Intrinsic Pathway
Intrinsic Pathway - Related Videos
01:31
The Intrinsic Apoptotic Pathway
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2023
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
01:20
Extrinsic and Intrinsic Pathways of Hemostasis
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2024
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot. The Extrinsic Pathway The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
02:18
Intrinsically Disordered Proteins
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2020
Intrinsically disordered proteins are a group of proteins that do not fold into specific three-dimensional structures. Their structural flexibility allows them to complement ordered proteins to perform functions that are inaccessible to rigid structures. They are more common in eukaryotes than prokaryotes and may either be exclusively intrinsically disordered or hybrid proteins, consisting of a mix of ordered and disordered regions. The absence of a rigid structure in these proteins can be...
02:18
Intrinsically Disordered Proteins
0 Views •
2023
Intrinsically disordered proteins are a group of proteins that do not fold into specific three-dimensional structures. Their structural flexibility allows them to complement ordered proteins to perform functions that are inaccessible to rigid structures. They are more common in eukaryotes than prokaryotes and may either be exclusively intrinsically disordered or hybrid proteins, consisting of a mix of ordered and disordered regions. The absence of a rigid structure in these proteins can be...
01:27
C4 Pathway and CAM
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2019
Most plants use the C3 pathway for carbon fixation. However, some plants, such as sugar cane, corn, and cacti that grow in hot conditions, use alternative pathways to fix carbon and conserve energy loss due to photorespiration. Photorespiration is the process that occurs when the oxygen concentration is high. Under such conditions, the rubisco enzyme in the Calvin cycle binds O2 instead of CO2, which halts photosynthesis and consumes energy. C4 Pathway The C4 pathway is used by plants such as...
FAQs
The decisive event is the shift in BCL-2 family protein balance at the mitochondrial outer membrane. Internal stress changes this balance, allowing membrane permeabilization and cytochrome c release. That release links an upstream condition, such as DNA damage or growth-factor withdrawal, to apoptosome formation and downstream caspase activation. Thus, the protein balance acts as a control point for cellular elimination.
Mitochondrial outer-membrane permeabilization connects internal stress to the cell-death signaling machinery. Before this event, signals such as oxidative stress or DNA damage remain upstream cellular disturbances. After permeabilization, cytochrome c can leave the mitochondrion and support apoptosome formation. This transition therefore converts diverse intracellular problems into a coordinated apoptotic response.
The apoptosome serves as the critical intermediate formed after cytochrome c is released from mitochondria. Its formation enables activation of caspase-9, placing this initiator caspase between the mitochondrial response and the execution phase. This organization gives the pathway a defined sequence, so an internal stress signal can be transmitted efficiently toward programmed cellular removal.
Caspase-9 functions as the initiator activated through apoptosome formation, whereas executioner caspases act downstream of that step. This ordering separates signal transmission from the final implementation of apoptosis. Interpreting these positions helps researchers determine whether a cellular disturbance has reached the mitochondrial signaling stage or progressed into the broader execution phase.
A useful sequence begins with internal stress, including DNA damage, oxidative stress, or growth-factor withdrawal. The stress alters BCL-2 family protein balance, followed by mitochondrial outer-membrane permeabilization and cytochrome c release. Cytochrome c then supports apoptosome formation, caspase-9 activation, and stimulation of executioner caspases. This sequence provides a framework for analyzing pathway progression.
Its normal biological roles include shaping tissues, removing damaged cells, and maintaining cellular homeostasis. The same pathway becomes medically important when its regulation is disturbed. The overview identifies links between dysregulation and cancer, neurodegeneration, and immune disorders, so investigators study its components both to understand disease mechanisms and to explore potential therapeutic targets.
Analysis of the pathway can connect an intracellular stress condition with specific signaling outcomes, including cytochrome c release, apoptosome formation, caspase-9 activation, and executioner-caspase activity. At the biological level, these events help explain how damaged cells are removed and tissues are shaped. At the disease level, altered regulation may provide context for cancer, neurodegeneration, or immune disorders.