GO:0071306 cellular response to vitamin E: Signaling, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0071306 cellular response to vitamin E describes any process by which a cell changes its state or activity in response to a vitamin E stimulus, including changes in gene expression, enzyme production, secretion, movement, and survival.
• Vitamin E is not a single molecule; the term covers responses to tocopherols and tocotrienols and their derivatives, including DL-alpha-tocopherol acetate and O-acetyl-alpha-tocopherol.
• A central mechanism is redox regulation: vitamin E scavenges lipid peroxyl radicals and modulates redox-sensitive signaling, thereby influencing ferroptosis, inflammation, and immune cell function.
• Vitamin E can directly modulate immune signaling; for example, it reinvigorates dendritic cells by targeting the checkpoint phosphatase SHP1, enhancing cancer immunotherapy responses.
• In T regulatory cells, vitamin E cooperates with GPX4 to protect against ferroptosis and to limit intestinal inflammatory damage in necrotizing enterocolitis.
• Studying GO:0071306 requires integrated approaches such as CRISPR knockout, point mutation, knock-in reporters, overexpression, RNA-seq, proteomics, and lipid peroxidation assays.
Description
GO:0071306 cellular response to vitamin E is a Gene Ontology biological process term that captures the full set of cellular changes triggered when a cell encounters vitamin E or a vitamin E-related stimulus. The official definition states that it is any process that results in a change in state or activity of a cell, in terms of movement, secretion, enzyme production, gene expression, and similar outputs, as a result of a vitamin E stimulus. This term is therefore broad and integrative: it does not describe a single pathway but rather the cellular response program initiated by vitamin E, including redox, immune, and survival signaling. Vitamin E is a family of lipid-soluble antioxidants, with alpha-tocopherol being the most biologically active form in humans. Cells respond to vitamin E through multiple mechanisms, including direct radical scavenging, modulation of enzyme activity, and changes in gene expression. Because vitamin E influences lipid peroxidation and redox balance, its cellular response is closely tied to ferroptosis, inflammation, and immune regulation. This makes GO:0071306 relevant to cancer immunology, intestinal inflammatory disease, and age-related immune dysfunction. For researchers, GO:0071306 provides a structured framework to annotate and interpret experiments in which vitamin E is used as a treatment, nutrient, or stress modifier. The term helps connect molecular readouts such as lipid peroxidation, cytokine secretion, and transcriptional changes to a defined biological process, enabling reproducible comparisons across cell types and disease models.
cellular response to vitamin E At A Glance
| GO ID | GO:0071306 |
|---|---|
| GO term | cellular response to vitamin E |
| Ontology | biological_process |
| Definition | Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a vitamin E stimulus. |
| Synonyms | cellular response to DL-alpha-tocopherol acetate; cellular response to DL-alpha-tocopheryl acetate; cellular response to O-Acetyl-alpha-tocopherol |
| Major function | Coordinating cellular redox, immune, and survival responses to vitamin E and its derivatives. |
| Related processes | Response to oxidative stress, ferroptosis, inflammatory signaling, immune cell activation, and lipid peroxidation. |
| Key cell types | Dendritic cells, T regulatory cells, endothelial cells, osteoblasts, hepatocytes, and lung cells. |
| Disease relevance | Cancer immunotherapy, necrotizing enterocolitis, age-related immune dysfunction, and oxidative stress-related pathology. |
What Is GO:0071306?
In simple terms, GO:0071306 cellular response to vitamin E describes everything a cell does after it senses vitamin E. According to the QuickGO definition, it is any process that results in a change in state or activity of a cell, such as movement, secretion, enzyme production, or gene expression, as a result of a vitamin E stimulus. The term includes responses to different vitamin E forms and derivatives, such as DL-alpha-tocopherol acetate and O-acetyl-alpha-tocopherol, and it is a biological process term rather than a molecular function or cellular component term.
Why Is cellular response to vitamin E Important in Cell Biology?
GO:0071306 is important because vitamin E is a widely consumed nutrient and a potential therapeutic agent, yet its cellular effects are context-dependent and can influence immunity, inflammation, and cell death. Understanding this process helps researchers explain how vitamin E modulates dendritic cell function to enhance cancer immunotherapy, how it cooperates with GPX4 to protect T regulatory cells from ferroptosis in necrotizing enterocolitis, and how it affects oxidative stress and inflammatory responses in endothelial and immune cells. The term also provides a standardized way to annotate and compare vitamin E responses across cell types, supporting reproducibility in nutrition, immunology, and cancer research.
• Vitamin E reinvigorates dendritic cells by targeting the checkpoint SHP1, linking GO:0071306 to cancer immunotherapy.
• Vitamin E and GPX4 cooperatively protect T regulatory cells from ferroptosis, reducing intestinal inflammatory damage in necrotizing enterocolitis.
• Vitamin E deficiency alters immunological regulation of lung cells, showing that this response is relevant to pulmonary immunity.
• Vitamin E modulates immune responses in aged individuals, with molecular mechanisms that have clinical implications for infection and vaccination.
• Vitamin E influences glutathione depletion and reactive oxygen species production in hepatocytes, connecting the term to redox biology.
• Vitamin E inhibits inflammatory endothelial responses through a pathway involving caspase activation and p65 cleavage.
• The term is relevant to osteoblast biology, as vitamin E-stabilized UHMWPE wear debris affects human osteoblast responses.
• Vitamin E deficiency can modify neurotoxicity and hepatotoxicity in experimental models, indicating broad physiological importance.
• GO:0071306 supports annotation of transcriptomic and proteomic changes induced by vitamin E in diverse cell models.
• Studying this process can reveal biomarkers and therapeutic targets for ferroptosis-related and inflammatory diseases.
What Happens During cellular response to vitamin E?
Vitamin E sensing and uptake
In simple terms: The cell first encounters vitamin E and takes it up or interacts with it at the membrane.
The cellular response to vitamin E begins when cells are exposed to vitamin E or its derivatives, such as alpha-tocopherol or DL-alpha-tocopherol acetate. Because vitamin E is lipid-soluble, it partitions into membranes and lipoproteins, where it can interact with redox-active lipids and proteins. This initial interaction is not a single receptor-ligand event but rather a membrane-associated process that sets the stage for downstream signaling. In immune cells, vitamin E exposure can directly influence signaling proteins such as SHP1, as shown by enhanced dendritic cell function in cancer immunotherapy models.
Redox modulation and lipid peroxidation control
In simple terms: Vitamin E acts as an antioxidant, stopping harmful lipid peroxidation and tuning the cell's redox state.
A core component of GO:0071306 is the modulation of redox balance. Vitamin E scavenges lipid peroxyl radicals, thereby limiting lipid peroxidation and protecting membrane integrity. This function is closely linked to glutathione metabolism and reactive oxygen species production, as demonstrated in hepatocyte suspensions where glutathione depletion and ROS generation are key readouts. In T regulatory cells, vitamin E cooperates with GPX4 to prevent ferroptosis, a form of lipid peroxidation-driven cell death, thereby maintaining immune homeostasis in necrotizing enterocolitis. These redox effects can also influence inflammatory signaling, as vitamin E inhibits endothelial inflammatory responses through caspase activation and p65 cleavage.
Immune signaling and checkpoint modulation
In simple terms: Vitamin E can change how immune cells communicate, sometimes boosting their ability to fight cancer.
Vitamin E can directly modulate immune cell signaling. In dendritic cells, vitamin E targets the checkpoint phosphatase SHP1, leading to reinvigoration of dendritic cells and enhanced cancer immunotherapy responses. This indicates that GO:0071306 includes changes in immune checkpoint pathways and antigen-presenting cell function. In aged individuals, vitamin E modulates immune responses through molecular mechanisms that affect T cell function and cytokine production, with clinical implications for infection and vaccination. Vitamin E deficiency also causes immunological dysregulation in lung cells, further supporting a role in pulmonary immune responses.
Transcriptional and enzyme production changes
In simple terms: The cell changes which genes and enzymes it makes in response to vitamin E.
According to the GO definition, cellular response to vitamin E includes changes in gene expression and enzyme production. Experimental studies show that vitamin E exposure alters transcriptional programs related to oxidative stress, inflammation, and immune function. For example, vitamin E-stabilized UHMWPE wear debris elicits biological responses in human osteoblasts, indicating changes in gene expression and enzyme activity in bone cells. These transcriptional and enzymatic changes are part of the cellular response and can be measured by RNA-seq, qPCR, and proteomics.
Cell survival, death, and ferroptosis regulation
In simple terms: Vitamin E can decide whether a cell lives or dies under stress, especially by preventing ferroptosis.
Vitamin E influences cell survival and death decisions. In T regulatory cells, vitamin E and GPX4 cooperatively protect against ferroptosis, a lipid peroxidation-dependent cell death pathway, thereby alleviating intestinal inflammatory damage in necrotizing enterocolitis. In endothelial cells, vitamin E inhibits inflammatory responses through a pathway involving caspase activation and p65 cleavage, linking redox regulation to apoptotic and inflammatory signaling. In dopaminergic neurotoxicity models, vitamin E deficiency exacerbates d-MDMA-induced neurotoxicity and hepatotoxicity, suggesting that vitamin E status affects cell survival under chemical stress.
Key Genes Involved in GO:0071306 cellular response to vitamin E
The following genes and proteins are experimentally linked to cellular responses to vitamin E, including redox regulation, immune signaling, ferroptosis, and inflammatory pathways.
| Gene | Major Role | Research Relevance |
|---|---|---|
| PTPN6 (SHP1) | Checkpoint phosphatase targeted by vitamin E in dendritic cells | Vitamin E reinvigorates dendritic cells via SHP1 to enhance cancer immunotherapy |
| GPX4 | Glutathione peroxidase that detoxifies lipid peroxides | Cooperates with vitamin E to protect Treg cells from ferroptosis in necrotizing enterocolitis |
| NFKB1 (p65) | Transcription factor subunit involved in inflammatory signaling | Vitamin E inhibits endothelial inflammatory responses via p65 cleavage |
| CASP3 / CASP8 | Caspases involved in apoptotic and inflammatory signaling | Vitamin E pathway involves caspase activation in endothelial cells |
| GSR / GCLC | Enzymes in glutathione synthesis and redox cycling | Glutathione depletion and ROS production are modulated by vitamin E in hepatocytes |
| IL6 | Pro-inflammatory cytokine | Vitamin E modulates immune responses and cytokine production in aged individuals |
| TNF | Pro-inflammatory cytokine | Vitamin E affects inflammatory signaling in endothelial and immune cells |
| IL10 | Anti-inflammatory cytokine | Vitamin E influences immune regulation in aged and lung cell models |
| ALOX15 | Lipoxygenase involved in lipid peroxidation | Lipid peroxidation pathways are central to vitamin E and ferroptosis responses |
| SLC7A11 (xCT) | Cystine/glutamate antiporter supporting glutathione synthesis | Redox and ferroptosis pathways intersect with vitamin E responses |
| NQO1 | NAD(P)H quinone dehydrogenase involved in redox balance | Vitamin E modulates redox-sensitive enzyme expression |
| HMOX1 | Heme oxygenase 1, stress-responsive enzyme | Vitamin E affects oxidative stress responses in immune and endothelial cells |
| MAPK1 / MAPK3 | Kinases in stress and inflammatory signaling | Vitamin E modulates inflammatory signaling pathways |
| PPARG | Nuclear receptor regulating lipid and inflammatory genes | Vitamin E can influence lipid-responsive transcription |
| SP1 | Transcription factor with redox-sensitive activity | Vitamin E affects gene expression programs in osteoblasts and immune cells |
| VDR | Vitamin D receptor, related to vitamin and immune regulation | Vitamin E and vitamin D pathways both modulate immune function |
| TP53 | Tumor suppressor and stress response transcription factor | Vitamin E responses intersect with cell survival and stress pathways |
How Is cellular response to vitamin E Regulated?
The cellular response to vitamin E is regulated at multiple levels. Redox status is a key regulator: glutathione availability and reactive oxygen species production influence how cells respond to vitamin E, as shown in hepatocyte suspensions where glutathione depletion alters ROS generation. Immune signaling checkpoints also regulate the response; SHP1 is a direct target of vitamin E in dendritic cells, and its activity determines the extent of immune reinvigoration. In T regulatory cells, the GPX4-dependent ferroptosis pathway is a critical regulator, and vitamin E cooperates with GPX4 to maintain cell survival. Inflammatory signaling through NF-kB p65 cleavage and caspase activation further modulates the endothelial response to vitamin E. Additionally, age-related changes in immune function can alter vitamin E responsiveness, as seen in aged individuals where vitamin E modulates immune responses through molecular mechanisms with clinical implications.
cellular response to vitamin E and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| PTPN6 (SHP1) | Cancer immunotherapy response | Dendritic cell knockout or point mutation followed by vitamin E treatment and T cell activation assays |
| GPX4 | Necrotizing enterocolitis and ferroptosis | Treg cell knockout of GPX4 with vitamin E treatment and lipid peroxidation measurement |
| NFKB1 (p65) | Endothelial inflammation | Endothelial cell knockout or overexpression with vitamin E and TNF stimulation |
| GSR / GCLC | Oxidative stress and glutathione depletion | Hepatocyte knockout or knockdown with vitamin E and ROS/glutathione assays |
| IL6 / TNF | Age-related immune dysfunction | Immune cell overexpression or knockout with vitamin E treatment and cytokine profiling |
Cancer immunotherapy
Vitamin E enhances cancer immunotherapy by reinvigorating dendritic cells via targeting the checkpoint SHP1. This places GO:0071306 at the intersection of nutrition, redox biology, and immuno-oncology. The cellular response to vitamin E in dendritic cells involves changes in signaling that overcome checkpoint inhibition, suggesting that vitamin E status could influence immunotherapy outcomes. Researchers can model this by treating dendritic cells with vitamin E and measuring SHP1 activity, antigen presentation, and T cell activation.
Necrotizing enterocolitis and intestinal inflammation
In necrotizing enterocolitis, vitamin E and GPX4 cooperatively protect T regulatory cells from ferroptosis and alleviate intestinal inflammatory damage. This links GO:0071306 to a severe neonatal intestinal disease characterized by inflammation and cell death. The mechanism involves lipid peroxidation control and maintenance of Treg survival, highlighting ferroptosis as a therapeutic target. Experimental models can use intestinal epithelial cells or Treg cells treated with ferroptosis inducers and vitamin E to assess protection.
Age-related immune dysfunction
Vitamin E modulates immune responses in aged individuals, with molecular mechanisms that have clinical implications for infection and vaccination. Aging is associated with chronic low-grade inflammation and impaired immune function, and vitamin E can influence cytokine production and T cell function. This makes GO:0071306 relevant to nutritional interventions aimed at improving immune responses in older adults.
Oxidative stress and inflammatory endothelial injury
Vitamin E inhibits inflammatory endothelial responses through a pathway involving caspase activation and p65 cleavage. This connects the cellular response to vitamin E to vascular inflammation and endothelial dysfunction. Additionally, vitamin E deficiency causes immunological dysregulation in lung cells, indicating that inadequate vitamin E status can exacerbate inflammatory responses in pulmonary tissue. These findings support the study of GO:0071306 in cardiovascular and pulmonary disease models.
From cellular response to vitamin E-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does SHP1 mediate vitamin E-induced dendritic cell activation? | PTPN6 knockout or point mutation in dendritic cells followed by vitamin E treatment |
| Does GPX4 cooperate with vitamin E to prevent Treg ferroptosis? | GPX4 knockout or knockdown in Treg cells with vitamin E and ferroptosis induction |
| Does p65 cleavage mediate vitamin E inhibition of endothelial inflammation? | NFKB1 knock-in of cleavage-resistant mutant or knockout in endothelial cells |
| Does vitamin E alter glutathione synthesis enzymes? | GSR or GCLC overexpression or knockout in hepatocytes with vitamin E and ROS assays |
| Does vitamin E modulate cytokine production in aged immune cells? | IL6 or TNF knock-in reporter or knockout in immune cells from aged models |
| Does vitamin E affect osteoblast gene expression? | Osteoblast overexpression or knockout of candidate genes with vitamin E-stabilized wear debris |
How to Study the cellular response to vitamin E Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA-seq | Global changes in gene expression | Identify transcriptional programs induced by vitamin E |
| Proteomics | Protein abundance and modifications | Detect SHP1 and p65 changes in immune and endothelial cells |
| Phosphoproteomics | Phosphorylation signaling events | Map kinase and checkpoint pathways modulated by vitamin E |
| Lipid peroxidation assay | Oxidative damage to lipids | Assess ferroptosis protection by vitamin E and GPX4 |
| Glutathione/ROS assay | Redox status and reactive oxygen species | Measure redox changes in hepatocytes and immune cells |
| Immunoblotting | Protein cleavage and expression | Detect p65 cleavage and caspase activation |
| Flow cytometry | Immune cell activation and cytokine production | Analyze dendritic cell and Treg responses to vitamin E |
| CRISPR screening | Gene essentiality and modifiers | Identify genes required for vitamin E responses |
Transcriptomic profiling by RNA-seq
RNA-seq is a primary method to measure changes in gene expression during the cellular response to vitamin E. Cells treated with vitamin E or its derivatives can be compared to untreated controls to identify differentially expressed genes involved in redox, inflammation, and immune pathways. This approach is useful for defining the transcriptional component of GO:0071306 and for generating hypotheses about upstream regulators.
Proteomics and phosphoproteomics
Proteomic methods measure changes in protein abundance and post-translational modifications, such as phosphorylation, during vitamin E responses. For example, SHP1 activity and p65 cleavage can be assessed by immunoblotting or mass spectrometry. Phosphoproteomics can reveal signaling nodes modulated by vitamin E in immune and endothelial cells.
Lipid peroxidation and ferroptosis assays
Because vitamin E controls lipid peroxidation, assays such as C11-BODIPY oxidation, malondialdehyde measurement, and ferroptosis inhibitors are essential to study GO:0071306. These methods have been used to show that vitamin E and GPX4 cooperatively protect Treg cells from ferroptosis. In hepatocytes, glutathione depletion and ROS production can be measured to assess redox changes.
Imaging and reporter assays
Fluorescence microscopy and reporter assays can visualize vitamin E uptake, subcellular localization, and signaling changes. For example, GFP-tagged proteins or luciferase reporters can monitor NF-kB activity or SHP1 function in live cells. Imaging of lipid peroxidation sensors can also reveal spatial aspects of ferroptosis protection by vitamin E.
How CRISPR Can Be Used to Study GO:0071306 cellular response to vitamin E
Knockout
CRISPR knockout is used to delete candidate genes such as PTPN6, GPX4, or NFKB1 to test their requirement in the cellular response to vitamin E. For example, knocking out PTPN6 in dendritic cells can determine whether SHP1 is necessary for vitamin E-induced immune activation. Similarly, GPX4 knockout in Treg cells can reveal whether vitamin E protection against ferroptosis depends on GPX4. Knockout studies provide causal evidence linking specific genes to GO:0071306.
Point Mutation
Point mutations can be introduced to dissect specific residues or domains. For instance, mutating the catalytic cysteine of SHP1 or the cleavage site in p65 can test whether these modifications are required for vitamin E responses. Point mutation models are valuable for separating enzymatic activity from scaffolding functions and for validating drug targets within the pathway.
Knock-in
Knock-in strategies can add tags, reporters, or disease-relevant alleles. A luciferase or GFP reporter knocked into an endogenous locus can monitor vitamin E-induced transcription in real time. Knock-in of a cleavage-resistant p65 allele can test whether p65 cleavage mediates vitamin E inhibition of endothelial inflammation. These models enable precise tracking of pathway activity.
Overexpression
Overexpression of genes such as GPX4, GSR, or SHP1 can test whether increased levels enhance or dampen the cellular response to vitamin E. For example, overexpressing GPX4 may synergize with vitamin E to protect against ferroptosis. Overexpression of antioxidant enzymes can also reveal whether redox capacity is limiting for vitamin E responses. These experiments complement loss-of-function studies.
How EDITGENE Supports cellular response to vitamin E Research
Researchers studying cellular response to vitamin E-related genes often need to determine whether a candidate gene is causally involved in redox regulation, immune signaling, or ferroptosis protection. EDITGENE provides CRISPR-based cell model services that enable precise knockout, point mutation, knock-in, and overexpression of genes such as PTPN6, GPX4, NFKB1, and GSR, supporting mechanistic studies of GO:0071306 in relevant cell types.
Contact EDITGENE today to design your custom CRISPR model for cellular response to vitamin E research.
Frequently Asked Questions About cellular response to vitamin E
What is GO:0071306 cellular response to vitamin E?
GO:0071306 is a Gene Ontology biological process term defined as any process that results in a change in state or activity of a cell as a result of a vitamin E stimulus, including changes in gene expression, enzyme production, secretion, and movement.
What genes are involved in cellular response to vitamin E?
Genes experimentally linked to this response include PTPN6 (SHP1), GPX4, NFKB1 (p65), caspases, glutathione synthesis enzymes, and inflammatory cytokines such as IL6 and TNF.
How does vitamin E affect dendritic cells?
Vitamin E reinvigorates dendritic cells by targeting the checkpoint phosphatase SHP1, which enhances cancer immunotherapy responses.
What is the role of GPX4 in vitamin E responses?
GPX4 cooperates with vitamin E to protect T regulatory cells from ferroptosis and to alleviate intestinal inflammatory damage in necrotizing enterocolitis.
Does vitamin E modulate inflammation?
Yes, vitamin E inhibits inflammatory endothelial responses through a pathway involving caspase activation and p65 cleavage, and it modulates immune responses in aged individuals.
How is cellular response to vitamin E studied?
Common methods include RNA-seq, proteomics, lipid peroxidation assays, glutathione/ROS measurements, immunoblotting, flow cytometry, and CRISPR screens.
What diseases are linked to cellular response to vitamin E?
Linked diseases and conditions include cancer immunotherapy response, necrotizing enterocolitis, age-related immune dysfunction, and oxidative stress-related inflammatory injury.
Can CRISPR be used to study cellular response to vitamin E?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models are used to test the causal roles of genes such as PTPN6, GPX4, and NFKB1 in vitamin E responses.
What are the synonyms of GO:0071306?
Synonyms include cellular response to DL-alpha-tocopherol acetate, cellular response to DL-alpha-tocopheryl acetate, and cellular response to O-Acetyl-alpha-tocopherol.
Why is vitamin E important for immune function?
Vitamin E modulates immune responses in aged individuals and affects dendritic cell and T regulatory cell function, with clinical implications for infection, vaccination, and cancer immunotherapy.
Conclusion
GO:0071306 cellular response to vitamin E is a broad biological process that encompasses redox regulation, immune signaling, transcriptional changes, and cell survival decisions triggered by vitamin E. Experimental evidence links this process to key genes such as PTPN6, GPX4, and NFKB1, and to diseases including cancer, necrotizing enterocolitis, and age-related immune dysfunction. Studying this term with CRISPR-based models and multi-omics methods can reveal new therapeutic opportunities and biomarkers. EDITGENE provides comprehensive CRISPR cell model services to support mechanistic and translational research on cellular response to vitamin E, from knockout and point mutation to knock-in, overexpression, and library screening.
References
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- 2. Luo S et al.. 2024. Vitamin E and GPX4 cooperatively protect treg cells from ferroptosis and alleviate intestinal inflammatory damage in necrotizing enterocolitis.. Redox Biol 75:103303 PMID: 39137584
- 3. Galliera E et al.. 2018. Vitamin E-stabilized UHMWPE: Biological response on human osteoblasts to wear debris.. Clin Chim Acta 486:18-25 PMID: 30006289
- 4. Johnson EA et al.. 2002. d-MDMA during vitamin E deficiency: effects on dopaminergic neurotoxicity and hepatotoxicity.. Brain Res 933(2):150-63 PMID: 11931860
- 5. Sabat R et al.. 2001. Immunological dysregulation of lung cells in response to vitamin E deficiency.. Free Radic Biol Med 30(10):1145-53 PMID: 11369505
- 6. Meydani SN et al.. 2005. Vitamin E and immune response in the aged: molecular mechanisms and clinical implications.. Immunol Rev 205(1):269-84 PMID: 15882360
- 7. Tirmenstein MA et al.. 2000. Glutathione depletion and the production of reactive oxygen species in isolated hepatocyte suspensions.. Chem Biol Interact 127(3):201-17 PMID: 10967318
- 8. Neuzil J et al.. 2001. Inhibition of inflammatory endothelial responses by a pathway involving caspase activation and p65 cleavage.. Biochemistry 40(15):4686-92 PMID: 11294636
