Affinage

MLST8

Target of rapamycin complex subunit LST8 · UniProt Q9BVC4

Length
326 aa
Mass
35.9 kDa
Annotated
2026-06-10
47 papers in source corpus 21 papers cited in narrative 21 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

mLST8 (GβL) is a WD-repeat scaffold protein that binds directly to the kinase domain of mTOR and serves as a shared, rate-limiting structural component of both mTOR complexes, coupling nutrient status to mTOR kinase output (PMID:12718876, PMID:24331524). In mTORC1 it stabilizes the raptor-mTOR association and stimulates mTOR kinase activity toward S6K1 and 4E-BP1 in a nutrient- and rapamycin-regulated manner (PMID:12718876). Its more essential role is in mTORC2: genetic ablation of mLST8 phenocopies rictor loss, and mLST8 is required to maintain mTOR association with the mTORC2 cofactors RICTOR and SIN1 — through a direct interaction with the SIN1 N-terminal domain — to drive hydrophobic-motif phosphorylation of AKT, PKCα, and FOXO3 (PMID:17141160, PMID:31085701). This division of labor is conserved, with the ortholog functioning selectively in TORC2 in Drosophila and in the TOR pathway in yeast (PMID:12719473, PMID:22493059). mLST8 abundance and complex partitioning are tightly controlled: CCT4-mediated folding supports its accumulation (PMID:35239512), while post-translational modifications dynamically tune mTOR complex assembly — SUMOylation promotes both mTOR-Raptor and mTOR-Rictor formation (PMID:38395307), and non-degradative ubiquitination by CRL3-Keap1 (via an ETGE motif), by UBE3C/SLAP, or by TRAF2 selectively reduces mTORC2 integrity and AKT activation (PMID:37688978, PMID:41398047, PMID:36927703), whereas CDK1 phosphorylation triggers FBXW7-mediated proteasomal degradation (PMID:34741373). Through control of mTORC1, mLST8 governs ULK1 phosphorylation and autophagy, a function exploited as a host factor during coronavirus replication and implicated in retinal pigment epithelium pathology (PMID:37377422, PMID:40205682). Independently of mTOR, mLST8 binds IKKα/IKKβ and acts as a scaffold recruiting PP4, PP2A, and PP6 phosphatases to IKKβ, negatively regulating TNFα-induced NF-κB signaling (PMID:18755269, PMID:21110129).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2003 High

    Established that mLST8 is a direct mTOR-binding subunit that positively controls kinase activity and gates nutrient regulation, defining it as a core mTOR pathway component rather than a passive associate.

    Evidence Co-immunoprecipitation, in vitro kinase assay, and biochemical fractionation in mammalian cells; reciprocal co-IP and genetic epistasis in yeast Lst8

    PMID:12718876 PMID:12719473

    Open questions at the time
    • Did not resolve whether mLST8 functions identically in mTORC2
    • Membrane localization observed in yeast not structurally explained
    • No structure of the mLST8-mTOR interface
  2. 2006 High

    Resolved the long-standing question of which complex mLST8 is essential for, showing in vivo that it is dispensable for mTORC1/S6K1 signaling but required for mTORC2 integrity and AKT/PKCα/FOXO3 phosphorylation.

    Evidence Conditional knockout mice with genetic epistasis against raptor and rictor knockouts and defined phosphorylation readouts

    PMID:17141160

    Open questions at the time
    • Molecular basis for selective mTORC2 requirement unknown
    • Did not identify the direct mTORC2 cofactor contact
  3. 2012 High

    Tested conservation of complex specificity, confirming the mTORC2-selective role of the ortholog in an intact animal and showing TORC2 controls growth independently of canonical AKT.

    Evidence Drosophila genetic knockout with Rheb-overexpression epistasis and cell-autonomous growth assays

    PMID:22493059

    Open questions at the time
    • AKT-independent TORC2 effectors not defined
    • Relevance to mammalian growth control not addressed
  4. 2019 High

    Pinpointed the structural mechanism of mTORC2-selectivity by identifying a direct mLST8-SIN1 N-terminal interaction and engineering a mutation pair that disrupts mTORC2 without affecting mTORC1.

    Evidence Co-IP, site-directed mutagenesis, and in vivo xenograft validation with AKT-S473 readout

    PMID:31085701

    Open questions at the time
    • No atomic structure of the mLST8-SIN1 interface
    • Whether the interaction is regulated dynamically unknown
  5. 2012 Low

    Proposed that mLST8 abundance is rate-limiting and that mTORC1 and mTORC2 compete for it, providing a quantitative model for reciprocal complex regulation.

    Evidence siRNA knockdown, Raptor-ΔCT overexpression, co-IP and S6K1/Akt phosphorylation

    PMID:24331524

    Open questions at the time
    • Competition model is indirect from a single study
    • Stoichiometry not measured directly
    • Not confirmed in vivo
  6. 2008 Medium

    Revealed an mTOR-independent function by showing mLST8 binds IKKβ and negatively regulates TNFα-induced NF-κB signaling.

    Evidence Yeast two-hybrid, reciprocal co-IP, domain mapping, siRNA, and NF-κB reporter assays

    PMID:18755269

    Open questions at the time
    • Mechanism of inhibition not defined in this study
    • Relationship to mTOR complex pool unclear
  7. 2010 Medium

    Defined the mechanism of NF-κB inhibition, showing mLST8 scaffolds PP4/PP2A/PP6 phosphatases onto IKKβ to suppress its activation.

    Evidence Co-IP with proteomic partner identification, siRNA rescue, and NF-κB reporter assays

    PMID:21110129

    Open questions at the time
    • Single lab; not independently replicated
    • Physiological context of phosphatase recruitment unclear
  8. 2013 Medium

    Linked mTOR pathway status to metabolism by showing mLST8 bridges mTOR and the pyrimidine-synthesis enzyme CAD.

    Evidence FLAG and endogenous co-IP, domain mapping, and CAD enzyme activity assays under nutrient depletion

    PMID:23594158

    Open questions at the time
    • Direct phosphorylation of CAD by mTOR via mLST8 not demonstrated here
    • Single lab
  9. 2021 Medium

    Identified degradative control of mLST8, showing CDK1 phosphorylation creates a phosphodegron recognized by FBXW7 for proteasomal degradation.

    Evidence Co-IP, in vitro ubiquitination, proteasome inhibition, and motif mapping

    PMID:34741373

    Open questions at the time
    • Cell-cycle context of CDK1-driven turnover not fully defined
    • Effect on mTORC1 vs mTORC2 partitioning not separated
  10. 2022 Medium

    Established upstream control of mLST8 levels via folding and mRNA stability, showing CCT4 chaperones mLST8 folding and ALKBH5/m6A regulates MLST8 transcript stability.

    Evidence RIP, polysome profiling, co-IP and xenografts (CCT4 axis); MeRIP-seq, RNA stability and luciferase assays (ALKBH5 axis)

    PMID:35239512 PMID:35579750

    Open questions at the time
    • Generality beyond glioblastoma/AML untested
    • Quantitative contribution to mTOR signaling output not measured
  11. 2024 Medium

    Built a layered post-translational regulatory model in which SUMOylation promotes mTOR complex assembly while distinct non-degradative ubiquitination events selectively dismantle mTORC2.

    Evidence Mass-spec site mapping, mutagenesis and rescue (SUMO); co-IP, ubiquitination and ETGE-motif mutagenesis for CRL3-Keap1, UBE3C/SLAP, and TRAF2

    PMID:36927703 PMID:37688978 PMID:38395307 PMID:41398047

    Open questions at the time
    • Interplay/hierarchy among these modifications not resolved
    • TRAF2 axis is Low-confidence single study
    • Structural consequence of ubiquitination on mTORC2 not visualized
  12. 2023 Medium

    Connected mLST8 to autophagy and disease physiology, showing mTORC1-dependent ULK1 phosphorylation controls autophagy with consequences for coronavirus replication and RPE pathology.

    Evidence CRISPR KO, autophagy flux, EM and viral replication assays; RPE-specific knock-in mouse with Torin1 rescue

    PMID:37377422 PMID:40205682

    Open questions at the time
    • Direct vs indirect contribution of mLST8 to ULK1 control not isolated
    • Tissue specificity of autophagy phenotypes unexplained
  13. 2024 Medium

    Began to place mLST8 in the activated mTORC1 architecture, showing membrane engagement aligns the mTOR active site with mLST8 as part of the assembled complex.

    Evidence Cryo-EM and membrane reconstitution with Rheb, Rags, and Ragulator (preprint)

    PMID:bio_10.1101_2024.11.15.623810

    Open questions at the time
    • Specific catalytic contribution of mLST8 not isolated structurally
    • No comparable mTORC2 membrane structure
    • Preprint, not peer-reviewed

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the competing post-translational modifications (SUMOylation, multiple ubiquitination routes, phosphodegron turnover) are integrated to dynamically allocate the limited mLST8 pool between mTORC1 and mTORC2 in vivo remains unresolved.
  • No unified quantitative model of mLST8 partitioning
  • No atomic structure of the mLST8-SIN1/mTORC2 interface
  • Crosstalk between mTOR-dependent and NF-κB scaffolding functions unexplored

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3
Localization
GO:0005764 lysosome 1 GO:0005768 endosome 1 GO:0005794 Golgi apparatus 1 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-168256 Immune System 2 R-HSA-9612973 Autophagy 2
Partners
CADFBXW7IKBKBKEAP1MAPKAP1MTORRICTORRPTOR
Complex memberships
IKK complexmTORC1mTORC2

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 GbetaL (mLST8) binds directly to the kinase domain of mTOR and stabilizes the interaction of raptor with mTOR. GbetaL binding strongly stimulates mTOR kinase activity toward S6K1 and 4E-BP1, an effect reversed by the stable interaction of raptor with mTOR. Nutrients and rapamycin regulate the mTOR-raptor association only in complexes that also contain GbetaL. Co-immunoprecipitation, in vitro kinase assay, biochemical fractionation Molecular cell High 12718876
2006 Genetic ablation of mLST8 in mice phenocopies rictor (mTORC2) loss, not raptor (mTORC1) loss. mLST8 is required to maintain the rictor-mTOR interaction but not the raptor-mTOR interaction. Both mLST8 and rictor are required for hydrophobic motif phosphorylation of Akt/PKB and PKCalpha, but not S6K1. Insulin signaling to FOXO3 but not to TSC2 or GSK3beta requires mLST8 and rictor. Conditional knockout mice, immunoprecipitation, immunoblot for pathway phosphorylation, genetic epistasis Developmental cell High 17141160
2003 Yeast Lst8p associates with both Tor1p and Tor2p and is a peripheral membrane protein localizing to endosomal or Golgi membranes, cofractioning with Tor1p. lst8 mutants display hypersensitivity to rapamycin and derepressed Gln3p activity, establishing Lst8p as a TOR pathway component. Different lst8 alleles selectively affect either Rtg1/3p or Gln3p transcription factor outputs, revealing two genetically separable TOR-Lst8 downstream branches. Co-immunoprecipitation, subcellular fractionation, genetic epistasis (rapamycin sensitivity, transcription factor reporter assays), temperature-sensitive mutant analysis The Journal of cell biology High 12719473
2012 In Drosophila, LST8 functions exclusively in TORC2 and is not required for TORC1 activity. In lst8 knockout mutants, expression of TOR, RAPTOR, and upstream activator Rheb was sufficient to provide TORC1 activity and stimulate cell and organ growth. TORC2 regulates cell growth cell-autonomously but not via its canonical target AKT. Genetic knockout in Drosophila, epistasis with Rheb overexpression, cell-autonomous growth assays, phosphorylation readouts Molecular and cellular biology High 22493059
2019 mLST8 loss blocks mTOR association with mTORC2 cofactors RICTOR and SIN1, abrogating mTORC2 activity, but has little to no impact on mTORC1 assembly or activity. A direct interaction between mLST8 and the NH2-terminal domain of the mTORC2 cofactor SIN1 was identified. A single pair of mutations on mLST8 with a corresponding mutation on mTOR selectively disrupts mTORC2 assembly and activity without affecting mTORC1. Co-immunoprecipitation, site-directed mutagenesis, in vivo xenograft tumor model, phosphorylation assays (AKT S473) Cancer research High 31085701
2015 mLST8 knockdown significantly suppresses mTORC1 and mTORC2 complex formation and inhibits tumor growth and invasiveness. mLST8 knockdown reduced mTORC2-mediated AKT phosphorylation in both cancer and normal cells, but potently inhibited mTORC1-mediated 4E-BP1 phosphorylation specifically in cancer cells, indicating distinct roles depending on expression level. siRNA knockdown, co-immunoprecipitation, phosphorylation assays, anchorage-independent growth assay PloS one Medium 25906254
2008 GbetaL (mLST8) interacts with IKKalpha and IKKbeta both in vitro and in vivo. The C-terminal WD domains of GbetaL are required for interaction with both the kinase domain and leucine zipper domain of IKKbeta. GbetaL overexpression inhibits TNFα-induced NF-κB signaling, while GbetaL knockdown enhances NF-κB activity. GbetaL constitutively interacts with IKKbeta, and this interaction is enhanced by TNFα treatment. Yeast two-hybrid screening, co-immunoprecipitation (in vitro and in vivo), siRNA knockdown, NF-κB reporter assays, domain mapping with deletion mutants Cellular signalling Medium 18755269
2010 GbetaL (mLST8) recruits protein phosphatases PP4, PP2A, and PP6 to IKKβ via immunoprecipitation. By mediating association of these phosphatases (which do not directly bind IKKβ) with the IKK complex, GbetaL acts as a scaffold to negatively regulate IKK activation and NF-κB signaling. siRNA knockdown of GbetaL diminishes the inhibitory effect of overexpressed phosphatases on NF-κB signaling. Co-immunoprecipitation, proteomic analysis, siRNA knockdown, NF-κB reporter assays Molecules and cells Medium 21110129
2013 mLST8 associates with CAD, a multifunctional protein catalyzing the initial three steps in de novo pyrimidine synthesis. mLST8 bridges CAD and mTOR, with mLST8 recognizing CAD and mTOR in distinct ways. CAD enzymatic activity decreases upon amino acid and serum depletion (conditions that suppress mTOR activity), suggesting mLST8 links mTOR pathway status to pyrimidine biosynthesis regulation. FLAG immunoprecipitation from transfected HEK293 cells, co-immunoprecipitation of endogenous proteins, domain mapping with deletion mutants, CAD enzyme activity assay Journal of biomedical science Medium 23594158
2021 CDK1 phosphorylates MLST8 at a consensus (T/S)PXX(S/T/D/E) motif, which is required for FBXW7-mediated recognition and ubiquitin-proteasome degradation of MLST8. FBXW7 (E3 ubiquitin ligase) directly interacts with MLST8 and promotes its ubiquitination and degradation. Co-immunoprecipitation, ubiquitination assay, proteasome inhibitor treatment, phosphorylation analysis with CDK1, domain/motif mapping Cancer science Medium 34741373
2022 YB-1 promotes translation of CCT4 mRNA by binding its 5'UTR; CCT4 (a subunit of the CCT chaperone complex) in turn promotes mLST8 protein folding, thereby activating both mTORC1 and mTORC2 signaling. This establishes a YB-1/CCT4/mLST8/mTOR axis in glioblastoma. RNA immunoprecipitation, polysome profiling, co-immunoprecipitation, knockdown/overexpression experiments, xenograft mouse model The Journal of clinical investigation Medium 35239512
2022 ALKBH5-mediated m6A demethylation of MLST8 mRNA stabilizes the transcript; when ALKBH5 is downregulated (by bioactive peptide), m6A levels on MLST8 mRNA increase, leading to mRNA decay and reduced MLST8 protein, which inhibits AML cell proliferation. MeRIP-seq, RNA-seq, MeRIP-qPCR, RNA stability assays, dual-luciferase reporter assays, Western blot Cellular oncology Medium 35579750
2023 Keap1 binds to mLST8 via a conserved ETGE motif. The CRL3-Keap1 ubiquitin ligase complex promotes non-degradative ubiquitination of mLST8, reducing mTORC2 complex integrity and mTORC2-AKT activation. Oxidative stress and ROS burst prevent this effect. Cancer-derived Keap1 or mLST8 mutations disrupt the Keap1-mLST8 interaction, allowing mLST8 to evade Keap1-mediated ubiquitination and enhancing mTORC2-AKT activation. Co-immunoprecipitation, ubiquitination assay, site-directed mutagenesis (ETGE motif), mTORC2 assembly assays, AKT phosphorylation readout Redox biology Medium 37688978
2024 SUMOylation of GβL (mLST8) at lysine residues K86, K215, K245, K261, and K305 by SUMO1, 2, and 3 isoforms promotes mTOR-Raptor and mTOR-Rictor complex formation and nutrient-induced mTOR signaling. Reconstitution with wild-type GbetaL but not SUMOylation-defective KR mutant GβL restores mTOR signaling in GβL-depleted cells. Mutagenesis, mass spectrometry, co-immunoprecipitation (mTOR complex assembly), rescue experiments with SUMOylation-defective mutant The Journal of biological chemistry Medium 38395307
2025 SLAP interacts with mLST8 and facilitates its non-degradative ubiquitination at lysines K86 and K215 via the E3 ubiquitin ligase UBE3C, thereby reducing mTORC2 integrity and mTORC2-AKT signaling. SLAP inhibition of colorectal cancer cell growth and invasion is dependent on mTORC2 signaling inhibition. Co-immunoprecipitation, ubiquitination assays, site-directed mutagenesis, loss-of-function cell assays, in vivo xenograft model Cell death and differentiation Medium 41398047
2023 mLST8 knockout reduces mTORC1-dependent phosphorylation of ULK1, promoting autophagy activation, which in turn inhibits coronavirus double-membrane vesicle formation and replication. mTORC1 (not mTORC2) is essential for coronavirus replication, establishing mLST8 as a host factor required for mTORC1-ULK1-autophagy regulation during CoV infection. CRISPR knockout, pharmacological inhibitors, transmission electron microscopy, autophagy flux assays, phosphorylation assays (ULK1), viral replication assays mBio Medium 37377422
2012 LST8 expression level determines basal mTORC1 and mTORC2 activities, as LST8 is the rate-limiting shared component present at the lowest level in both complexes. mTORC1 (Raptor-mTOR) and mTORC2 (Rictor-mTOR) complexes compete for association with LST8; displacement of Raptor from LST8 leads to reciprocal enhancement of mTORC2 activity. siRNA knockdown, overexpression of Raptor deletion mutant (Raptor-ΔCT), co-immunoprecipitation, phosphorylation assays (S6K1, Akt) Obesity research & clinical practice Low 24331524
2023 In fission yeast, the mLST8 ortholog Wat1 undergoes hyper-phosphorylation at S116 in response to osmotic stress. Wat1 interacts with the C-terminal/FATC domain-containing region of Tor1. Phosphorylation of Wat1 at S116 is required for its physical interaction with Gad8 (AGC kinase, AKT ortholog), and this phosphorylation is required for vacuolar integrity and sexual differentiation. Co-immunoprecipitation, molecular modelling, phosphomutant analysis, growth/phenotypic assays in fission yeast European journal of cell biology Low 29699848
2025 MLST8 overexpression in retinal pigment epithelium (RPE) cells drives upregulation of mTORC1 and mTORC2 complexes, which disrupts autophagy by suppressing autophagosome formation genes and impairing LC3 processing, leading to autophagosome accumulation and defective autolysosome formation. Torin1 (mTOR inhibitor) or CRYBA1 overexpression rescues these autophagy defects. RPE-specific MLST8 knock-in mouse model, Western blot (LC3 processing), autophagosome quantification, pharmacological rescue with Torin1 Autophagy Medium 40205682
2023 In a maternal hyperglycemia (GDM) model, high glucose promotes TRAF2-dependent ubiquitination of GβL (mLST8), which increases the GβL/Raptor association (favoring mTORC1) while decreasing GβL/Rictor and GβL/Sin1 association (reducing mTORC2), impairing pulmonary vasculogenesis. TRAF2 knockdown inhibited high-glucose-induced GβL ubiquitination and GβL/Raptor association and restored tube formation. Immunoprecipitation of ubiquitinated GβL, co-IP of GβL with Raptor/Rictor/Sin1, TRAF2 knockdown, tube formation assay Diabetology & metabolic syndrome Low 36927703
2024 Cryo-EM structural reconstitution of mTORC1 (comprising mTOR, Raptor, and mLST8) on lysosomal membranes shows that Raptor and mTOR directly interact with the membrane at anchor points separated by up to 230 Å. Full membrane engagement is required for maximal mTORC1 kinase activation via alignment of catalytic residues in the mTOR active site, with mLST8 as part of the complex. Cryo-EM structure determination, biochemical reconstitution on membranes with physiological concentrations of Rheb, Rags, and Ragulator bioRxivpreprint Medium bio_10.1101_2024.11.15.623810

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Ablation in mice of the mTORC components raptor, rictor, or mLST8 reveals that mTORC2 is required for signaling to Akt-FOXO and PKCalpha, but not S6K1. Developmental cell 1207 17141160
2003 GbetaL, a positive regulator of the rapamycin-sensitive pathway required for the nutrient-sensitive interaction between raptor and mTOR. Molecular cell 771 12718876
1997 Control of amino acid permease sorting in the late secretory pathway of Saccharomyces cerevisiae by SEC13, LST4, LST7 and LST8. Genetics 119 9409822
2003 LST8 negatively regulates amino acid biosynthesis as a component of the TOR pathway. The Journal of cell biology 116 12719473
2007 Target of rapamycin and LST8 proteins associate with membranes from the endoplasmic reticulum in the unicellular green alga Chlamydomonas reinhardtii. Eukaryotic cell 64 18039939
2022 Upregulated YB-1 protein promotes glioblastoma growth through a YB-1/CCT4/mLST8/mTOR pathway. The Journal of clinical investigation 58 35239512
2016 Genetic variants near MLST8 and DHX57 affect the epigenetic age of the cerebellum. Nature communications 52 26830004
2019 Phosphorus Availability Regulates TORC1 Signaling via LST8 in Chlamydomonas. The Plant cell 51 31712405
2015 mLST8 Promotes mTOR-Mediated Tumor Progression. PloS one 51 25906254
2011 Simultaneous determination of γ-Hydroxybutyrate (GHB) and its analogues (GBL, 1.4-BD, GVL) in whole blood and urine by liquid chromatography coupled to tandem mass spectrometry. Journal of analytical toxicology 41 21219697
2019 Disruption of the Scaffolding Function of mLST8 Selectively Inhibits mTORC2 Assembly and Function and Suppresses mTORC2-Dependent Tumor Growth In Vivo. Cancer research 40 31085701
2015 Evolutionary conservation of TORC1 components, TOR, Raptor, and LST8, between rice and yeast. Molecular genetics and genomics : MGG 40 25956502
2013 Pharmacokinetics of GHB and detection window in serum and urine after single uptake of a low dose of GBL - an experiment with two volunteers. Drug testing and analysis 36 23733593
2012 LST8 regulates cell growth via target-of-rapamycin complex 2 (TORC2). Molecular and cellular biology 35 22493059
2023 Gamma-hydroxybutyrate (GHB), 1,4-butanediol (1,4BD), and gamma-butyrolactone (GBL) intoxication: A state-of-the-art review. Regulatory toxicology and pharmacology : RTP 27 37343712
2014 GHB, GBL and 1,4-BD addiction. Current pharmaceutical design 25 24001290
2013 Association of CAD, a multifunctional protein involved in pyrimidine synthesis, with mLST8, a component of the mTOR complexes. Journal of biomedical science 21 23594158
1988 Presynaptic inhibition of nigrostriatal dopamine release in the mouse: lack of cross tolerance between apomorphine, GBL and CGS 10746B. Life sciences 21 3352463
2007 Cataleptic effects of gamma-hydroxybutyrate (GHB), its precursor gamma-butyrolactone (GBL), and GABAB receptor agonists in mice: differential antagonism by the GABAB receptor antagonist CGP35348. Psychopharmacology 20 17277933
2022 Bioactive peptide inhibits acute myeloid leukemia cell proliferation by downregulating ALKBH5-mediated m6A demethylation of EIF4EBP1 and MLST8 mRNA. Cellular oncology (Dordrecht, Netherlands) 18 35579750
2022 Intestinal microbial composition changes induced by Lactobacillus plantarum GBL 16, 17 fermented feed and intestinal immune homeostasis regulation in pigs. Journal of animal science and technology 17 36812041
2010 Regulation of IκB kinase by GβL through recruitment of the protein phosphatases. Molecules and cells 16 21110129
2006 Lack of effects of GHB precursors GBL and 1,4-BD following i.c.v. administration in rats. The European journal of neuroscience 13 17100847
2020 Enhanced mLST8 Expression Correlates with Tumor Progression in Hepatocellular Carcinoma. Annals of surgical oncology 12 32157528
2018 Phosphorylation of Wat1, human Lst8 homolog is critical for the regulation of TORC2 -Gad8 dependent pathway in fission yeast Schizosacchromyces pombe. European journal of cell biology 12 29699848
2023 mLST8 is essential for coronavirus replication and regulates its replication through the mTORC1 pathway. mBio 11 37377422
2021 CDK1/FBXW7 facilitates degradation and ubiquitination of MLST8 to inhibit progression of renal cell carcinoma. Cancer science 11 34741373
2007 UFT and its metabolite gamma-butyrolactone (GBL) inhibit angiogenesis induced by vascular endothelial growth factor in advanced cervical carcinoma. Medical oncology (Northwood, London, England) 11 17968681
2012 Gamma butyrolactone (GBL) and gamma valerolactone (GVL): similarities and differences in their effects on the acoustic startle reflex and the conditioned enhancement of startle in the rat. Pharmacology, biochemistry, and behavior 9 22349589
2023 Disruption of the Keap1-mTORC2 axis by cancer-derived Keap1/mLST8 mutations leads to oncogenic mTORC2-AKT activation. Redox biology 8 37688978
2008 GbetaL regulates TNFalpha-induced NF-kappaB signaling by directly inhibiting the activation of IkappaB kinase. Cellular signalling 8 18755269
2006 Evaluation for the withdrawal syndrome from gamma-hydroxybutyric acid (GHB), gamma-butyrolactone (GBL), and 1,4-butanediol (1,4-BD) in different rat lines. Annals of the New York Academy of Sciences 8 17105952
2014 Regional Fos-expression induced by γ-hydroxybutyrate (GHB): comparison with γ-butyrolactone (GBL) and effects of co-administration of the GABAB antagonist SCH 50911 and putative GHB antagonist NCS-382. Neuroscience 7 25088910
2023 Maternal hyperglycemia inhibits pulmonary vasculogenesis during mouse fetal lung development by promoting GβL Ubiquitination-dependent mammalian target of Rapamycin assembly. Diabetology & metabolic syndrome 5 36927703
2017 Physicochemical and electrochemical characterisation of imidazolium based IL + GBL mixtures as electrolytes for lithium-ion batteries. Physical chemistry chemical physics : PCCP 5 29022022
2017 Identifying novel small molecule antagonists for mLST8 protein using computational approaches. Journal of receptor and signal transduction research 5 29041842
2025 MLST8 overexpression in RPE cells disrupts autophagy through novel mechanisms affecting AMD pathogenesis. Autophagy 4 40205682
2024 SUMO modifies GβL and mediates mTOR signaling. The Journal of biological chemistry 4 38395307
2019 Incorporation of γ-butyrolactone (GBL) dramatically lowers the phase transition temperature of formamidinium-based metal halide perovskites. Chemical communications (Cambridge, England) 3 31513197
2012 LST8 level controls basal p70 S6 kinase and Akt phosphorylations, and mTORC1 and mTORC2 negatively regulate each other by competing for association with LST8. Obesity research & clinical practice 3 24331524
2019 Cloning and characterization of the target protein subunit lst8 of rapamycin in Apostichopus japonicus. Fish & shellfish immunology 2 31233778
2000 [Anti-angiogenic activities of UFT and its metabolites, GHB and GBL, in the dorsal air sac (DAS) model in mice]. Gan to kagaku ryoho. Cancer & chemotherapy 2 10660738
2008 Gamma-butyrolactone (GBL) disruption of passive avoidance learning in the day-old chick appears to be due to its effect on GABAB not gamma-hydroxybutyric [corrected] acid (GHB) receptors. Behavioural brain research 1 18948143
2026 Transcranial direct current stimulation exerts neuroprotective effects in Parkinson's disease by restoring Mlst8-mediated autophagic homeostasis. Journal of translational medicine 0 41484879
2026 Gene model for the ortholog of Lst8 in Drosophila yakuba. bioRxiv : the preprint server for biology 0 42182478
2025 Anatomical Insights into Frontal Branch Preservation in Minimally Invasive Brow Lift Techniques: A Comparative Analysis of Anatomical Lift Prantl's Suture Suspension (ALPS) Versus Gliding Brow Lift (GBL). Aesthetic plastic surgery 0 41286172
2025 SLAP controls mTORC2 integrity via UBE3C-mediated non-degradative mLST8 ubiquitination to suppress colorectal tumorigenesis. Cell death and differentiation 0 41398047

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