Cellular Biology I - Cell Death Mechanisms

<p>There is an opening of Ca2+-permeable channels (A)</p> Signup and view all the answers

<p>Cell death characterized by multinucleation during failed mitosis (A)</p> Signup and view all the answers

<p>Apoptosis is orderly and highly regulated. (D)</p> Signup and view all the answers

<p>Direct damage to the cell. (C)</p> Signup and view all the answers

<p>A cleanly executed cellular death mechanism. (C)</p> Signup and view all the answers

<p>The morphological and biochemical interpretations of cell death. (A)</p> Signup and view all the answers

<p>Induced by physiological signals. (C)</p> Signup and view all the answers

<p>Based on signal dependency and specific triggers. (D)</p> Signup and view all the answers

<p>Necrosis. (D)</p> Signup and view all the answers

<p>Predetermined genetic signals. (B)</p> Signup and view all the answers

<p>fragmentation into apoptotic bodies (A)</p> Signup and view all the answers

<p>massive activation of caspases (D)</p> Signup and view all the answers

<p>to cleave specific proteins leading to cell disassembly (C)</p> Signup and view all the answers

<p>intrinsic pathway (D)</p> Signup and view all the answers

<p>complete fragmentation of the nucleus (A)</p> Signup and view all the answers

<p>exposure of phosphatidylserine residues (C)</p> Signup and view all the answers

<p>necrotic cell death (B)</p> Signup and view all the answers

<p>activation of immune pathways (C)</p> Signup and view all the answers

<p>It is triggered by signals from other cells. (B)</p> Signup and view all the answers

<p>permeabilization of the mitochondrial outer membrane (C)</p> Signup and view all the answers

<p>Caspase-9 (A)</p> Signup and view all the answers

<p>It forms the apoptosome with APAF1. (B)</p> Signup and view all the answers

<p>They are activated through dimerization and cleavage. (B)</p> Signup and view all the answers

<p>Interferon (D)</p> Signup and view all the answers

<p>Interaction of surface receptors with their ligands (A)</p> Signup and view all the answers

<p>Cleaving target proteins post-activation (A)</p> Signup and view all the answers

<p>Formation of membrane introflexions (C)</p> Signup and view all the answers

<p>Caspase-8 (C)</p> Signup and view all the answers

<p>They dimerize and undergo proteolytic cleavage. (B)</p> Signup and view all the answers

<p>They must be cleaved to become active. (B)</p> Signup and view all the answers

<p>Pannexin 1 (D)</p> Signup and view all the answers

<p>Apoptosis (D)</p> Signup and view all the answers

<p>Death receptor-ligand binding (B)</p> Signup and view all the answers

<p>Cell contents are released due to membrane breakdown (A)</p> Signup and view all the answers

<p>Progression dependent on caspase activity (C)</p> Signup and view all the answers

<p>Find-me signals (D)</p> Signup and view all the answers

<p>It progresses as a form of programmed necrosis (D)</p> Signup and view all the answers

<p>Inflammatory response (A)</p> Signup and view all the answers

<p>They eliminate the debris of dead cells (D)</p> Signup and view all the answers

<p>Mitochondria (A)</p> Signup and view all the answers

The irreversible breakdown of essential cell functions, leading to loss of cell integrity. This includes disruption of ATP production and the ability to maintain a balanced redox state.

A form of programmed cell death that is orderly, controlled, and often needed for normal tissue development and maintenance.

An uncontrolled and often traumatic form of cell death that is initiated by damage to the cell, leading to inflammation.

The process of cell death can be triggered by various stimuli, such as physical damage (burns, irradiation), chemical agents (toxins, lack of nutrients), or internal signals.

The process of cell death can be regulated by various intracellular pathways, including biochemical cascades, signaling molecules, and transcription factors.

The study of cell death is crucial for understanding both normal physiological development and disease processes.

The Nomenclature Committee on Cell Death provides a framework for classifying and interpreting cell death based on morphological, biochemical, and functional characteristics.

Cell death can occur in various ways, including apoptosis, necrosis, and other less common forms. These forms differ in their pathways, triggers, and resulting outcomes.

A type of cell death where the cell self-digests its components through a process called autophagy, leading to the formation of autophagosomes and eventual breakdown by lysosomes.

A cell death modality characterized by the presence of multiple nuclei within a single cell, often occurring after a failed or disrupted cell division.

Apoptosis triggered by the loss of cell-to-cell or cell-to-substrate contact.

Neuron death caused by excessive activation of glutamate receptors, leading to a surge of calcium ions and triggering lethal signaling pathways.

The final stage of epidermal cell differentiation, during which cells become filled with keratin and form a tough, protective layer of the skin.

Apoptosis is a neat, orderly process where the cell shrinks, loses adhesion to neighbors, and forms blebs. Its chromatin breaks down into small fragments, and it's quickly engulfed by phagocytosis.

The release of cytochrome c from the mitochondria is a crucial step in the intrinsic pathway of apoptosis. It triggers a cascade of events leading to cell death.

Caspases are a family of enzymes that break down proteins during apoptosis. They are activated in a cascade, like dominoes falling.

The intrinsic pathway of apoptosis is triggered by internal cellular stresses, like DNA damage, while the extrinsic pathway is initiated by external signals from other cells.

The cell's plasma membrane loses its integrity during apoptosis, allowing vital dyes to enter, marking the cell's death.

The point of no return in cell death is when the cell passes certain thresholds, like massive caspase activation or complete permeabilization of the mitochondrial outer membrane.

ADCD, ICD, LDCD, and MPT are different types of cell death classified based on their molecular mechanisms.

Exposure of phosphatidylserine residues on the cell surface acts as an 'eat me' signal, attracting phagocytes to engulf the dying cell.

The morphology of apoptosis includes cell shrinkage, loss of adhesion, blebbing, chromatin fragmentation, and fast engulfment by phagocytosis.

The cell can reverse the death process until it passes a point-of-no-return, like massive caspase activation or mitochondrial membrane permeabilization.

A programmed form of cell death, a process of cellular self-destruction that is activated when apoptosis is otherwise prevented. It progresses independently of caspase activity.

The process where a cell breaks down into multiple vesicles (apoptotic bodies) that are then engulfed by phagocytes.

Specialized cells that engulf and remove dead or damaged cells and cellular debris.

Signals released by dying cells that attract phagocytes.

Signals released by dying cells that indicate to phagocytes that they should be engulfed.

Elongated membrane protrusions that extend outward from a cell, facilitating the transport of cellular material.

Damage-associated molecular patterns (DAMPs) are molecules released from damaged or dying cells that can activate the immune system and trigger inflammation.

A protein kinase that plays a crucial role in necroptosis. It phosphorylates MLKL, leading to the formation of pores in the plasma membrane.

A family of proteases involved in programmed cell death (apoptosis). They are synthesized as inactive precursors (pro-caspases) and activated through a cascade of events.

Initiator caspases activate downstream effector caspases, ultimately leading to cell death.

Caspases are also known as cysteine-aspartic proteases because they contain a cysteine residue in their active site that cleaves target proteins after an aspartic acid residue.

Examples of pro-apoptotic stimuli include FasL, TNF, Granzyme-B, GRB, DNA damage, Ca2+ channels, and ER stress.

Pro-caspases are inactive precursors. Upon activation, they dimerize or oligomerize, leading to cleavage into smaller subunits. These subunits then associate to form an active heterodimer caspase.

The extrinsic pathway is triggered by external stimuli like FasL, TNF, and TRAIL. These ligands bind to their respective death receptors, initiating a signaling cascade.

The intrinsic pathway is triggered by stressors like DNA damage, hypoxia, or oxidative stress. It involves the release of cytochrome c from mitochondria, leading to the formation of the apoptosome.

The apoptosome is a complex formed by cytochrome c, APAF1, and caspase-9. It activates caspase-9, which in turn activates effector caspases like caspase-3, -6, and -7.

Effector caspases like caspase-3, -6, and -7 are responsible for executing the apoptotic program by cleaving key cellular substrates.

During apoptosis, the cell membrane contracts, forming introflexions. This process is mediated by ROCK1, a kinase that regulates cytoskeletal changes.