Bid, una proteína que interactúa con Bcl2, media la liberación del citocromo c de las mitocondrias en respuesta a la activación de los receptores de muerte celular en la superficie celular
Video Experimental Relacionado
Updated: May 5, 2026
07:42
Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
Published on: June 29, 2011
16.9K
1Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, 75235, USA.
Cell
|September 4, 1998
Resumen
Este estudio identifica Bid como una proteína clave que transmite señales apoptóticas. La escisión de Caspase-8 de Bid desencadena la liberación del citocromo c de las mitocondrias, iniciando la muerte celular programada.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- Los receptores de muerte de la superficie celular inician la apoptosis.
- La caspasa-8 es una caspasa apical activada por estos receptores.
- La permeabilización de la membrana externa mitocondrial (MOMP) es un paso crítico en la apoptosis.
Objetivo del estudio:
- Para identificar la proteína citosólica mediadora de la liberación del citocromo c.
- Para aclarar el papel de Bid en la vía apoptótica.
- Para entender el mecanismo del MOMP inducido por la oferta.
Principales métodos:
- Purificación de proteínas a partir de extractos de células.
- Las huellas dactilares de masa de péptidos para la identificación de proteínas.
- Pruebas de inmunodepleción.
- Análisis de la escisión y translocación de las ofertas.
- Ensayos funcionales para la liberación del citocromo c.
Principales resultados:
- Una proteína citosólica que induce la liberación del citocromo c fue purificada e identificada como Bid.
- Caspase-8 divide Bid, y el fragmento COOH-terminal se transloca a las mitocondrias.
- Bid desencadena la liberación del citocromo c, un proceso antagonizado por Bcl2.
- Una mutación en el dominio BH3 de Bid redujo su actividad.
Conclusiones:
- Bid actúa como un intermediario crucial, transmitiendo señales apoptóticas de los receptores de muerte a las mitocondrias.
- La liberación del citocromo c inducida por la oferta es un evento clave en la vía apoptótica intrínseca.
- La función de Bid está regulada por la escisión de la caspasa-8 y la interacción con Bcl2.
Videos de Conceptos Relacionados
01:24Caspases
8.7K
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
8.7K
01:17The Extrinsic Apoptotic Pathway
6.2K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.2K
01:31The Intrinsic Apoptotic Pathway
6.2K
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...
6.2K
01:18Autophagic Cell Death
3.3K
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
3.3K
01:11Cellular Injury IlI: Cellular Death
93
Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
93
01:22Cellular Injury V: Apoptosis and Autophagy
121
Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
121