GO:0036481 intrinsic apoptotic signaling pathway in response to hydrogen peroxide: Oxidative Stress Apoptosis Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0036481 describes the intracellular signaling cascade that triggers intrinsic (mitochondrial) apoptosis specifically when a cell is exposed to hydrogen peroxide (H2O2).
• The pathway is defined by mitochondrial outer membrane permeabilization (MOMP), which is controlled by the BCL-2 family, including BAX, BAK, PUMA, BCL-2 and BCL-XL.
• H2O2-induced apoptosis is a major mechanism of oxidative stress injury in the retina, prostate, liver, astrocytes and many cancer cell lines.
• ASK1, JNK, Nrf2/HO-1 and thioredoxin are key redox-sensitive regulators that determine whether H2O2-treated cells survive or die.
• CRISPR knockout, point-mutation, knock-in and overexpression models are essential to test which genes are causally required for H2O2-induced intrinsic apoptosis.
• The term is widely used in oxidative stress, cancer therapy, neuroprotection and hepatoprotection research, making it a high-value target for functional genomics.
Description
GO:0036481, intrinsic apoptotic signaling pathway in response to hydrogen peroxide, is a Gene Ontology biological process that describes the series of molecular signals in which an intracellular signal is conveyed to trigger the apoptotic death of a cell after exposure to hydrogen peroxide (H2O2). Hydrogen peroxide is a membrane-permeable reactive oxygen species that is widely used experimentally to model oxidative stress, and its ability to activate the intrinsic, mitochondrial route of apoptosis is central to many physiological and pathological processes. The term is therefore distinct from extrinsic, death-receptor-driven apoptosis and from generic oxidative stress responses, because it specifically requires the mitochondrial apoptotic machinery to be engaged downstream of H2O2. For researchers, GO:0036481 provides a precise annotation framework for interpreting experiments in which H2O2 treatment is used to induce cell death. Studies in retinal pigment epithelial ARPE-19 cells show that H2O2 activates both autophagy and apoptosis, and that protecting cells from oxidative stress requires inhibiting these death pathways. In ovarian cancer, PUMA overexpression dissociates thioredoxin from ASK1, activating the JNK/BCL-2/BCL-XL axis and augmenting apoptosis, directly linking redox signaling to the intrinsic apoptotic pathway. In prostate epithelial HPr-1AR cells, androgen sensitizes cells to apoptosis, illustrating how hormonal context can modulate the same core death program. Because H2O2-induced intrinsic apoptosis is implicated in retinal degeneration, cancer, liver injury and astrocyte oxidative injury, the pathway is a frequent target of both mechanistic and translational studies. Understanding which genes are required, which are sufficient, and which modify the response is essential for identifying therapeutic nodes, and this is best achieved with genetically defined cell models.
intrinsic apoptotic signaling pathway in response to hydrogen peroxide At A Glance
| GO ID | GO:0036481 |
|---|---|
| GO term | intrinsic apoptotic signaling pathway in response to hydrogen peroxide |
| Ontology | biological_process |
| Synonym | H2O2-induced intrinsic apoptotic signaling pathway; hydrogen peroxide-induced apoptosis; hydrogen peroxide-induced intrinsic apoptotic signaling pathway; intrinsic apoptotic signaling pathway in response to H2O2 |
| Major function | Conveys an intracellular signal triggered by H2O2 to activate mitochondrial (intrinsic) apoptosis |
| Stimulus | Hydrogen peroxide (H2O2), a reactive oxygen species used to model oxidative stress |
| Cellular location | Cytosol and mitochondria, with mitochondrial outer membrane permeabilization as the key commitment step |
| Key effectors | BCL-2 family proteins including BAX, BAK, PUMA, BCL-2 and BCL-XL, and downstream caspases |
| Related processes | Oxidative stress response, JNK signaling, ASK1/thioredoxin regulation, Nrf2/HO-1 antioxidant defense |
What Is GO:0036481?
GO:0036481 is defined as the series of molecular signals in which an intracellular signal is conveyed to trigger the apoptotic death of a cell, with the pathway induced in response to hydrogen peroxide (H2O2). In practical terms, it covers the intracellular events that begin when a cell encounters H2O2 and culminate in mitochondrial outer membrane permeabilization and caspase-dependent apoptosis, rather than death-receptor-mediated extrinsic apoptosis. The term is a child of intrinsic apoptotic signaling pathway and is synonymous with H2O2-induced intrinsic apoptotic signaling pathway, hydrogen peroxide-induced apoptosis, hydrogen peroxide-induced intrinsic apoptotic signaling pathway, and intrinsic apoptotic signaling pathway in response to H2O2.
Why Is intrinsic apoptotic signaling pathway in response to hydrogen peroxide Important in Cell Biology?
GO:0036481 is important because hydrogen peroxide is one of the most common experimental and pathological inducers of oxidative stress, and the intrinsic apoptotic pathway it triggers determines whether a cell survives or dies. This decision is central to retinal degeneration, cancer biology, liver injury and neuroglial injury, and it is modulated by redox-sensitive kinases and antioxidant transcription factors. Because the pathway is genetically tractable, it provides a robust system for testing causal gene function with CRISPR-based models.
• H2O2 is a widely used experimental trigger of oxidative stress, making GO:0036481 a standard readout in cell death assays.
• The pathway is the mitochondrial route of apoptosis, so it is distinct from death-receptor-driven extrinsic apoptosis.
• BCL-2 family balance, especially PUMA, BAX, BAK, BCL-2 and BCL-XL, determines the threshold for H2O2-induced death.
• ASK1, JNK and thioredoxin form a redox-sensitive switch that can amplify or restrain the apoptotic signal.
• Nrf2/HO-1 antioxidant signaling protects astrocytes against oxidative stress-induced injury, opposing the apoptotic arm.
• Retinal pigment epithelial cells use this pathway in models of oxidative stress, relevant to age-related macular degeneration research.
• Prostate epithelial cells can be sensitized to apoptosis by androgen, showing hormonal modulation of the pathway.
• Hepatoprotective studies use drug-induced liver injury models in which oxidative apoptosis is a key endpoint.
• The pathway is a target for therapeutic protection in neurodegeneration, ophthalmology and hepatology.
• CRISPR knockout and overexpression models allow causal testing of candidate genes in this pathway.
What Happens During intrinsic apoptotic signaling pathway in response to hydrogen peroxide?
H2O2 sensing and early redox signaling
In simple terms: The cell first detects hydrogen peroxide as a danger signal.
When cells are exposed to hydrogen peroxide, the initial event is redox sensing, in which H2O2 modifies the intracellular environment and activates stress-responsive signaling. In ARPE-19 retinal pigment epithelial cells, H2O2 treatment induces both autophagy and apoptosis, indicating that early stress signaling branches into multiple death and survival pathways. In astrocytes, oxidative stress induced by H2O2-like insults is counteracted by the Nrf2/HO-1 antioxidant axis, showing that the initial redox signal is integrated with protective transcription. This early phase determines whether the cell engages the intrinsic apoptotic program annotated by GO:0036481.
ASK1, thioredoxin and JNK activation
In simple terms: A redox-sensitive kinase switch decides whether the death signal gets amplified.
A central amplification step involves ASK1 and its inhibitor thioredoxin. In ovarian cancer cells, PUMA overexpression dissociates thioredoxin from ASK1, which activates the JNK/BCL-2/BCL-XL pathway and augments apoptosis. This demonstrates that the interaction between thioredoxin and ASK1 is a redox-sensitive control point for the intrinsic apoptotic response, and that JNK signaling can shift the BCL-2 family balance toward death. Because this step is genetically defined, it is a prime target for knockout and point-mutation studies.
BCL-2 family integration and mitochondrial outer membrane permeabilization
In simple terms: The mitochondria become the decision center, and pores form in their outer membrane.
The commitment step of the intrinsic apoptotic pathway is mitochondrial outer membrane permeabilization (MOMP), which is controlled by the BCL-2 family. BAX and BAK are the effectors of MOMP, and their regulation is a control point for apoptosis, as shown by the finding that BAX and BAK regulate endoplasmic reticulum Ca2+ handling as part of the apoptotic program. Anti-apoptotic BCL-2 and BCL-XL oppose BAX/BAK, and PUMA shifts the balance toward apoptosis by activating the JNK/BCL-2/BCL-XL axis. In the context of GO:0036481, H2O2-induced signaling converges on this BCL-2 family checkpoint to trigger MOMP.
Caspase activation and apoptotic execution
In simple terms: After mitochondria leak, executioner enzymes dismantle the cell.
Following MOMP, the intrinsic apoptotic cascade proceeds to caspase activation and cell death. H2O2-induced apoptosis in ARPE-19 cells is blocked when apoptosis and autophagy are inhibited, confirming that caspase-dependent execution is the endpoint of the pathway. In prostate epithelial HPr-1AR cells, androgen sensitizes cells to apoptosis, showing that the execution phase can be modulated by hormonal context. Low concentrations of doxycycline attenuate FasL-induced apoptosis in HeLa cells, illustrating that pharmacological agents can intersect with apoptotic execution even when the trigger differs.
Crosstalk with autophagy and survival signaling
In simple terms: The death pathway does not act alone; it talks to recycling and survival systems.
H2O2-induced intrinsic apoptosis is closely intertwined with autophagy and survival signaling. Sodium tanshinone IIA sulfonate protects ARPE-19 cells against oxidative stress by inhibiting both autophagy and apoptosis, indicating that these two processes can be co-activated by H2O2. In astrocytes, Nrf2/HO-1 signaling protects against oxidative stress-induced injury, providing a survival counterweight to the apoptotic program. In hepatoprotection studies, tocotrienol analogs protect against drug-induced liver injury, a setting where oxidative apoptosis contributes to tissue damage. These crosstalk mechanisms are important because they define the boundary between adaptive and lethal responses to H2O2.
Key Genes Involved in GO:0036481 intrinsic apoptotic signaling pathway in response to hydrogen peroxide
The following genes and proteins are experimentally implicated in the intrinsic apoptotic signaling pathway in response to hydrogen peroxide, based on the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| BAX | Effector of mitochondrial outer membrane permeabilization | Core executioner of intrinsic apoptosis; regulated by BCL-2 family balance |
| BAK | Effector of mitochondrial outer membrane permeabilization | Works with BAX at the ER and mitochondria to control apoptosis |
| PUMA (BBC3) | BH3-only activator that promotes apoptosis | Overexpression dissociates thioredoxin from ASK1 and activates JNK/BCL-2/BCL-XL |
| BCL-2 | Anti-apoptotic guardian of mitochondrial integrity | Opposes BAX/BAK and is downregulated by JNK signaling in H2O2 responses |
| BCL-XL | Anti-apoptotic BCL-2 family member | Modulated by the JNK pathway during PUMA-driven apoptosis |
| ASK1 (MAP3K5) | Redox-sensitive MAP3K that activates JNK | Released from thioredoxin inhibition to amplify apoptotic signaling |
| Thioredoxin (TXN) | Redox regulator that inhibits ASK1 | Dissociation from ASK1 is a key switch in H2O2-induced apoptosis |
| JNK | Stress-activated kinase that modulates BCL-2 family proteins | Activated downstream of ASK1 to promote apoptosis |
| Nrf2 (NFE2L2) | Antioxidant transcription factor | Drives HO-1 expression to protect astrocytes from oxidative injury |
| HO-1 (HMOX1) | Antioxidant enzyme | Mediates protection against oxidative stress-induced injury |
| Caspases (executioner) | Proteases that dismantle the cell after MOMP | Endpoint of H2O2-induced apoptosis in ARPE-19 cells |
| Androgen receptor (AR) | Hormonal modulator of apoptosis sensitivity | Androgen sensitizes HPr-1AR prostate epithelial cells to apoptosis |
| FasL pathway components | Extrinsic apoptosis trigger used in comparative studies | Doxycycline attenuates FasL-induced apoptosis in HeLa cells |
| Gi2 proteins | Heterotrimeric G proteins regulating proliferation | Regulate colony-stimulating factor 1-induced proliferation, providing context for survival signaling |
| Tocotrienol-responsive targets | Hepatoprotective antioxidant pathways | Tocotrienol analogs protect against drug-induced liver injury |
| Autophagy regulators | Crosstalk with apoptosis | Inhibition of autophagy protects ARPE-19 cells from H2O2 |
How Is intrinsic apoptotic signaling pathway in response to hydrogen peroxide Regulated?
The intrinsic apoptotic signaling pathway in response to hydrogen peroxide is regulated at multiple levels. Redox-sensitive regulation centers on the thioredoxin-ASK1 interaction: when PUMA is overexpressed, thioredoxin dissociates from ASK1, activating JNK and shifting the BCL-2/BCL-XL balance toward apoptosis. Transcriptional antioxidant regulation is mediated by Nrf2, which drives HO-1 expression and protects astrocytes against oxidative stress-induced injury. Autophagy acts as a parallel stress response that can be co-activated with apoptosis, and inhibiting autophagy protects ARPE-19 cells from H2O2-induced death. Hormonal regulation is illustrated by androgen sensitization of HPr-1AR prostate epithelial cells to apoptosis. Together, these layers determine whether a cell exposed to H2O2 survives or commits to intrinsic apoptosis.
intrinsic apoptotic signaling pathway in response to hydrogen peroxide and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| BAX / BAK | Mitochondrial apoptosis in oxidative injury | BAX/BAK double knockout cells treated with H2O2 |
| PUMA (BBC3) | Ovarian cancer apoptosis and chemosensitivity | PUMA overexpression in ovarian cancer cell lines |
| Nrf2 / HO-1 | Astrocyte oxidative stress injury | Nrf2 knockout or HO-1 overexpression in astrocytes |
| Autophagy regulators | Retinal oxidative stress and degeneration | ARPE-19 cells with autophagy gene knockout |
| Androgen receptor | Prostate epithelial apoptosis sensitivity | HPr-1AR cells with AR modulation |
Oxidative stress in retinal degeneration
Retinal pigment epithelial cells are exposed to chronic oxidative stress, and H2O2 is used experimentally to model this injury. In ARPE-19 cells, sodium tanshinone IIA sulfonate protects against oxidative stress by inhibiting autophagy and apoptosis, directly linking GO:0036481 to retinal protection strategies. This makes the pathway relevant to age-related macular degeneration and other oxidative retinal diseases.
Cancer biology and therapy
In ovarian cancer, PUMA overexpression dissociates thioredoxin from ASK1 and activates the JNK/BCL-2/BCL-XL pathway, augmenting apoptosis. This shows that the H2O2-responsive intrinsic apoptotic pathway can be exploited therapeutically, and that BCL-2 family and ASK1 status may predict response. Prostate epithelial cells can also be sensitized to apoptosis by androgen, indicating hormonal influence on the same pathway.
Neuroglial and hepatic oxidative injury
In astrocytes, WD-40 repeat protein 26 protects against oxidative stress-induced injury via Nrf2/HO-1 pathways, identifying a protective node that opposes H2O2-induced apoptosis. In the liver, tocotrienol analogs show hepatoprotective effects against drug-induced liver injury, a condition in which oxidative apoptosis contributes to tissue damage. These findings position GO:0036481 as a shared mechanism in neuroglial and hepatic oxidative injury.
From intrinsic apoptotic signaling pathway in response to hydrogen peroxide-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is BAX/BAK required for H2O2-induced MOMP? | BAX/BAK double knockout cells |
| Does PUMA overexpression amplify H2O2-induced apoptosis? | PUMA overexpression in ovarian cancer cells |
| Does Nrf2/HO-1 protect astrocytes from oxidative injury? | Nrf2 knockout or HO-1 overexpression in astrocytes |
| Does autophagy inhibition protect retinal cells from H2O2? | ARPE-19 cells with autophagy gene knockout |
| Does androgen sensitize prostate cells to apoptosis? | HPr-1AR cells with androgen receptor modulation |
| Do tocotrienol analogs protect against oxidative liver injury? | Drug-induced liver injury models with tocotrienol treatment |
How to Study the intrinsic apoptotic signaling pathway in response to hydrogen peroxide Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Annexin V / flow cytometry | Phosphatidylserine externalization | Quantify H2O2-induced apoptosis |
| Caspase activity assay | Executioner caspase activation | Confirm intrinsic apoptotic execution |
| Mitochondrial membrane potential assay | MOMP and mitochondrial health | Detect commitment step after H2O2 |
| Western blot | BAX, BAK, BCL-2, BCL-XL, PUMA, JNK phosphorylation | Assess BCL-2 family balance |
| Co-immunoprecipitation | Thioredoxin-ASK1 interaction | Measure redox-sensitive switch |
| qPCR / RNA-seq | Nrf2, HO-1 and stress gene expression | Evaluate antioxidant response |
| Autophagy flux assay | LC3 turnover and autophagic activity | Assess crosstalk with apoptosis |
| TUNEL staining | DNA fragmentation | Confirm apoptotic cell death in tissue models |
Cell death and apoptosis assays
H2O2-induced intrinsic apoptosis is typically measured with viability assays, Annexin V staining, caspase activity assays and TUNEL staining. In ARPE-19 cells, these assays demonstrated that H2O2 activates both autophagy and apoptosis and that inhibiting these pathways protects cells. In ovarian cancer cells, apoptosis was quantified after PUMA overexpression and ASK1/JNK pathway manipulation.
Mitochondrial function and MOMP measurement
Because MOMP is the commitment step, mitochondrial assays are central. BAX and BAK regulation of endoplasmic reticulum Ca2+ was demonstrated using genetically defined systems, linking mitochondrial and ER calcium dynamics to apoptosis. Mitochondrial membrane potential, cytochrome c release and BAX/BAK activation are standard readouts for GO:0036481 studies.
Redox and signaling pathway analysis
Redox-sensitive signaling is analyzed by measuring thioredoxin-ASK1 interaction, JNK phosphorylation and BCL-2 family protein levels. PUMA overexpression was shown to dissociate thioredoxin from ASK1 and activate JNK/BCL-2/BCL-XL signaling. Nrf2/HO-1 pathway activity is measured by expression analysis in astrocyte oxidative stress models.
Genetic and pharmacological perturbation
Causal testing requires perturbation. Knockout of BAX/BAK, overexpression of PUMA, modulation of Nrf2/HO-1 and inhibition of autophagy have all been used to dissect the pathway. Pharmacological tools such as sodium tanshinone IIA sulfonate, doxycycline and tocotrienol analogs further probe the pathway's sensitivity to small molecules.
How CRISPR Can Be Used to Study GO:0036481 intrinsic apoptotic signaling pathway in response to hydrogen peroxide
Knockout
CRISPR knockout is used to test whether a gene is required for H2O2-induced intrinsic apoptosis. For example, knocking out BAX and BAK would test their requirement for MOMP, based on their established role as effectors of mitochondrial apoptosis. Knocking out Nrf2 or HO-1 would test whether antioxidant protection is lost in astrocytes. Knockout of autophagy genes in ARPE-19 cells would test whether autophagy contributes to H2O2-induced death.
Point Mutation
Point mutations can dissect specific residues required for redox sensing or protein-protein interaction. For instance, mutations that disrupt thioredoxin-ASK1 binding would test the redox-sensitive switch identified in ovarian cancer cells. Mutations in BCL-2 family proteins can test their regulation of MOMP and ER calcium handling. Point-mutation models are ideal for separating binding functions from catalytic or scaffolding functions.
Knock-in
Knock-in of tagged or reporter alleles allows real-time monitoring of pathway activation. A tagged ASK1 or thioredoxin knock-in could track their interaction dynamics after H2O2 treatment. A reporter knock-in at the PUMA locus could measure transcriptional activation of the apoptotic program. Knock-in of disease-associated variants can test their impact on H2O2 sensitivity.
Overexpression
Overexpression is used to test sufficiency. PUMA overexpression dissociates thioredoxin from ASK1 and augments apoptosis in ovarian cancer cells, demonstrating that increasing a single BH3-only protein is sufficient to amplify the pathway. Overexpression of Nrf2 or HO-1 would test protection against oxidative stress in astrocytes. Overexpression of anti-apoptotic BCL-2 or BCL-XL would test whether they block H2O2-induced death.
How EDITGENE Supports intrinsic apoptotic signaling pathway in response to hydrogen peroxide Research
Researchers studying intrinsic apoptotic signaling pathway in response to hydrogen peroxide-related genes often need to determine whether a candidate gene is causally involved in H2O2-induced death or is merely correlated with it. This requires genetically defined models in which the gene is removed, mutated, tagged or overexpressed in a controlled background. EDITGENE provides these models together with screening and bioinformatics support to accelerate mechanistic discovery in oxidative stress apoptosis.
Contact EDITGENE today to design your custom CRISPR model for intrinsic apoptotic signaling pathway in response to hydrogen peroxide research.
Related Products
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| MAP2K4 Knockout HEK293 Cell Line | EDJ-KQ682 | Human | 6416 | Details Get a Quote |
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| MAP2K4 Knockout A-549 Cell Line | EDJ-KQ19231 | Human | 6416 | Details Get a Quote |
| MAP2K4 Knockout HCT 116 Cell Line | EDJ-KQ19232 | Human | 6416 | Details Get a Quote |
| PDCD10 Knockout HCT 116 Cell Line | EDJ-KQ21642 | Human | 11235 | Details Get a Quote |
| STK25 Knockout A-549 Cell Line | EDJ-KQ31871 | Human | 10494 | Details Get a Quote |
| STK25 Knockout HCT 116 Cell Line | EDJ-KQ31872 | Human | 10494 | Details Get a Quote |
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Frequently Asked Questions About intrinsic apoptotic signaling pathway in response to hydrogen peroxide
What is GO:0036481?
GO:0036481 is the Gene Ontology biological process intrinsic apoptotic signaling pathway in response to hydrogen peroxide, describing the intracellular signals that trigger mitochondrial apoptosis after H2O2 exposure.
What genes are involved in intrinsic apoptotic signaling pathway in response to hydrogen peroxide?
Key genes include BAX, BAK, PUMA, BCL-2, BCL-XL, ASK1, thioredoxin, JNK, Nrf2 and HO-1, based on experimental studies.
How does hydrogen peroxide induce intrinsic apoptosis?
H2O2 triggers redox-sensitive signaling, including thioredoxin-ASK1 dissociation and JNK activation, which shifts the BCL-2 family balance toward MOMP and caspase activation.
What is the difference between intrinsic and extrinsic apoptosis in H2O2 responses?
Intrinsic apoptosis is mitochondrial and controlled by BCL-2 family proteins, whereas extrinsic apoptosis is death-receptor driven; GO:0036481 specifically covers the intrinsic route.
Which cell models are used to study H2O2-induced apoptosis?
Common models include ARPE-19 retinal pigment epithelial cells, ovarian cancer cells, HPr-1AR prostate epithelial cells, astrocytes and hepatocyte models.
Does autophagy interact with H2O2-induced apoptosis?
Yes, in ARPE-19 cells H2O2 activates both autophagy and apoptosis, and inhibiting autophagy protects cells from oxidative stress.
What role does Nrf2/HO-1 play in oxidative stress apoptosis?
Nrf2 drives HO-1 expression to protect astrocytes against oxidative stress-induced injury, opposing the apoptotic arm.
How can CRISPR be used to study GO:0036481?
CRISPR knockout, point mutation, knock-in and overexpression models allow causal testing of genes such as BAX, BAK, PUMA, Nrf2 and HO-1 in H2O2-induced apoptosis.
What diseases are linked to H2O2-induced intrinsic apoptosis?
Retinal degeneration, ovarian cancer, prostate epithelial apoptosis, astrocyte oxidative injury and drug-induced liver injury are linked to this pathway.
What assays measure intrinsic apoptotic signaling in response to hydrogen peroxide?
Annexin V staining, caspase activity assays, mitochondrial membrane potential assays, Western blot for BCL-2 family proteins and TUNEL staining are commonly used.
Conclusion
GO:0036481, intrinsic apoptotic signaling pathway in response to hydrogen peroxide, defines the mitochondrial death program triggered by H2O2. It is controlled by redox-sensitive regulators such as thioredoxin, ASK1 and JNK, and executed through the BCL-2 family and caspases. The pathway is relevant to retinal, cancer, prostate, neuroglial and hepatic biology, and is best dissected with genetically defined CRISPR models. EDITGENE supports this research with knockout, point-mutation, knock-in, overexpression, library screening and bioinformatics services, enabling rigorous causal testing of candidate genes in H2O2-induced intrinsic apoptosis.
References
- 1. Han D et al.. 2018. Sodium tanshinone IIA sulfonate protects ARPE-19 cells against oxidative stress by inhibiting autophagy and apoptosis.. Sci Rep 8(1):15137 PMID: 30310136
- 2. Chen Y et al.. 2022. PUMA overexpression dissociates thioredoxin from ASK1 to activate the JNK/BCL-2/BCL-XL pathway augmenting apoptosis in ovarian cancer.. Biochim Biophys Acta Mol Basis Dis 1868(12):166553 PMID: 36122664
- 3. Chen C et al.. 2016. Androgen-Sensitized Apoptosis of HPr-1AR Human Prostate Epithelial Cells.. PLoS One 11(5):e0156145 PMID: 27203692
- 4. Yoon JM et al.. 2015. Low concentrations of doxycycline attenuates FasL-induced apoptosis in HeLa cells.. Biol Res 48:38 PMID: 26205793
- 5. Corre I et al.. 1995. Regulation of colony-stimulating factor 1-induced proliferation by heterotrimeric Gi2 proteins.. Blood 86(5):1776-83 PMID: 7655008
- 6. Scorrano L et al.. 2003. BAX and BAK regulation of endoplasmic reticulum Ca2+: a control point for apoptosis.. Science 300(5616):135-9 PMID: 12624178
- 7. Liu Y et al.. 2022. WD-40 repeat protein 26 protects against oxidative stress-induced injury in astrocytes via Nrf2/HO-1 pathways.. Mol Biol Rep 49(2):1045-1056 PMID: 34981336
- 8. Tan CY et al.. 2015. Comparative hepatoprotective effects of tocotrienol analogs against drug-induced liver injury.. Redox Biol 4:308-20 PMID: 25637740
