Gsta4

UniProt ID: P14942
Organism: Rattus norvegicus
Review Status: COMPLETE
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Gene Description

Gsta4 encodes rat glutathione S-transferase alpha-4 (GSTA4-4), an alpha-class cytosolic GST that conjugates reduced glutathione to hydrophobic electrophiles. Among the alpha-class paralogs (Gsta1/2/3/4), Gsta4 is functionally distinguished by its high catalytic efficiency toward lipid peroxidation-derived alpha,beta-unsaturated aldehydes, especially 4-hydroxynonenal (4-HNE), which it detoxifies by GSH conjugation (Michael addition). The review treats glutathione transferase activity and glutathione/xenobiotic metabolism as core or direct functions; stress-response and toxicant-response annotations are retained only as context from expression or perturbation studies. Note that much of the strongest mechanistic/kinetic and loss-of-function evidence derives from mouse Gsta4-null models, human GSTA4-4 enzyme assays, or unspecified GSTA4-4, not rat P14942 specifically; these are treated as orthology-based support rather than rat-specific facts.

Existing Annotations Review

GO Term Evidence Action Reason
GO:0004364 glutathione transferase activity
IBA
GO_REF:0000033
ACCEPT
Summary: Gsta4's glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles supports retaining glutathione transferase activity as a direct annotation (IBA, GO_REF:0000033).
Reason: glutathione transferase activity is a specific catalytic activity matching Gsta4's documented role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0004364; F:glutathione transferase activity; ISO:RGD.
file:rat/Gsta4/Gsta4-deep-research-falcon.md
For 4-HNE and related substrates, GSTA4-4 forms glutathionylated adducts such as **GS-HNE/GS-NE**, supporting phase II detoxification and control of reactive aldehyde signaling.
GO:0006749 glutathione metabolic process
IBA
GO_REF:0000033
ACCEPT
Summary: Gsta4's glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles supports retaining glutathione metabolic process as a direct annotation (IBA, GO_REF:0000033).
Reason: glutathione metabolic process is a direct metabolic process expected from Gsta4's documented role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0006749; P:glutathione metabolic process; ISO:RGD.
file:rat/Gsta4/Gsta4-deep-research-falcon.md
The best-supported biological role is **detoxification of reactive lipid aldehydes**, especially **4-HNE**, thereby limiting **protein carbonylation**, oxidative damage, and downstream stress signaling.
GO:0006805 xenobiotic metabolic process
IBA
GO_REF:0000033
ACCEPT
Summary: Gsta4's glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles supports retaining xenobiotic metabolic process as a direct annotation (IBA, GO_REF:0000033).
Reason: xenobiotic metabolic process is a direct metabolic process expected from Gsta4's documented role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0006805; P:xenobiotic metabolic process; ISO:RGD.
GO:0004364 glutathione transferase activity
IEA
GO_REF:0000120
ACCEPT
Summary: Gsta4's glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles supports retaining glutathione transferase activity as a direct annotation (IEA, GO_REF:0000120).
Reason: glutathione transferase activity is a specific catalytic activity matching Gsta4's documented role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0004364; F:glutathione transferase activity; ISO:RGD.
GO:0005737 cytoplasm
IEA
GO_REF:0000044
KEEP AS NON CORE
Summary: cytoplasm is retained as useful context for Gsta4, but it is not the defining core function (IEA, GO_REF:0000044).
Reason: cytoplasm records where Gsta4 has been observed, but localization does not define the gene product's primary activity.
Supporting Evidence:
UniProtKB:P14942
FUNCTION: Conjugation of reduced glutathione to a wide number of exogenous and endogenous hydrophobic electrophiles.
file:rat/Gsta4/Gsta4-deep-research-falcon.md
Although GSTs are classically described as **cytosolic**, GSTA4-4 has strong evidence for **mitochondrial association**
GO:0042802 identical protein binding
ISO
GO_REF:0000121
KEEP AS NON CORE
Summary: identical protein binding is retained as useful context for Gsta4, but it is not the defining core function (ISO, GO_REF:0000121).
Reason: identical protein binding records substrate, cofactor, or quaternary-structure context for Gsta4, but the curated core function is glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0042802; F:identical protein binding; ISO:RGD.
GO:0061771 response to caloric restriction
ISO
GO_REF:0000121
MARK AS OVER ANNOTATED
Summary: response to caloric restriction is treated as over-annotation because it reflects context or consequence rather than Gsta4's direct role (ISO, GO_REF:0000121).
Reason: response to caloric restriction reflects exposure, expression, phenotype, or downstream pathway context rather than the direct Gsta4 role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Propagation Review
Root cause: PROPAGATION BAD
Failure modes: CONTEXT OR TISSUE MISMATCH ROLE CONFLATION
Sources checked:
MGI:MGI:1309515 Β· mouse Gsta4 SUPPORTS SOURCE BUT NOT TARGET
The mouse Gsta4 donor annotation records altered expression under caloric restriction; dietary regulation of the gene is not a glutathione-conjugation function of rat Gsta4.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0061771; P:response to caloric restriction; ISO:RGD.
GO:0005739 mitochondrion
ISO
GO_REF:0000121
KEEP AS NON CORE
Summary: mitochondrion is retained as useful context for Gsta4, but it is not the defining core function (ISO, GO_REF:0000121). Falcon deep research indicates mitochondrial association is stress-inducible (phosphorylation/Hsp70-dependent import) rather than incidental, supporting a genuine but secondary compartment for protecting mitochondria from reactive lipid aldehydes.
Reason: mitochondrion records a functionally relevant but secondary compartment for Gsta4 (stress-inducible mitochondrial targeting), and localization does not define the gene product's primary activity. Note the detailed import-mechanism evidence (Ser189/Thr193 phosphorylation, Hsp70) derives from reviews of GSTA4-4 generally, not rat P14942 specifically.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0005739; C:mitochondrion; ISO:RGD.
file:rat/Gsta4/Gsta4-deep-research-falcon.md
mitochondrial targeting can be activated by phosphorylation (e.g., **Ser189/Thr193**) and involves enhanced Hsp70 interaction, enabling import competence and increasing mitochondrial localization under oxidative/electrophilic stress (including 4-HNE exposure).
GO:0005829 cytosol
ISO
GO_REF:0000121
KEEP AS NON CORE
Summary: cytosol is retained as useful context for Gsta4, but it is not the defining core function (ISO, GO_REF:0000121).
Reason: cytosol records where Gsta4 has been observed, but localization does not define the gene product's primary activity.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0005829; C:cytosol; ISO:RGD.
file:rat/Gsta4/Gsta4-deep-research-falcon.md
Functionally, GSTA4-4 is best known as a **cytosolic** GST, but multiple studies also support **mitochondrial localization**.
GO:0015643 toxic substance binding
IPI
PMID:11018474
Characterization of 4-hydroxy-2-nonenal metabolism in stella...
MARK AS OVER ANNOTATED
Summary: toxic substance binding is treated as over-annotation because the IPI evidence (4-HNE/CHEBI:58968) captures H-site substrate binding within the catalytic cycle rather than an independent non-catalytic binding activity (IPI, PMID:11018474).
Reason: The 4-HNE interaction supporting this IPI annotation is the H-site substrate-binding step of the glutathione-conjugation catalytic cycle, which is already fully captured by the ACCEPTED GO:0004364 glutathione transferase activity. The falcon evidence ("GSH conjugation (Michael addition) catalyzed predominantly by GSTA4-4") supports catalysis, not a standalone binding function, so toxic substance binding is redundant over-annotation rather than a distinct activity.
Supporting Evidence:
PMID:11018474
During oxidative stress, reactive aldehydes, including trans-4-hydroxy-2-nonenal (4-HNE), are generated by peroxidation of membrane lipids and purportedly stimulate hepatic stellate cells to produce excessive extracellular matrix, including type I collagen.
file:rat/Gsta4/Gsta4-deep-research-falcon.md
A major cellular clearance pathway is **GSH conjugation (Michael addition)** catalyzed predominantly by **GSTA4-4**.
GO:0009635 response to herbicide
IEP
PMID:20553223
Effect of zinc and paraquat co-exposure on neurodegeneration...
MARK AS OVER ANNOTATED
Summary: response to herbicide is treated as over-annotation because it reflects context or consequence rather than Gsta4's direct role (IEP, PMID:20553223).
Reason: response to herbicide reflects exposure, expression, phenotype, or downstream pathway context rather than the direct Gsta4 role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
PMID:20553223
Oxidative stress is implicated in Parkinson's disease (PD). Metallothioneins (MT), cytochrome P450 IIE1 (CYP2E1) and glutathione S-transferases alpha4-4 (GSTA4-4) are involved in oxidative stress-mediated damage.
GO:0010043 response to zinc ion
IEP
PMID:20553223
Effect of zinc and paraquat co-exposure on neurodegeneration...
MARK AS OVER ANNOTATED
Summary: response to zinc ion is treated as over-annotation because it reflects context or consequence rather than Gsta4's direct role (IEP, PMID:20553223).
Reason: response to zinc ion reflects exposure, expression, phenotype, or downstream pathway context rather than the direct Gsta4 role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles. It derives from the same zinc/paraquat co-exposure expression experiment (PMID:20553223, IEP) as response to herbicide, with no mechanistic evidence that zinc directly modulates GSTA4-4 activity, so it is harmonized with response to herbicide as over-annotation.
Supporting Evidence:
PMID:20553223
Oxidative stress is implicated in Parkinson's disease (PD). Metallothioneins (MT), cytochrome P450 IIE1 (CYP2E1) and glutathione S-transferases alpha4-4 (GSTA4-4) are involved in oxidative stress-mediated damage.
GO:0035094 response to nicotine
IEP
PMID:9774145
Preferential effects of nicotine and 4-(N-methyl-N-nitrosami...
MARK AS OVER ANNOTATED
Summary: response to nicotine is treated as over-annotation because it reflects context or consequence rather than Gsta4's direct role (IEP, PMID:9774145).
Reason: response to nicotine reflects exposure, expression, phenotype, or downstream pathway context rather than the direct Gsta4 role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
PMID:9774145
We have investigated the in vivo effects of the tobacco-specific toxins nicotine and 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) on antioxidant defense systems in the mitochondrial, microsomal, and cytosolic compartments of rat brain, lung, and liver.
GO:0071285 cellular response to lithium ion
IEP
PMID:18082333
The effect of mood stabilizer lithium on expression and acti...
MARK AS OVER ANNOTATED
Summary: cellular response to lithium ion is treated as over-annotation because it reflects context or consequence rather than Gsta4's direct role (IEP, PMID:18082333).
Reason: cellular response to lithium ion reflects exposure, expression, phenotype, or downstream pathway context rather than the direct Gsta4 role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
PMID:18082333
Chronic treatment with the mood stabilizer lithium is required to generate its mood stabilizing effect in the treatment of bipolar disorder.
GO:0006749 glutathione metabolic process
ISO
GO_REF:0000121
ACCEPT
Summary: Gsta4's glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles supports retaining glutathione metabolic process as a direct annotation (ISO, GO_REF:0000121).
Reason: glutathione metabolic process is a direct metabolic process expected from Gsta4's documented role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0006749; P:glutathione metabolic process; ISO:RGD.
GO:0006805 xenobiotic metabolic process
ISO
GO_REF:0000121
ACCEPT
Summary: Gsta4's glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles supports retaining xenobiotic metabolic process as a direct annotation (ISO, GO_REF:0000121).
Reason: xenobiotic metabolic process is a direct metabolic process expected from Gsta4's documented role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0006805; P:xenobiotic metabolic process; ISO:RGD.
GO:0042803 protein homodimerization activity
ISO
GO_REF:0000121
KEEP AS NON CORE
Summary: protein homodimerization activity is retained as useful context for Gsta4, but it is not the defining core function (ISO, GO_REF:0000121).
Reason: protein homodimerization activity records substrate, cofactor, or quaternary-structure context for Gsta4, but the curated core function is glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0042803; F:protein homodimerization activity; ISO:RGD.
GO:0004364 glutathione transferase activity
ISO
GO_REF:0000121
ACCEPT
Summary: Gsta4's glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles supports retaining glutathione transferase activity as a direct annotation (ISO, GO_REF:0000121).
Reason: glutathione transferase activity is a specific catalytic activity matching Gsta4's documented role in glutathione conjugation of lipid peroxidation products and xenobiotic electrophiles.
Supporting Evidence:
UniProtKB:P14942
GO; GO:0004364; F:glutathione transferase activity; ISO:RGD.

Core Functions

Gsta4 encodes rat glutathione S-transferase alpha-4 (GSTA4-4). FUNCTION: Conjugation of reduced glutathione to a wide number of exogenous and endogenous hydrophobic electrophiles, with characteristic high catalytic efficiency toward lipid peroxidation-derived alpha,beta-unsaturated aldehydes, especially 4-hydroxynonenal (4-HNE), which it clears by GSH conjugation (Michael addition).

Supporting Evidence:
  • UniProtKB:P14942
    FUNCTION: Conjugation of reduced glutathione to a wide number of exogenous and endogenous hydrophobic electrophiles.
  • file:rat/Gsta4/Gsta4-deep-research-falcon.md
    GSTA4-4 is repeatedly characterized as unusually efficient for **lipid-derived Ξ±,Ξ²-unsaturated aldehydes**, especially **4-HNE**

References

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Suggested Questions for Experts

Q: Falcon deep research highlights Scian et al. 2023 (Biomolecules, DOI:10.3390/biom13020329) showing GSTA4-4 catalyzes the retro-Michael reaction (GS-alkenal -> GSH + alkenal) with low commitment to forward catalysis, supporting a homeostatic/regulatory role in setting steady-state lipid alkenal pools rather than purely unidirectional detoxification. Does this reversibility/set-point framing warrant a new or modified BP annotation (e.g., capturing alkenal homeostasis or regulation of reactive lipid signaling) beyond the current detoxification/xenobiotic-metabolism terms?

Suggested experts: William M. Atkins

Deep Research

Falcon

(Gsta4-deep-research-falcon.md)

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πŸ“š Additional Documentation

Notes

(Gsta4-notes.md)

Gsta4 review notes

Evidence summary

  • [UniProtKB:P14942] UniProt describes Gsta4 as conjugating reduced glutathione to exogenous and endogenous hydrophobic electrophiles.
  • PMID:11018474 The fetched GOA file uses this publication for toxic-substance binding, kept as non-core context rather than the defining activity.

Curation decisions

  • Core function: glutathione S-transferase alpha-4 (glutathione transferase activity, GO:0004364).
  • Specific catalytic activities and direct metabolic processes were accepted.
  • Broad parent, localization, binding, and stimulus-response annotations were modified, kept non-core, or marked over-annotated according to support.

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