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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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...
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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 cells.
The Intrinsic Apoptotic Pathway01:31

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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...
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
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Evaluation of Caspase Activation to Assess Innate Immune Cell Death
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El TNF-alfa induce dos vías distintas de activación de la caspasa-8

Lai Wang1, Fenghe Du, Xiaodong Wang

  • 1Howard Hughes Medical Institute and Department of Biochemistry, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.

Cell
|May 20, 2008
PubMed
Resumen

El factor de necrosis tumoral alfa (TNF-alfa) desencadena la apoptosis a través de dos vías distintas. Estas vías implican ya sea cicloheximida o Smac mimético, que regula diferencialmente la activación de la caspasa-8 a través de cIAP1/2 y c-FLIP.

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Área de la Ciencia:

  • Biología celular Biología celular.
  • Los mecanismos moleculares de la muerte celular
  • Inmunología Inmunología.

Sus antecedentes:

  • El factor de necrosis tumoral alfa (TNF-alfa) es una citocina clave en las respuestas inflamatorias.
  • El cambio de la inflamación a la apoptosis es un proceso celular crítico.
  • La caspasa-8 es un mediador central en la apoptosis inducida por el TNF-alfa.

Objetivo del estudio:

  • Para dilucidar los distintos mecanismos moleculares por los cuales el TNF-alfa induce la apoptosis.
  • Para investigar las funciones de la cicloheximida y Smac mimetic en la regulación de la activación de la caspasa-8.
  • Diferenciar las funciones reguladoras de c-FLIP y cIAP1/2 en la señalización del TNF-alfa.

Principales métodos:

  • Utilizó cicloheximida, un inhibidor de la síntesis de proteínas.
  • Empleó Smac mimético, una pequeña molécula que imita a Smac/Diablo.
  • Investigó la participación de la caspasa-8, el c-FLIP, el cIAP1/2, el RIPK1 y el CYLD.

Principales resultados:

  • La cicloheximida promueve la activación de la caspasa-8 mediante la degradación de la c-FLIP.
  • Smac mimetic desencadena la apoptosis mediante la degradación de cIAP1/2, liberando RIPK1 para formar un complejo de activación de la caspasa-8.
  • RIPK1 es esencial para la activación de la caspasa-8 inducida por Smac mimetic pero no inducida por cicloheximida.
  • La activación de la caspasa-8 inducida por Smac mimetic es independiente de la c-FLIP endógena.

Conclusiones:

  • El TNF-alfa induce la apoptosis a través de al menos dos vías distintas de activación de la caspasa-8.
  • Estas vías están reguladas diferencialmente por los inhibidores celulares cIAP1/2 y c-FLIP.
  • Comprender estas vías ofrece información sobre estrategias terapéuticas específicas para enfermedades que involucran la señalización del TNF-alfa.