Cellular Bioenergetics and Homeostasis

The maintenance of stable conditions in cells for optimal function, growth, and survival.

Maintaining cellular homeostasis prevents stress, dysfunction, and diseases, ensuring cell health.

A cellular process that degrades and recycles components, aiding in homeostasis.

A metabolic pathway in mitochondria that produces ATP using an electron transport chain.

The primary energy carrier in cells, powering cellular functions.

A series of protein complexes that facilitate electron transfer to produce ATP.

A difference in proton concentration across the mitochondrial membrane that helps synthesize ATP.

High-energy molecules that donate electrons to the electron transport chain during metabolism.

A cellular process parallel to ubiquitination, modifying proteins with SUMO.

A small ubiquitin-like modifier that tags proteins for modification.

The SUMO activating enzyme that initiates the sumoylation process using ATP.

The conjugating enzyme (e.g., UBC9) that receives activated SUMO for transfer to targets.

An enzyme that facilitates the attachment of SUMO to target proteins.

The process of removing SUMO from proteins, reversing sumoylation.

The abnormal accumulation of proteins, like tau, leading to disease.

A protein that, when sumoylated abnormally, contributes to Alzheimer's disease progression.

A critical process impacted by sumoylation, influencing cell division and proliferation.

Sumoylation modifies proteins critical for DNA repair, apoptosis, and cell cycle, affecting cancer development.

An enzyme that synthesizes ATP from ADP and Pi using energy from proton flow.

Molecular oxygen (O2) that accepts electrons in the electron transport chain.

A metabolic pathway that generates ATP using energy from electron transport and oxygen.

Neuromuscular diseases caused by mitochondrial dysfunction, leading to energy deficiency.

Chemically reactive molecules containing oxygen that can damage cellular components.

Mechanisms that identify and degrade malfunctioning cellular components.

Processes ensuring damaged proteins and organelles are removed to prevent toxicity.

The process where cells reuse valuable molecules from degraded components.

A condition resulting from inadequate ATP production, impairing cellular functions.

A protein released from mitochondria that activates apoptosis signaling by forming the apoptosome.

A pro-apoptotic molecule that promotes the release of CytoC from mitochondria, altering membrane permeability.

A process where the mitochondrial membrane becomes permeable, leading to CytoC release and apoptosis.

A protein that binds to CytoC to form the apoptosome, activating procaspase 9 in the apoptosis pathway.

An effector caspase activated by the apoptosome, leading to downstream caspase activation and cell death.

Anti-apoptotic proteins that inhibit CytoC release, promoting cell survival by preventing apoptosis.

An oncogene that stimulates cell growth and metabolism but can induce apoptosis when CytoC is released.

A serine protease that targets nuclear proteins like linker histone H1.

Immune cells that destroy infected cells and tumors via granule exocytosis.

A type of immune cell that targets and kills infected or cancerous cells.

Mechanism used by CTLs and NK cells to release perforin and granzymes.

A serine protease that induces apoptosis through caspase-dependent mechanisms.

The process by which granzyme B activates caspases to execute apoptosis.

A pro-apoptotic protein cleaved by granzyme B that disrupts mitochondria.

A process triggered by truncated BID, leading to further activation of caspases.

The breaking down of DNA, a key event in apoptosis, facilitated by granzyme B.