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Event: 2124
Key Event Title
increased, Bax expression
Short name
Biological Context
Level of Biological Organization |
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Molecular |
Cell term
Organ term
Key Event Components
Key Event Overview
AOPs Including This Key Event
AOP Name | Role of event in AOP | Point of Contact | Author Status | OECD Status |
---|---|---|---|---|
Co-activation of IP3R and RyR to lower IQ | KeyEvent | Karine Audouze (send email) | Under development: Not open for comment. Do not cite | |
AhR activation leading to Premature ovarian insufficiency | KeyEvent | Sapana Kushwaha (send email) | Under development: Not open for comment. Do not cite |
Taxonomic Applicability
Life Stages
Sex Applicability
Key Event Description
Bax (Bcl-2-associated X protein) is a pro-apoptotic member of the Bcl-2 family that plays a critical role in regulating apoptosis. It is primarily localized in the cytoplasm and translocates to the mitochondria during apoptotic signaling. Bax plays a critical role in regulating apoptosis, including the apoptosis of oocytes during early development. When apoptotic signals are received, pro-apoptotic members like Bax are activated, often through phosphorylation or cleavage (e.g., in response to cellular stress). Once activated, Bax translocate to the outer mitochondrial membrane, where they form pores, leading to the release of cytochrome c and other apoptotic factors from the mitochondria into the cytoplasm. Increased expression of pro-apoptotic proteins (like Bax or Bad) can lead to excessive apoptosis, which might contribute to diseases such as neurodegenerative disorders, autoimmune diseases, or reproductive cell depletion (like oocyte loss).
Increased Bax expression is a key event in the pathway leading to oocyte apoptosis in fetal ovaries, specifically in response to PAH exposure mediated by AHR activation. This event underscores the role of Bax in the damage to the developing female germ line. In Bax-deficient mice, the follicle pool at birth appears normal but expands in size during postnatal development, indicating that Bax plays a role in regulating postnatal oocyte apoptosis. Bax deficiency can prevent the oocyte depletion that normally occurs, suggesting that its expression is necessary for the reduction of the oocyte population. The extent of increased Bax expression refers to its upregulation as a response to apoptotic signals, particularly in toxic conditions promotes mitochondrial-mediated apoptosis in oocytes. After an apoptotic stimulus, Bax translocates from the cytoplasm to the outer mitochondrial membrane, where it triggers mitochondrial membrane permeabilization and the release of pro-apoptotic factors. This step is crucial for initiating the apoptotic cascade in oocytes, which could potentially lead to the depletion of the oocyte pool.