Affinage

GSTP1

Glutathione S-transferase P · UniProt P09211

Round 2 corrected
Length
210 aa
Mass
23.4 kDa
Annotated
2026-04-28
130 papers in source corpus 30 papers cited in narrative 30 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GSTP1 is a pi-class glutathione S-transferase that integrates detoxification catalysis with non-enzymatic regulation of stress signaling and protein S-glutathionylation. As a homodimeric enzyme (crystal structure at 2.8 Å), it conjugates glutathione to electrophilic substrates including 4-hydroxynonenal and lipid hydroperoxides, with catalytic efficiency modulated by coding polymorphisms (Ile105Val, Ala114Val) in the H-site and by PKCα-mediated serine phosphorylation (PMID:1522586, PMID:9092542, PMID:20654585). In its monomeric form, GSTP1 directly binds the C-terminus of JNK1 (Kd ~188 nM) and suppresses JNK kinase activity; oxidative stress triggers GSTP1 oligomerization via S-glutathionylation at Cys47/Cys101, releasing active JNK — a switch autoregulated by GSTP1's own catalytic forward S-glutathionylation activity (PMID:10064598, PMID:18990698). GSTP1 also catalyzes S-glutathionylation of specific client proteins, including KEAP1 at Cys434 to activate NRF2-dependent antioxidant transcription and Pik3r1 at Cys498/Cys670 to suppress AKT–mTOR signaling and modulate autophagy (PMID:38479222, PMID:36870110). Protein turnover is controlled by at least three E3 ubiquitin ligases — SMURF2, FBX8/SCF, and Parkin — that target GSTP1 for proteasomal or autophagy-mediated degradation, while SIRT5-dependent demalonylation stabilizes the protein (PMID:38016474, PMID:31024008, PMID:36871745, PMID:38169591).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1985 High

    Establishing that cytosolic GSTs comprise distinct evolutionary classes (alpha, mu, pi) resolved how GSTP1 fits within the transferase superfamily and defined its unique substrate and immunological identity.

    Evidence Protein purification, N-terminal sequencing, substrate/inhibitor profiling, and immunoprecipitation across rat, mouse, and human tissues

    PMID:3864155

    Open questions at the time
    • No structural basis for class-specific substrate selectivity yet determined
    • Tissue-specific regulatory mechanisms uncharacterized
  2. 1987 High

    Cloning the full-length human GSTP1 cDNA from placenta established the primary sequence (209 aa) and confirmed broad expression in normal and malignant tissues, enabling all subsequent molecular studies.

    Evidence cDNA library screening, sequencing, and Northern blot hybridization across human tissues

    PMID:3664469

    Open questions at the time
    • Promoter elements and transcriptional regulation unknown
    • Post-translational modifications uncharacterized
  3. 1992 High

    The 2.8 Å crystal structure with bound S-hexylglutathione defined the architecture of the G-site and H-site and the homodimeric interface, providing the structural framework for understanding catalysis and polymorphism effects.

    Evidence X-ray crystallography of human placental GSTP1-1 with competitive inhibitor

    PMID:1522586

    Open questions at the time
    • No structure of apo form or with physiological substrates
    • Conformational dynamics during catalysis not addressed
  4. 1997 High

    Demonstrating that common GSTP1 polymorphisms (Ile105Val, Ala114Val) in the H-site produce enzymes with 3–4-fold differences in catalytic efficiency answered how genetic variation translates to functional diversity in detoxification capacity.

    Evidence Recombinant expression of three allelic variants in E. coli with kinetic analysis (Km, Kcat/Km)

    PMID:9092542

    Open questions at the time
    • In vivo phenotypic consequences of allelic variants not established
    • Whether allelic variants differentially affect non-catalytic functions (e.g., JNK binding) was unknown
  5. 1999 High

    The discovery that monomeric GSTP1 directly inhibits JNK and that stress-induced oligomerization releases active JNK established a non-catalytic signaling-regulatory role, fundamentally expanding GSTP1 biology beyond detoxification.

    Evidence Protein purification, co-IP, in vitro kinase assays, GSTP1-null MEFs with re-expression rescue

    PMID:10064598

    Open questions at the time
    • Binding interface on GSTP1 not mapped
    • Whether JNK inhibition extends to JNK2/JNK3 isoforms unclear
  6. 2001 High

    Mapping the GSTP1–JNK1 interaction to the JNK C-terminus (residues 200–424) with nanomolar affinity, and showing a dominant-negative C-terminal JNK fragment activates JNK, provided the structural basis for the inhibitory complex.

    Evidence FRET with recombinant proteins, co-IP, dominant-negative expression in inducible NIH3T3 cells

    PMID:11279197

    Open questions at the time
    • Atomic-resolution structure of GSTP1–JNK complex not determined
    • Stoichiometry of inhibitory complex unclear
  7. 2002 Medium

    Showing that basal hepatic GSTP1 expression depends on NRF2 but that preneoplastic cells express GSTP1 independently of NRF2 revealed dual transcriptional programs and explained why GSTP1 is a robust preneoplastic marker.

    Evidence Nrf2-KO mouse model with BHA induction and DEN-initiated hepatocarcinogenesis, quantitative GSTP1 immunohistochemistry

    PMID:11895860

    Open questions at the time
    • Identity of Nrf2-independent transcription factors in preneoplastic cells unknown
    • Whether this applies to human preneoplastic lesions not tested
  8. 2008 High

    Establishing that GSTP1 catalyzes forward S-glutathionylation of low-pKa cysteines on target proteins — and that GSTP1 itself is autoregulated by S-glutathionylation at Cys47/Cys101 — unified the catalytic and JNK-regulatory functions into a redox-sensing switch.

    Evidence In vitro S-glutathionylation assays with site-directed mutagenesis of catalytic residues and Cys47/Cys101

    PMID:18990698

    Open questions at the time
    • Full client repertoire for GSTP1-catalyzed S-glutathionylation uncharacterized
    • Kinetics of autoregulatory S-glutathionylation in vivo not measured
  9. 2010 High

    PKCα-dependent serine phosphorylation of GSTP1 was shown to activate cisplatin–GSH conjugation, linking post-translational modification to drug resistance and demonstrating that GSTP1 catalytic output is tunable by upstream kinase signaling.

    Evidence PKC activation assays, siRNA knockdown of GSTP1/PKCα, glutathionylplatinum metabolite quantification, and DNA cross-link assays in glioma cells

    PMID:20654585

    Open questions at the time
    • Specific phosphorylation site(s) not mapped
    • Whether other kinases similarly regulate GSTP1 unknown
  10. 2011 High

    Gstp-null mice crossed with H-ras-initiated mice showed increased tumor multiplicity with altered lipid metabolism, Wnt signaling, and cytoskeletal gene programs, establishing that GSTP1 suppresses tumorigenesis through microenvironment regulation beyond direct detoxification.

    Evidence Gstp−/− × Tg.AC mouse genetic cross, TPA carcinogenesis, microarray with GSEA, immunohistochemistry

    PMID:21975931

    Open questions at the time
    • Direct molecular targets mediating Wnt and lipid metabolic changes not identified
    • Contribution of S-glutathionylation versus detoxification not dissected
  11. 2019 Medium

    Identification of FBX8/SCF as an E3 ligase that ubiquitinates and degrades GSTP1 revealed a first ubiquitin-dependent turnover mechanism, with FBX8 loss stabilizing GSTP1 to promote colorectal cancer progression.

    Evidence Co-IP, ubiquitination assays, FBX8-KO transgenic mice, chemical colon carcinogenesis model

    PMID:31024008

    Open questions at the time
    • Ubiquitination site(s) on GSTP1 not mapped
    • Whether FBX8 regulation is tissue-specific unknown
  12. 2020 Medium

    C/EBPβ was identified as a direct transcriptional activator of GSTP1 downstream of EGFR/ROS signaling, establishing a second transcription factor axis (alongside NRF2) for GSTP1 induction in cancer.

    Evidence ChIP for C/EBPβ on GSTP1 promoter, overexpression/knockdown, ROS quantification, in vivo GBM models

    PMID:32526700

    Open questions at the time
    • Relative contributions of C/EBPβ vs NRF2 to GSTP1 expression in different cancer types not compared
    • Specific promoter elements bound by C/EBPβ not fully mapped
  13. 2023 High

    Three independent studies expanded the regulatory and functional landscape: SMURF2 was identified as an E3 ligase degrading GSTP1 during ferroptosis (revealing GSTP1 as a GPX4-independent ferroptosis suppressor via lipid hydroperoxide clearance), Parkin was shown to ubiquitinate GSTP1 for proteasomal and autophagic degradation in lens epithelial cells, and GSTP1-catalyzed S-glutathionylation of Pik3r1 at Cys498/670 was shown to suppress AKT–mTOR signaling and osteoclastogenesis.

    Evidence Proteomics during ferroptosis with ubiquitination assays and in vivo tumor models (SMURF2); co-IP, ubiquitination, and non-ubiquitinatable mutant in lens cells (Parkin); S-glutathionylation assays with Cys mutagenesis and OVX mouse model (Pik3r1)

    PMID:36870110 PMID:36871745 PMID:38016474

    Open questions at the time
    • Whether SMURF2 and Parkin compete for GSTP1 or act in different contexts not addressed
    • Full spectrum of GSTP1 S-glutathionylation substrates remains uncharacterized
    • Lipid peroxidase activity kinetic parameters not fully defined
  14. 2023 Medium

    CaMK2A was shown to phosphorylate NRF2 at Ser558 under hypoxia, driving NRF2 nuclear translocation and GSTP1 transcription to support cancer stem cell self-renewal and TKI resistance, revealing a hypoxia-specific transcriptional activation route.

    Evidence NRF2 phospho-mutagenesis (Ser558), ChIP of NRF2 on GSTP1 promoter, CSC sphere assays, patient-derived organoids

    PMID:36709476

    Open questions at the time
    • Whether CaMK2A-NRF2-GSTP1 axis operates in non-cancer contexts unknown
    • Direct structural impact of Ser558 phosphorylation on NRF2-GSTP1 promoter interaction not resolved
  15. 2024 High

    GSTP1-catalyzed S-glutathionylation of KEAP1 at Cys434 was identified as the mechanism by which GSTP1 activates NRF2 signaling, establishing a positive-feedback loop where GSTP1 promotes its own transcription factor's nuclear translocation.

    Evidence Mass spectrometry, molecular docking, Cys434 mutagenesis, co-IP (KEAP1–NRF2), AAV-GSTP in vivo mouse model of acute lung injury

    PMID:38479222

    Open questions at the time
    • Kinetics and stoichiometry of KEAP1 S-glutathionylation by GSTP1 not determined
    • Whether other GSTs can substitute for GSTP1 in this reaction unknown
  16. 2024 Medium

    SIRT5-mediated demalonylation was shown to stabilize GSTP1 protein; loss of this regulation in diabetic cardiomyopathy leads to GSTP1 destabilization, oxidative stress, and pyroptosis, linking GSTP1 post-translational regulation to metabolic disease.

    Evidence SIRT5-KO mice, malonylation proteomics, co-IP, GSTP1 knockdown/overexpression in cardiomyocytes, ChIP for SPI1 on SIRT5 promoter

    PMID:38169591

    Open questions at the time
    • Specific lysine malonylation sites on GSTP1 not mapped
    • Whether demalonylation affects GSTP1 catalytic activity or only stability not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the full repertoire of GSTP1 S-glutathionylation substrates, the atomic structure of the GSTP1–JNK inhibitory complex, whether allelic variants differentially affect non-catalytic functions, the relative contributions of multiple E3 ligases in tissue-specific GSTP1 turnover, and the identity of NRF2-independent transcription factors driving GSTP1 in preneoplastic cells.
  • No co-crystal structure of GSTP1–JNK complex
  • Systematic identification of S-glutathionylation substrates lacking
  • Tissue-specific hierarchy of SMURF2, FBX8, and Parkin in GSTP1 degradation not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 6 GO:0098772 molecular function regulator activity 4 GO:0016209 antioxidant activity 2
Localization
GO:0005829 cytosol 3
Pathway
R-HSA-1430728 Metabolism 5 R-HSA-162582 Signal Transduction 4 R-HSA-8953897 Cellular responses to stimuli 4 R-HSA-5357801 Programmed Cell Death 3 R-HSA-9612973 Autophagy 2
Partners
FBX8JNK1KEAP1PARK2PIK3R1SIRT5SMURF2STAT3

Evidence

Reading pass · 30 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 GSTP1 (GSTp) was identified as an endogenous inhibitor of JNK signaling: monomeric GSTP1 binds directly to JNK and inhibits its kinase activity. UV or H2O2 stress causes GSTP1 oligomerization and dissociation of the GSTP1–JNK complex, releasing active JNK. Forced GSTP1 expression decreased MKK4 and JNK phosphorylation and c-Jun-mediated transcription; GSTp-null mouse embryo fibroblasts showed elevated basal JNK activity reversible by GSTP1 re-expression. The inhibitory effect on JNK was independent of the MEKK1–MKK4 module. Protein purification, co-immunoprecipitation, in vitro kinase assays, GSTp inhibitor/peptide experiments, forced expression/immunodepletion, GSTp-null MEFs The EMBO journal High 10064598
2001 GSTP1-1 interacts directly with the C-terminus of JNK1 (residues 200–424; apparent Kd ~188–217 nM for full-length JNK). An N-terminal JNK fragment (residues 1–206) did not bind GSTP1-1. Overexpression of the C-terminal JNK fragment acted as a dominant negative, competing with endogenous JNK for GSTP1-1 binding and activating JNK under normal growth conditions. Co-immunoprecipitation of GSTP1-1 by HA-tagged C-JNK confirmed the direct interaction. FRET with purified recombinant proteins, dominant-negative expression in tetracycline-inducible NIH3T3 cells, co-immunoprecipitation The Journal of biological chemistry High 11279197
1992 Crystal structure of human placental GSTP1-1 (class pi GST) solved at 2.8 Å in complex with competitive inhibitor S-hexylglutathione, defining the glutathione-binding G-site and electrophilic substrate H-site. The H-site is lined by Tyr7, Phe8, Val10, Val35, and Tyr106; the enzyme is a homodimer. X-ray crystallography (Patterson search refinement, R-factor 19.6%) Journal of molecular biology High 1522586
1985 Cytosolic glutathione S-transferases were classified into three classes (alpha, mu, pi) based on amino-terminal sequences, substrate specificities, inhibitor sensitivities, and immunological cross-reactivity across rat, mouse, and human; the pi class (including GSTP1) was established as a distinct evolutionary and functional grouping. Protein purification, amino-terminal sequencing, substrate specificity assays, inhibitor sensitivity, immunoprecipitation with class-specific antibodies, pattern recognition analysis Proceedings of the National Academy of Sciences of the United States of America High 3864155
1997 Three human GSTP1 allelic variants (hGSTP1*A, *B, *C) were cloned and expressed in E. coli. Variants *B and *C carry Ile105Val (codon 313 A→G) and *C additionally Ala114Val (codon 341 C→T), both in the electrophile-binding H-site. The *A-encoded protein showed ~3-fold lower Km for CDNB and 3–4-fold higher Kcat/Km than *B- and *C-encoded proteins, demonstrating that these polymorphisms cause functionally distinct catalytic activities. cDNA cloning, E. coli expression, GSH-affinity purification, kinetic enzyme assays (Km, Kcat/Km), computer modeling of active site The Journal of biological chemistry High 9092542
1987 The complete coding sequence of human GST-pi (GSTP1) mRNA was cloned from a human placenta cDNA library; the deduced protein contains 209 amino acids (Mr ~23,224) with 85.6% amino acid homology to rat GST-P, sharing identical chain length but differing pI (5.5 vs 6.9). Expression was confirmed in normal and cancerous human tissues. cDNA library screening, sequencing, Northern blot/hybridization analysis Cancer research High 3664469
1989 Human GST pi-1 (GSTP1) cDNA was isolated from multidrug-resistant MCF-7 cells; GSTP1 mRNA was expressed broadly in human normal and malignant tissues with lowest levels in liver and lymphoma and highest in lung, esophagus, and placenta, establishing tissue-specific expression patterns. cDNA library construction from MDR MCF-7 cells, sequencing, Northern blot across 170 human tissue and tumor specimens Cancer research High 2466554
2008 GSTP1 (GSTpi) catalyzes forward S-glutathionylation of low-pKa cysteine residues in target proteins following oxidative and nitrosative stress, requiring its catalytic activity (shown by mutational analysis). GSTP1 itself is autoregulated by S-glutathionylation at Cys47 and Cys101, which breaks its interaction with JNK and promotes GSTP1 multimer formation. In vitro S-glutathionylation assays, site-directed mutagenesis of catalytic residues, S-glutathionylation detection in vivo and in vitro, mutational mapping of Cys47/Cys101 The Journal of biological chemistry High 18990698
2006 GSTP1 has ligand-binding properties beyond detoxification catalysis and regulates signaling kinases (including JNK) through direct protein–protein interaction; the forward rate of protein S-glutathionylation is influenced by GSTP1, while the reverse is controlled by glutaredoxin, thioredoxin, and sulfiredoxin. Review integrating prior biochemical, mutational, and cell-based experimental evidence (mechanistic synthesis) Biochemical pharmacology Medium 17098212
2010 PKCα-dependent serine phosphorylation of GSTP1 functionally activates GSTP1 to catalyze cisplatin–glutathione conjugation (glutathionylplatinum formation), reducing DNA interstrand cross-links and increasing cisplatin resistance in malignant glioma cells. siRNA knockdown of GSTP1 or PKCα similarly decreased cisplatin IC50 and glutathionylplatinum levels; combined inhibition was synergistic. PKC activation assays, GSTP1/PKCα siRNA knockdown, glutathionylplatinum metabolite quantification, DNA cross-link assays, apoptosis (Bax/cytochrome c/caspase) analysis in MGR1/MGR3 glioma cells Biochemical pharmacology High 20654585
2023 SMURF2 is an E3 ubiquitin ligase that ubiquitinates and degrades GSTP1 at early stages of ferroptosis. GSTP1 acts as a GPX4/FSP1-independent ferroptosis suppressor by catalyzing GSH conjugation of 4-hydroxynonenal (4-HNE) and exhibiting selenium-independent GSH peroxidase activity toward lipid hydroperoxides. Genetic or pharmacological inhibition of the SMURF2/GSTP1 axis sensitized tumors to ferroptosis-inducing drugs. Proteomics during ferroptosis, co-IP for SMURF2–GSTP1 interaction, ubiquitination assays, enzymatic activity assays (4-HNE conjugation, GSH peroxidase), genetic KO/overexpression, in vitro and in vivo tumor models Molecular cell High 38016474
2007 GSTP1 alleles have differential effects on JNK-dependent and -independent regulation of proliferation and apoptosis: GSTP1*A reduces cellular proliferation and protects against apoptosis via a JNK-independent mechanism, while GSTP1*C protects against apoptosis through JNK-mediated mechanisms (reduced JNK activity). Analysis of JNK phosphorylation and colony-forming efficiency in soft agar under oxidative stress supported these allele-specific differences. Inducible expression of GSTP1*A vs *C in NIH3T3 fibroblasts, JNK activity measurement, cell proliferation (doubling time, G1-S transition), apoptosis assays, colony-forming efficiency in soft agar Carcinogenesis Medium 17557902
2011 GSTP-null mice (Gstp−/−) interbred with Tg.AC (H-ras-initiated) mice showed increased skin tumor incidence and multiplicity upon TPA treatment, accompanied by elevated nitrotyrosine (inflammation marker) but no differences in proliferation, apoptosis, or oxidative stress markers. Gene expression analysis revealed altered lipid/sterol metabolism, Wnt signaling, cytoskeletal control, and epidermal morphogenesis, indicating GSTP regulates the tumor microenvironment and carcinogenesis independently of detoxification. Gstp−/− × Tg.AC mouse genetic model, TPA skin carcinogenesis protocol, immunohistochemistry, microarray gene expression with GSEA, histopathology Cancer research High 21975931
2014 In vivo regulation of human GSTP1 by chemopreventive agents (ethoxyquin, butylated hydroxyanisole) was characterized using a transgenic reporter mouse. Surprisingly, genetic deletion of Nrf2 increased rather than decreased GSTP1 expression, demonstrating that additional factors beyond Nrf2 control GSTP1 transcription in vivo. Transgenic hGSTP1 reporter mouse, Nrf2-knockout crosses, chemopreventive agent treatment, reporter gene analysis, mouse embryonic fibroblast in vitro studies Cancer research Medium 24934809
2019 An irreversible covalent inhibitor (CNBSF) of GSTP1-1 was developed that works by first reacting with intracellular glutathione via aromatic substitution, then the resulting GSH conjugate covalently modifies Tyr108 in the active site of GSTP1-1 via sulfonyl ester bond formation, achieving irreversible intracellular inhibition. In vitro enzyme inhibition assays, cellular permeability studies, mechanism-of-action characterization (aromatic substitution + sulfonyl fluoride-Tyr108 covalent bond), in cellulo GSTP1-1 inhibition Chembiochem : a European journal of chemical biology Medium 30548113
2020 Co-crystal structure of MNPC with NQO1 and molecular docking with GSTP1 showed the inhibitor binds the active sites of both enzymes. Dual inactivation of NQO1 and GSTP1 via siRNA or the inhibitor caused imbalanced redox homeostasis, inducing apoptosis selectively in EGFRvIII-mutant GBM cells. High-throughput screen, co-crystal structure (MNPC–NQO1), molecular docking (MNPC–GSTP1), siRNA knockdown, in vitro and in vivo GBM tumor models Journal of hematology & oncology Medium 33087132
2020 C/EBPβ, a ROS-responsive transcription factor upregulated by EGFR overexpression in GBM, directly binds the promoters of NQO1 and GSTP1 and drives their transcription. C/EBPβ overexpression selectively decreased ROS and promoted proliferation via NQO1 and GSTP1 upregulation; C/EBPβ knockdown elevated ROS and reduced proliferation by repressing these reductases. ChIP assay (C/EBPβ binding to GSTP1/NQO1 promoters), C/EBPβ overexpression/knockdown, ROS measurement, in vitro proliferation, in vivo tumor growth Redox biology Medium 32526700
2023 GSTP1-mediated S-glutathionylation of Pik3r1 (PI3K regulatory subunit p85α) at Cys498 and Cys670 decreases Pik3r1 phosphorylation, suppresses the Pik3r1–AKT–mTOR axis, alters autophagic flux, and inhibits osteoclastogenesis. In vivo GSTP1 knockdown/overexpression in OVX mice altered bone loss outcomes. S-glutathionylation assays, site-directed mutagenesis (Cys498/Cys670), co-IP, AKT-mTOR pathway analysis, autophagic flux assays, in vivo OVX mouse model Redox biology Medium 36870110
2024 GSTP promotes S-glutathionylation of KEAP1 specifically at Cys434, inhibiting the KEAP1–NRF2 interaction, promoting NRF2 nuclear translocation, and activating downstream antioxidant gene expression. This mechanism protects against LPS-induced acute lung injury; AAV-GSTP mice confirmed the pathway in vivo. Protein mass spectrometry, molecular docking, site-directed mutagenesis (Cys434), co-IP (KEAP1–NRF2), AAV-GSTP in vivo mouse model, NRF2 target gene expression Redox biology High 38479222
2024 SIRT5-mediated lysine demalonylation of GSTP1 stabilizes GSTP1 protein; SIRT5 loss in diabetic cardiomyopathy increases GSTP1 lysine malonylation, destabilizes GSTP1, and leads to cardiomyocyte pyroptosis and oxidative stress. SPI1 transcriptionally activates SIRT5 to maintain GSTP1 stability; SIRT5 overexpression protected against DCM-related injury, reversed by GSTP1 knockdown. SIRT5 KO mice, high-glucose primary cardiomyocytes, malonylation proteomics, co-IP, GSTP1 knockdown/overexpression, pyroptosis/senescence/DNA damage assays, ChIP (SPI1–SIRT5 promoter) International journal of biological sciences Medium 38169591
2019 FBX8, the F-box component of an SCF E3 ubiquitin ligase, directly targets GSTP1 for ubiquitin-mediated proteasomal degradation in colorectal cancer. FBX8 loss stabilizes GSTP1 and promotes CRC proliferation, invasion, and metastasis; FBX8–GSTP1 axis identified in both clinical CRC tissues and FBX8-knockout transgenic mice. Co-IP (FBX8–GSTP1 interaction), ubiquitination assays, FBX8 KO transgenic mice, chemical colon carcinogenesis model, CRC cell proliferation/invasion/metastasis assays Cell death & disease Medium 31024008
2023 Parkin (an E3 ubiquitin ligase) ubiquitinates GSTP1 and promotes its degradation via both the ubiquitin-proteasome system and autophagy-lysosome/mitophagy pathways under oxidative stress. GSTP1 loss leads to lens epithelial cell apoptosis; a non-ubiquitinatable GSTP1 mutant retained anti-apoptotic function while wild-type did not when co-expressed with Parkin. Mechanistically, GSTP1 promotes mitochondrial fusion through upregulation of MFN1/2. Co-IP (Parkin–GSTP1), ubiquitination assays, proteasome/autophagy inhibitor experiments, GSTP1 overexpression/knockdown, non-ubiquitinatable GSTP1 mutant, MFN1/2 expression analysis, human cataract tissue and Emory mouse model Biochimica et biophysica acta. Molecular cell research Medium 36871745
2023 CaMK2A phosphorylates NRF2 at Ser558, promoting NRF2 nuclear translocation and GSTP1 transcription under hypoxia. This CaMK2A/NRF2/GSTP1 axis supports lung cancer stem cell self-renewal, metastasis, and TKI resistance. GSTP1 in turn suppresses ROS to maintain CSC phenotypes. The GSTP1 inhibitor ezatiostat synergized with the ALK inhibitor crizotinib in patient-derived organoids. CaMK2A overexpression/knockdown, NRF2 phospho-mutagenesis (Ser558), ChIP (NRF2 on GSTP1 promoter), CSC sphere assays, in vitro/in vivo tumor models, patient-derived organoids Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 36709476
2024 Tryptanthrin (TRYP) directly binds GSTP1 and inhibits its enzymatic activity, leading to ROS accumulation, DNA damage response (DDR), and cellular senescence in liver cancer cells via the GSTP1/ROS/DDR/NF-κB/SASP axis. Senescent cells were then sensitized to apoptosis by the senolytic ABT263 (Bcl2 inhibitor). Natural product library screen, drug-target identification (molecular docking, CETSA, enzymatic activity assay), GSTP1 knockdown/overexpression, ROS/DDR/NF-κB pathway analysis, in vitro and in vivo senescence assays Redox biology Medium 39180983
2008 GSTP1-1 expression enhances intracellular accumulation of sulforaphane (SFN) and its GSH conjugate SFN-SG, increasing ARE-driven phase II gene induction. MRP1 co-expression with GSTP1-1 greatly reduced SFN/SFN-SG accumulation and attenuated ARE reporter induction and sustained Nrf2 nuclear levels, demonstrating that GSTP1-1-catalyzed GSH conjugation and MRP1-mediated efflux cooperate to modulate cellular Nrf2 signaling. GSTP1-1 and MRP1 transgenic MCF7 derivatives, intracellular SFN/SFN-SG accumulation assays, ARE reporter gene assays, Nrf2 nuclear level measurement, GSH depletion experiments Carcinogenesis Medium 18204073
2017 GSTP1-containing exosomes transfer drug resistance between breast cancer cells; GSTP1 partially re-localizes from nucleus to cytoplasm upon chemotherapy treatment, coinciding with increased co-localization with the exosomal marker TSG101 in the cytoplasm, suggesting exosomal packaging of GSTP1 as a mechanism of resistance transfer. Exosome isolation, immunofluorescence (GSTP1 subcellular re-localization), cell apoptosis assays, exosome transfer experiments, IHC of patient samples Gene Low 28438694
2017 CLDN6 promotes chemoresistance in breast cancer through GSTP1: CLDN6 interacts with p53 and promotes its translocation from nucleus to cytoplasm, which in turn upregulates GSTP1 expression and GST enzyme activity. GSTP1 overexpression restored resistance in CLDN6-silenced cells; silencing GSTP1 abrogated CLDN6-induced resistance. CLDN6 lentiviral overexpression/shRNA, GSTP1 lentiviral overexpression/shRNA, GST activity kit, co-IP (CLDN6–p53), p53 nuclear/cytoplasmic fractionation, cck-8 cytotoxicity, IHC of patient tissues Journal of experimental & clinical cancer research : CR Medium 29116019
2022 GSTP1 overexpression promotes colorectal cancer cell proliferation, invasion, and metastasis by directly binding and upregulating STAT3. Co-IP confirmed direct GSTP1–STAT3 protein interaction in CRC cells. This interaction is regulated upstream by FBX8 (which degrades GSTP1 by ubiquitination). Co-IP and immunofluorescence (GSTP1–STAT3 co-localization/interaction), GSTP1 overexpression, JAK-STAT3 pathway western blotting, IHC correlation in human CRC tissues Advances in clinical and experimental medicine Medium 35195960
2020 Formononetin (FN) selectively binds to His129 and Lys131 in the BTB domain of KEAP1 (confirmed by Bio-FN pulldown), activating the NRF2 pathway. RNA interference showed FN protection against oxaliplatin-induced peripheral neuropathy is mediated directly through NRF2-downstream GSTP1 (as the key oxaliplatin metabolism enzyme in neurons), and FN does not activate GSTP1 in colorectal cancer cells (different NRF2 downstream activation), preserving chemotherapy efficacy. RNA interference (NRF2, GSTP1 knockdown), Bio-FN target pulldown identifying KEAP1 BTB domain binding sites, expression profile sequencing, in vivo mouse nociception assays Redox biology Medium 32823168
2002 Nrf2 is a key transcriptional activator of GSTP1 in normal hepatocytes (basal hepatic GSTP1 expression was 60% lower in Nrf2-KO female mice; BHA induction of GSTP1 was abolished in Nrf2-KO mice). However, DEN-induced GSTP1-positive preneoplastic single cells in female mouse liver express GSTP1 independent of Nrf2, indicating a distinct transcriptional program in initiated/preneoplastic cells. Nrf2-KO mouse model, quantitative GSTP1 expression analysis, BHA treatment, DEN-induced hepatocarcinogenesis model, immunohistochemistry Carcinogenesis Medium 11895860

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2005 Loss of acetylation at Lys16 and trimethylation at Lys20 of histone H4 is a common hallmark of human cancer. Nature genetics 1390 15765097
1985 Identification of three classes of cytosolic glutathione transferase common to several mammalian species: correlation between structural data and enzymatic properties. Proceedings of the National Academy of Sciences of the United States of America 1165 3864155
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2014 A proteome-scale map of the human interactome network. Cell 977 25416956
1999 Regulation of JNK signaling by GSTp. The EMBO journal 920 10064598
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2001 Metabolic gene polymorphism frequencies in control populations. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 701 11751440
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2008 Large-scale proteomics and phosphoproteomics of urinary exosomes. Journal of the American Society of Nephrology : JASN 607 19056867
1997 Molecular cloning, characterization, and expression in Escherichia coli of full-length cDNAs of three human glutathione S-transferase Pi gene variants. Evidence for differential catalytic activity of the encoded proteins. The Journal of biological chemistry 585 9092542
2003 Exploring proteomes and analyzing protein processing by mass spectrometric identification of sorted N-terminal peptides. Nature biotechnology 485 12665801
2005 NAT2 slow acetylation, GSTM1 null genotype, and risk of bladder cancer: results from the Spanish Bladder Cancer Study and meta-analyses. Lancet (London, England) 477 16112301
2009 Prenatal tobacco smoke exposure affects global and gene-specific DNA methylation. American journal of respiratory and critical care medicine 451 19498054
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
1989 Expression of anionic glutathione-S-transferase and P-glycoprotein genes in human tissues and tumors. Cancer research 399 2466554
2005 Human ISG15 conjugation targets both IFN-induced and constitutively expressed proteins functioning in diverse cellular pathways. Proceedings of the National Academy of Sciences of the United States of America 383 16009940
2010 Dynamics of cullin-RING ubiquitin ligase network revealed by systematic quantitative proteomics. Cell 318 21145461
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