Apoptosis and Cell Death Quiz

A process of cell death that is programmed and controlled by the cell itself, leading to a neat and clean dismantling without causing inflammation or damaging neighboring cells.

A form of cell death that occurs due to external factors such as injury or toxins, resulting in uncontrolled cell breakdown and inflammation.

The process of cell death plays a crucial role in maintaining a healthy population of cells by removing cells that are damaged, old, or no longer needed.

Apoptosis is essential for development, eliminating unwanted cells during embryonic growth. For example, the tadpole's tail disappears through apoptosis.

Apoptosis is a continuous process in adults, removing billions of healthy cells each hour. This ensures proper regulation and eliminates cells that fail quality control checks.

The process of breaking down DNA in the nucleus into fragments containing multiples of nucleosomes, creating a ladder-like pattern during apoptosis.

These are inactive precursors to caspases, activated by specific signals triggering apoptosis.

A type of programmed cell death that is activated by external signals, often involving death receptor proteins on the cell surface.

Apoptotic bodies are formed during apoptosis as the cell's cytoplasm fragments, each enclosed within a membrane.

A class of enzymes involved in apoptosis, specifically targeting and breaking down proteins within the cell.

Programmed cell death (PCD) is a controlled process where a cell self-destructs to maintain tissue homeostasis.

Apoptosis requires ATP, while necrosis occurs when ATP is depleted.

Apoptosis involves phagocytosis of the cell by immune cells, preventing tissue inflammation. In contrast, necrosis results in cell lysis and inflammation.

Apoptosis is triggered by either the withdrawal of positive signals (growth factors) or the receipt of negative signals (such as DNA damage or death activators).

Apoptotic pathways involve a series of steps, including the decision to activate the pathway, the actual cell death process, engulfment by phagocytes, and degradation of the remains.

Examples of negative signals that trigger apoptosis include DNA damage by X-ray or UV light, chemotherapeutic drugs, misfolded proteins, and death activators like TNF-α and FasL.

A gene that promotes cell growth and division. When mutated, it becomes an oncogene and can contribute to cancer development.

A gene that normally prevents uncontrolled cell growth. When mutated, it loses its tumor suppressor function, leading to increased cancer risk.

Genes involved in repairing damaged DNA. When mutated, they increase the likelihood of mutations accumulating in other genes, including proto-oncogenes and tumor suppressor genes, increasing cancer risk.

The escape from programmed cell death (apoptosis) by cancer cells, allowing them to survive and proliferate.

Cancer can be considered a genetic disease resulting from mutations in genes involved in cell growth, division, and DNA repair.

Caspases are a family of proteases (enzymes that break down proteins) that play a crucial role in apoptosis, also known as programmed cell death.

Caspases are activated by proteolytic cleavage, where a specific part of the caspase molecule is removed, enabling it to become active.

The extrinsic pathway is triggered when a death receptor on the cell surface binds to its specific ligand, initiating a signaling cascade that leads to caspase activation.

The intrinsic pathway is activated by internal cellular stress, such as DNA damage or mitochondrial dysfunction, leading to the release of cytochrome c from mitochondria, ultimately activating caspases.

FasL, TNF, and TRAIL are ligands that bind to their respective receptors on the cell surface, triggering the extrinsic apoptotic pathway.

The Fas (CD95) receptor, TNF-R, and DR4 (TRAIL-R) are death receptors that bind to their specific ligands and initiate the extrinsic apoptotic pathway.

When a ligand binds to its receptor, it triggers a series of events, including the assembly of death-inducing signaling complex (DISC) and activation of caspase-8, ultimately leading to apoptosis.

The mitochondrial pathway is initiated by internal stress and involves the release of cytochrome c from mitochondria, forming a complex with Apaf-1 and caspase-9, ultimately activating other caspases and leading to apoptosis.

A mutated version of a proto-oncogene that is constantly active, promoting excessive cell growth and contributing to cancer.

The p53 gene is a crucial tumor suppressor gene responsible for halting the cell cycle when DNA damage occurs. It allows for DNA repair and, if unsuccessful, triggers programmed cell death (apoptosis).