Evidence Co-IP, ACBD3/PI4KB knockdown with viral replication readout, colocalization imaging

    PMID:22124328

    Open questions at the time
    • Structural basis of ACBD3–PI4KB binding not yet defined
    • Did not address whether recruitment alters catalytic output
  4. 2016 High

    Provided structural and biochemical mechanism for ACBD3-dependent activation, showing membrane recruitment via ACBD3 boosts PI4KB kinase activity and that viral 3A protein directly activates the kinase, sensitized by ACBD3.

    Evidence NMR and crystal structures, HDX-MS interface mapping, in vitro membrane recruitment and lipid kinase activity assays, mutagenesis

    PMID:27009356 PMID:27989622

    Open questions at the time
    • Did not establish the activation mechanism at atomic resolution for the full membrane-bound complex
    • Relevance of in vitro activation magnitudes to cellular PI4P pools not quantified
  5. 2016 High

    Validated PI4KB as a druggable antiviral target by defining the ATP-site binding mode of selective inhibitors.

    Evidence X-ray crystallography, enzyme inhibition and antiviral assays

    PMID:28004945

    Open questions at the time
    • Selectivity against the full lipid kinase family not exhaustively profiled
    • In vivo efficacy not addressed
  6. 2017 High

    Clarified the post-translational control of PI4KB stability by showing 14-3-3 forms a 2:2 complex upon phosphorylation that protects PI4KB from proteolysis without altering activity or blocking ACBD3 recruitment.

    Evidence SAXS, fluorescence biophysics, proteolysis-protection and activity assays, structural analysis; conserved 14-3-3 recognition shown by crystallography

    PMID:27827352 PMID:28864297

    Open questions at the time
    • Cellular consequences of disrupting 14-3-3 binding not tested
    • Identity of the kinase generating the 14-3-3 site in vivo unresolved
  7. 2019 High

    Distinguished adaptor-specific recruitment routes by establishing ACBD3 as essential for viral 3A-driven recruitment and characterizing a separate c10orf76–PI4KB complex (via the kinase linker, PKA-modulated) that raises Golgi PI4P and supports Arf1 activation.

    Evidence ACBD3/PI4KB KO and reconstitution with defined mutants, HDX-MS, PI4P measurement, virus replication assays

    PMID:30755512 PMID:31829496

    Open questions at the time
    • Whether c10orf76 and ACBD3 pools are physically segregated not yet shown
    • Role of PKA phosphorylation in physiological signaling undefined
  8. 2019 Medium

    Mapped the conformational architecture of PI4KB heterocomplexes, defining stoichiometries (14-3-3:PI4KB:Rab11 of 2:1:1) and membrane-dependent assembly of the ACBD3:PI4KB:Rab11 complex.

    Evidence SAXS, in vitro reconstitution

    PMID:30679637

    Open questions at the time
    • Low-resolution flexible models lack atomic detail
    • Functional output of Rab11-containing complexes not tested
  9. 2020 High

    Demonstrated a physiological, organ-level requirement for PI4KB by showing Schwann-cell-specific deletion disrupts Golgi morphology, OSBP/GOLPH3 localization, and lipid metabolism, impairing myelination.

    Evidence Conditional PI4KB knockout mice, EM, immunofluorescence, lipid analysis, nerve conduction velocity

    PMID:33106410

    Open questions at the time
    • Did not separate trafficking versus lipid-transport contributions to the myelin defect
    • Human relevance to peripheral neuropathy not established
  10. 2022 Medium

    Identified ARL5A/B GTPases as additional trans-Golgi recruiters of PI4KB that promote PI4P synthesis and secretion.

    Evidence miniTurboID proximity biotinylation, quantitative MS, interaction and functional secretion assays

    PMID:35844135

    Open questions at the time
    • PI4KB was one of many hits in a broad Arf-family screen
    • Direct versus indirect ARL5–PI4KB binding not fully resolved
  11. 2023 High

    Resolved that distinct adaptor-defined PI4P pools serve different effectors: the C10orf76/ARMH3 distal-Golgi pool feeds CERT-mediated ceramide transport and directs cGAMP-triggered STING trafficking via PI4P-binding AP-1/GGA2.

    Evidence Genome-wide CRISPR screens, super-resolution microscopy, ceramide transport assays, co-IP, RNAi of PI4P-binding proteins, in vivo Armh3 mouse model

    PMID:36921576 PMID:37195633

    Open questions at the time
    • How spatial specificity of pools is biophysically maintained not defined
    • Cross-talk between trafficking and innate-immune pools unexplored
  12. 2024 High

    Placed PI4KB at the output of a defined GTPase signaling axis, showing ARMH3 is the active-ARL5 effector that activates PI4KB to generate the main TGN PI4P pool controlling GOLPH3 recruitment and glycosylation.

    Evidence Proximity biotinylation, binding assays with active/inactive ARL5 mutants, PI4P measurement, knockdown/knockout functional readouts

    PMID:39580461

    Open questions at the time
    • Direct activation mechanism of PI4KB by ARMH3 not structurally resolved
    • Quantitative partitioning between ARMH3 and ACBD3 pools not measured
  13. 2025 High

    Extended PI4KB into signal-driven non-canonical autophagy by showing ULK1 phosphorylates PI4KB at S256/T263 downstream of P38 to drive PI4P production and ATG8ylation in oncogenic KRAS contexts, and identifying SCAMP5 as a TGN recruiter enabling AP-4/ATG9A-dependent presynaptic autophagy.

    Evidence Phosphosite mutagenesis, genetic knockouts, PI4P and autophagy-flux assays, xenograft/KPC mouse models; co-IP and trafficking assays for SCAMP5

    PMID:40055523 PMID:40958389

    Open questions at the time
    • SCAMP5 axis rests on single-lab co-IP and knockdown data
    • How ULK1-driven and Golgi housekeeping PI4P pools are kept distinct unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the cell biophysically segregates the multiple adaptor-defined PI4KB/PI4P pools (ACBD3, ARMH3/ARL5, RAB30, SCAMP5) so that each delivers PI4P to a dedicated effector pathway without cross-interference.
  • No unified spatial model integrating all adaptors
  • Stoichiometry and dynamics of competing complexes in living cells unmeasured
  • Functional hierarchy among adaptors under physiological signaling undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 4 GO:0140097 catalytic activity, acting on DNA 1
Localization
GO:0005794 Golgi apparatus 5 GO:0005654 nucleoplasm 1
Pathway
R-HSA-1643685 Disease 3 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-9612973 Autophagy 3 R-HSA-1430728 Metabolism 2 R-HSA-168256 Immune System 1
Partners
ACBD3ANXA2ARL5AARL5BC10ORF76/ARMH3RAB30SCAMP5YWHA (14-3-3)
Complex memberships
14-3-3:PI4KB (2:2) complex14-3-3:PI4KB:Rab11 complexACBD3:PI4KB complexC10orf76(ARMH3):PI4KB complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 ACBD3 (a Golgi-resident protein) interacts with PI4KB and recruits it to Aichi virus RNA replication sites, forming a viral protein/ACBD3/PI4KB complex that synthesizes PI4P at replication sites essential for viral RNA replication. Co-immunoprecipitation, knockdown of ACBD3 or PI4KB (loss-of-function with viral replication readout), colocalization imaging The EMBO journal High 22124328
2016 NMR structure of the PI4KB–ACBD3 complex was determined; ACBD3 recruits PI4KB to membranes both in vitro and in vivo and membrane recruitment increases PI4KB enzymatic (lipid kinase) activity; the ACBD3:PI4KB complex is essential for proper Golgi function. NMR structure determination, in vitro membrane recruitment assay, in vivo localization, enzymatic activity assay Scientific reports High 27009356
2016 Crystal structure of the ACBD3 GOLD domain revealed a unique N-terminus mediating interaction with Aichi virus 3A protein; 3A directly activates PI4KIIIβ lipid kinase activity, and this activation is sensitized by ACBD3; complex-disrupting mutations in ACBD3 and PI4KIIIβ abrogated this sensitization. Interfaces were mapped by hydrogen-deuterium exchange mass spectrometry (HDX-MS). Biochemical reconstitution, crystal structure determination, HDX-MS interface mapping, mutagenesis, lipid kinase activity assay Structure High 27989622
2016 PI4KB inhibitors bind in the ATP-binding site of PI4KB; crystallographic analysis confirmed the binding mode and explains their inhibitory activity against PI4KB, with selectivity over other kinases. X-ray crystallography, enzyme inhibition assays, antiviral assays Journal of medicinal chemistry High 28004945
2017 PI4KB forms a tight 2:2 complex with 14-3-3 proteins upon phosphorylation; 14-3-3 binding does not directly modulate PI4KB enzymatic activity but protects PI4KB from proteolytic degradation in vitro; structural analysis showed 14-3-3 binding does not interfere with ACBD3-mediated membrane recruitment. Biophysical characterization (SAXS, fluorescence methods), proteolysis protection assay, enzymatic activity assay, structural analysis Journal of structural biology High 28864297
2019 ACBD3 is an essential mediator of enterovirus 3A-dependent PI4KB recruitment to replication organelles; ACBD3 knockout prevented PI4KB recruitment and impaired 3A Golgi localization; a PI4KB mutant unable to bind ACBD3 failed to restore replication in PI4KB-KO cells; the ACB and CAR domains of ACBD3 are dispensable for PI4KB recruitment. ACBD3 and PI4KB knockout cells, reconstitution with wild-type and mutant proteins, fluorescence microscopy localization, virus replication assays mBio High 30755512
2019 c10orf76 forms a complex with PI4KB mediated by the kinase linker of PI4KB; PKA-dependent phosphorylation modulates complex formation; PI4KB is required for membrane recruitment of c10orf76 to the Golgi; the intact c10orf76–PI4KB complex increases Golgi PI4P levels and is required for replication of specific enteroviruses; c10orf76 contributes to Arf1 activation at the Golgi. HDX-MS complex characterization, complex-disrupting mutagenesis, PI4P level measurement, virus replication assay, localization studies EMBO reports High 31829496
2019 PI4KB forms highly flexible heterocomplexes including ACBD3, 14-3-3, and Rab11 proteins; the 14-3-3:PI4KB:Rab11 complex has 2:1:1 stoichiometry; the ACBD3:PI4KB complex exists in very compact and extended conformations; membrane is necessary for formation of the ACBD3:PI4KB:Rab11 complex at physiological concentrations. Small angle X-ray scattering (SAXS), in vitro reconstitution Scientific reports Medium 30679637
2006 PI4K92 (PI4KB) phosphorylated at Ser-294 localizes exclusively to the Golgi and this phosphorylation increases lipid kinase activity; PI4K92 phosphorylated at Ser-496 and Thr-504 localizes to nuclear speckles dynamically and is required for cell viability (microinjection of anti-pSer-496 antibody caused apoptosis). Anti-phosphopeptide antibodies, indirect immunofluorescence, microinjection, lipid kinase activity assay The Journal of biological chemistry Medium 16606619
2001 Recombinant PI4K92 (PI4KB) produces PtdIns4P as product; is characterized as a type III PI4K (high Km for ATP and PtdIns in millimolar range, IC50 ~300 nM for Wortmannin); multiple phosphorylation sites mapped by MALDI-MS and LC-MS/MS at S258, T263, S266, S277, S294, T423, S496, T504 within a designated phosphorylation domain. Recombinant protein expression, in vitro lipid kinase assay, MALDI-MS, LC-MS/MS phosphorylation site mapping European journal of biochemistry High 11277933
2022 ARL5A and ARL5B GTPases interact with PI4KB at the trans-Golgi and recruit it, thereby promoting PI4KB's function in PI4P synthesis and protein secretion. Proximity biotinylation (miniTurboID), quantitative mass spectrometry, protein interaction assays The EMBO journal Medium 35844135
2024 ARMH3 (C10orf76) is an effector of active ARL5 at the TGN; ARMH3 activates PI4KB to account for the main pool of PI4P at the TGN; this contributes to GOLPH3 recruitment and glycan modifications; the SYS1-ARFRP1-ARL5-ARMH3 axis regulates PI4KB-dependent PI4P generation at the TGN. Proximity biotinylation, protein interaction assays (active vs. inactive ARL5 mutants), PI4P level measurement, knockdown/knockout with functional readouts (GOLPH3 localization, glycan modification) Nature communications High 39580461
2023 ARMH3 interacts with STING at the Golgi upon cGAMP stimulation and recruits PI4KB to synthesize PI4P, which directs STING Golgi-to-endosome trafficking via PI4P-binding proteins AP-1 and GGA2; disrupting PI4P-dependent transport impaired STING activation; elevated cellular PI4P was sufficient for cGAS-independent STING activation. Genome-wide CRISPR-Cas9 screen, co-immunoprecipitation, PI4P measurement, RNAi of PI4P-binding proteins, in vivo mouse model (Armh3fl/fl LyzCre/Cre) Immunity High 36921576
2023 The C10orf76–PI4KB axis generates a specific pool of PI4P at distal Golgi subregions; CERT preferentially utilizes PI4P generated by PI4KB recruited via C10orf76 (not ACBD3) for ER-to-Golgi ceramide trafficking; C10orf76 localizes predominantly at distal Golgi where sphingomyelin synthesis occurs, while ACBD3 is at more proximal regions. Genome-wide screening, PI4P measurement, super-resolution microscopy, ceramide transport assays The Journal of cell biology High 37195633
2018 RAB30 interacts with PI4KB and recruits it to the Golgi apparatus and GAS-containing autophagosome-like vacuoles (GcAVs); PI4KB knockout suppressed autophagy by inhibiting GcAV formation, resulting in increased GAS survival; PtdIns4P is crucial for GcAV formation. Co-immunoprecipitation (RAB30–PI4KB interaction), PI4KB knockout cells, autophagy/GcAV formation assay, PI4P depletion/repletion experiments Autophagy Medium 30290718
2019 PI4KB is recruited to inclusion bodies formed by ER membrane remodeling during HPIV3 infection; the HPIV3 phosphoprotein (P) recruits PI4KB to IBs to generate PI4P, creating a PI4P-enriched microenvironment that promotes viral replication; HRSV nucleoprotein similarly recruits PI4KB to IBs. Co-immunoprecipitation, PI4P measurement, colocalization imaging, knockdown/loss-of-function viral replication assays Cell reports Medium 31747597
2017 Under PI4KB inhibition, PI4KB activity has distinct functions in both proteolytic processing of the enteroviral polyprotein and in replication organelle (RO) biogenesis; a PI4KB-inhibitor-resistant escape mutation corrects a proteolytic processing defect, revealing an unexpected role of PI4KB in viral polyprotein processing. PI4KB inhibitor-resistant mutant virus selection, electron tomography of ROs, viral polyprotein processing analysis Cell reports Medium 29045829
2020 SC-specific genetic inactivation of PI4KB in mice disrupts Golgi morphology in Schwann cells, causes disappearance of OSBP at cis-Golgi and loss of GOLPH3 from the entire Golgi, reduces cholesterol and sphingomyelin in sciatic nerves, reduces caveolae, and results in thinner myelin, abnormal nodes of Ranvier, and impaired engulfment of nerve fibers; demonstrating PI4KB Golgi function is required for myelination through lipid metabolism and protein glycosylation control. Conditional PI4KB knockout mice (SC-specific), electron microscopy, immunofluorescence, lipid analysis, nerve conduction velocity measurement PNAS High 33106410
2025 Oncogenic KRAS induces a non-canonical autophagy pathway (RINCAA) involving a P38-ULK1-PI4KB-WIPI2 signaling cascade; ULK1 phosphorylates PI4KB at S256 and T263, triggering PI4P production, ATG8ylation, and non-canonical autophagosome formation; inhibiting these phosphorylation sites reduces RINCAA activity and tumor growth in xenograft and KPC pancreatic cancer models. Genetic knockouts, phosphorylation site mutagenesis, PI4P measurement, autophagy flux assays, in vivo xenograft and KPC mouse models Cell research High 40055523
2021 ANXA2 interacts with both EV71 3D polymerase and PI4KB; the annexin domain of ANXA2 mediates 3D binding; ANXA2 localizes to replication organelles; ANXA2 overexpression stimulates PI4P production and promotes the PI4KB–3D interaction, facilitating formation of a higher-order ANXA2–PI4KB–3D protein complex at the viral replication site. Co-immunoprecipitation, ANXA2 knockout, PI4P level measurement, colocalization imaging Virologica Sinica Medium 34196914
2025 SCAMP5 is a binding partner of PI4KB/PI4KIIIβ at the TGN; SCAMP5 controls PI4KB recruitment to the TGN and subsequent PI4P production; PI4P is essential for AP-4 recruitment; SCAMP5 depletion disrupts AP-4-mediated ATG9A trafficking to presynaptic sites, impairing presynaptic autophagy. Co-immunoprecipitation (SCAMP5–PI4KB interaction), SCAMP5 knockdown with PI4P measurement, AP-4 localization, ATG9A trafficking assay, autophagosome formation assay Autophagy Medium 40958389
2014 HCV NS5A competes with PI4KB for binding to ACBD3 in a genotype-dependent manner; ACBD3 binds GT1b NS5A with higher affinity than GT2a NS5A, correlating with higher PI4KB/PI4P colocalization in GT1b-infected cells; NS5A displaces PI4KB from ACBD3 to allow PI4KB relocation to replication sites. Co-immunoprecipitation (competitive binding), colocalization imaging Antiviral research Medium 24792752
2016 A yeast 14-3-3 protein crystal structure bound to a phosphopeptide derived from human PI4KB was determined, demonstrating that the 14-3-3 recognition mode for PI4KB phosphopeptide is highly evolutionarily conserved. X-ray crystallography of 14-3-3 bound to PI4KB-derived phosphopeptide Acta crystallographica Section F Medium 27827352

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 ACBD3-mediated recruitment of PI4KB to picornavirus RNA replication sites. The EMBO journal 158 22124328
2023 ARMH3-mediated recruitment of PI4KB directs Golgi-to-endosome trafficking and activation of the antiviral effector STING. Immunity 80 36921576
2016 Structural insights and in vitro reconstitution of membrane targeting and activation of human PI4KB by the ACBD3 protein. Scientific reports 80 27009356
2016 Rational Design of Novel Highly Potent and Selective Phosphatidylinositol 4-Kinase IIIβ (PI4KB) Inhibitors as Broad-Spectrum Antiviral Agents and Tools for Chemical Biology. Journal of medicinal chemistry 56 28004945
2019 ACBD3 Is an Essential Pan-enterovirus Host Factor That Mediates the Interaction between Viral 3A Protein and Cellular Protein PI4KB. mBio 54 30755512
2017 Escaping Host Factor PI4KB Inhibition: Enterovirus Genomic RNA Replication in the Absence of Replication Organelles. Cell reports 52 29045829
2016 The Molecular Basis of Aichi Virus 3A Protein Activation of Phosphatidylinositol 4 Kinase IIIβ, PI4KB, through ACBD3. Structure (London, England : 1993) 44 27989622
2019 Characterization of the c10orf76-PI4KB complex and its necessity for Golgi PI4P levels and enterovirus replication. EMBO reports 36 31829496
2014 Amplification of Chromosome 1q Genes Encoding the Phosphoinositide Signalling Enzymes PI4KB, AKT3, PIP5K1A and PI3KC2B in Breast Cancer. Journal of Cancer 32 25368680
2006 Subcellular localization and structural function of endogenous phosphorylated phosphatidylinositol 4-kinase (PI4K92). The Journal of biological chemistry 30 16606619
2017 Structural analysis of phosphatidylinositol 4-kinase IIIβ (PI4KB) - 14-3-3 protein complex reveals internal flexibility and explains 14-3-3 mediated protection from degradation in vitro. Journal of structural biology 29 28864297
2000 Immunohistochemical localisation of two phosphatidylinositol 4-kinase isoforms, PI4K230 and PI4K92, in the central nervous system of rats. Experimental brain research 29 11045352
2022 Defining the proximal interaction networks of Arf GTPases reveals a mechanism for the regulation of PLD1 and PI4KB. The EMBO journal 22 35844135
2019 Phosphatidylinositol 4-kinase IIIβ (PI4KB) forms highly flexible heterocomplexes that include ACBD3, 14-3-3, and Rab11 proteins. Scientific reports 22 30679637
2001 Human phosphatidylinositol 4-kinase isoform PI4K92. Expression of the recombinant enzyme and determination of multiple phosphorylation sites. European journal of biochemistry 22 11277933
2023 CircRNA-PI4KB Induces Hepatic Lipid Deposition in Non-Alcoholic Fatty Liver Disease by Transporting miRNA-122 to Extra-Hepatocytes. International journal of molecular sciences 21 36674813
2020 Myelination of peripheral nerves is controlled by PI4KB through regulation of Schwann cell Golgi function. Proceedings of the National Academy of Sciences of the United States of America 21 33106410
2021 ANXA2 Facilitates Enterovirus 71 Infection by Interacting with 3D Polymerase and PI4KB to Assist the Assembly of Replication Organelles. Virologica Sinica 20 34196914
2019 PI4KB on Inclusion Bodies Formed by ER Membrane Remodeling Facilitates Replication of Human Parainfluenza Virus Type 3. Cell reports 20 31747597
2016 Fluorescent Inhibitors as Tools To Characterize Enzymes: Case Study of the Lipid Kinase Phosphatidylinositol 4-Kinase IIIβ (PI4KB). Journal of medicinal chemistry 19 28004946
2022 Cytoplasmic domain and enzymatic activity of ACE2 are not required for PI4KB dependent endocytosis entry of SARS-CoV-2 into host cells. Virologica Sinica 18 35272059
2018 RAB30 regulates PI4KB (phosphatidylinositol 4-kinase beta)-dependent autophagy against group A Streptococcus. Autophagy 17 30290718
2014 Hepatitis C virus NS5A competes with PI4KB for binding to ACBD3 in a genotype-dependent manner. Antiviral research 17 24792752
2021 circSLC6A6 Sponges miR-497-5p to Promote Endometrial Cancer Progression via the PI4KB/Hedgehog Axis. Journal of immunology research 15 34258297
2023 The C10orf76-PI4KB axis orchestrates CERT-mediated ceramide trafficking to the distal Golgi. The Journal of cell biology 14 37195633
2025 Oncogenic RAS induces a distinctive form of non-canonical autophagy mediated by the P38-ULK1-PI4KB axis. Cell research 13 40055523
2019 Identification of novel Plasmodium falciparum PI4KB inhibitors as potential anti-malarial drugs: Homology modeling, molecular docking and molecular dynamics simulations. Computational biology and chemistry 12 30928871
2016 Crystal structures of a yeast 14-3-3 protein from Lachancea thermotolerans in the unliganded form and bound to a human lipid kinase PI4KB-derived peptide reveal high evolutionary conservation. Acta crystallographica. Section F, Structural biology communications 12 27827352
2015 PI4K-beta and MKNK1 are regulators of hepatitis C virus IRES-dependent translation. Scientific reports 10 26323588
2024 Bithiazole inhibitors of PI4KB show broad-spectrum antiviral activity against different viral families. Antiviral research 9 39265657
2025 Targeting PI4KB and Src/Abl host kinases as broad-spectrum antiviral strategy: Myth or real opportunity? Antiviral research 8 39922541
2023 CUR-N399, a PI4KB inhibitor, for the treatment of Enterovirus A71 infection. Antiviral research 8 37657668
2019 Identification and functional characterization of two novel mutations in KCNJ10 and PI4KB in SeSAME syndrome without electrolyte imbalance. Human genomics 8 31640787
2024 N-terminal acetyltransferase 6 facilitates enterovirus 71 replication by regulating PI4KB expression and replication organelle biogenesis. Journal of virology 7 38189249
2024 ARMH3 is an ARL5 effector that promotes PI4KB-catalyzed PI4P synthesis at the trans-Golgi network. Nature communications 7 39580461
2020 Another hijack! Some enteroviruses co-opt the c10orf76/PI4KB complex for their own good. EMBO reports 5 31919962
2024 Locational and functional characterization of PI4KB in the mouse embryo. Journal of cellular physiology 4 38230579
2023 Inhibition of Pi4kb activity causes malformation of vestibular apparatus in zebrafish by downregulating hey1. Gene 3 38135256
2024 PI4KB is an essential host factor for duck hepatitis a virus 1 replication and translation. International journal of biological macromolecules 1 39393728
2026 Chlamydia pneumoniae facilitates its development by recruiting PI4P to inclusion bodies via the Cpn0308-ACBD3-PI4KB pathway. Infection and immunity 0 42240327
2025 SCAMP5 regulates AP-4-dependent sorting and trafficking of ATG9A for presynaptic autophagy via PI4KB/PI4KIIIβ recruitment and PtdInsP4 production at the TGN. Autophagy 0 40958389
2025 MAPK/p38-ULK1-PI4KB signaling defines a non-canonical autophagy mechanism in KRAS-Mutant tumors. Autophagy 0 41450005

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