Cell Death Mechanisms in Biology

An enzyme that synthesizes ATP using energy from protons.

Molecular oxygen (O2) that accepts electrons in the ETC to form water.

A metabolic pathway for producing ATP using the electron transport chain.

Neuromuscular diseases caused by mutations affecting mitochondria, leading to energy deficiency.

Chemically reactive molecules that can damage cellular components and lead to cell death.

Processes that degrade obsolete or malfunctioning cellular components to maintain health.

A process that degrades and recycles cellular components for maintenance and energy.

Processes ensuring proper cellular function by removing damaged proteins and organelles.

A cellular mechanism that controls protein breakdown and signaling.

Balance of protein synthesis, folding, and degradation in cells.

Proteins that regulate the cell cycle and are degraded by ubiquitination.

Ubiquitin-activating enzyme that initiates the ubiquitination process.

Ubiquitin-conjugating enzyme that transfers activated ubiquitin from E1.

Ubiquitin ligase that transfers ubiquitin to target proteins, conferring specificity.

The process of tagging proteins with ubiquitin for degradation or signaling.

Large protein complex that degrades ubiquitinated proteins into peptides.

Cellular process of fixing DNA damage, aided by ubiquitination.

Regulation of signaling pathways influenced by ubiquitin’s stability effect on proteins.

A regulated process of programmed cell death essential for removing unwanted cells.

Uncontrolled cell death due to injury or disease, often leading to inflammation.

Activated by internal signals like DNA damage, involving mitochondrial changes.

Triggered by signals from other cells through death receptors like TNF family.

A group of proteins that regulate apoptosis by promoting or inhibiting cell death.

Proteins that play essential roles in programmed cell death by executing apoptosis.

Immune cells that induce apoptosis in infected or cancerous cells by recognizing foreign epitopes.

A family of proteins involved in the extrinsic apoptosis pathway by activating death receptors.

Conditions caused by abnormalities in apoptosis, such as cancer and neurodegenerative diseases.

Proteins released during intrinsic apoptosis that activate caspases leading to cell death.

An enzyme that activates apoptosis by cleaving substrates like BID.

A pro-apoptotic protein cleaved by Granzyme-B to form tBID.

Truncated version of BID that promotes cell death.

Cells that remove apoptotic cell fragments, reducing inflammation.

Elevation of intracellular Ca2+ triggers T-cell activation.

A receptor on T-cells that binds to antigens presented by APCs.

An enzyme activated during T-cell signaling that generates second messengers.

Second messengers produced by PLC-γ1 that help raise intracellular Ca2+.

A tyrosine kinase that promotes early T-cell activation.

A DNA damage sensor that granzyme B directly cleaves, impacting repair mechanisms.

A proto-oncogene playing a key role in cell growth and apoptosis regulation.

Mechanisms that promote programmed cell death, such as DNA damage and stress.

The process by which the tumor suppressor p53 is kept stable to respond to DNA damage.

A signaling route that stabilizes p53 in response to genotoxic stress.

Increased granzyme secretion has been linked to autoimmune disorders like Sjogren's syndrome.