APOPTOSIS VA INTRINSECA Y EXTRINSECA PDF

En las celulas mamiferas, la apoptosis es mediada por dos vias: una ruta extrinseca de receptor de muerte y una ruta intrinseca mitocondrial. La via extrinseca. Explicar la conformación de la pleura indicando su función y drenaje. BIBLIOGRAFÍA: . Via intrinseca y extrinseca de la apoptosis. Enviado por. Apoptosis, mecanismo de acción. Jorge Pérez Machado,1 Alejandro Eliécer Lie Concepción2. Diana Valentina Moreno. Juan Sebastian Hernandez. MEDICINA .

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For more than a decade, it has been apparent that apoptosis and other aopptosis of cell death are often controlled at one or more crucial steps involving the mitochondria.

The new study shows that one type, MMP-3, causes normal cells to express a protein, Rac1b, that has previously been found only in cancers. Me gustaria que todos lo leyeran, sobre todo por nuestro resultados de smac y lo que planeo hacer extriseca continuacion.

Laboratorio Biologia Molecular: July

Interesante por el hecho de que la modificacion externa, mediada por el estroma, puede incidir en la progresion del cancer. Este es el corte de p65 por caspasa 3. The emerging, if preliminary, perspective these new studies provide may represent either a refinement of our views of how cells die or, perhaps, the beginnings of what amounts to a reformulation of our ideas. Sin embargo no existian las contrapartes de las caspasas de la via extrinseca.

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Esto coincide con papers previos en los que los niveles relativos de IKK1 y 2 determinaban la activacion de NFkB y un articulo previo de IKK1 como inhibidor en macrofagos. Bissell, appears in the 7 July issue of Nature.

Este es nuestro blog. Tuesday, July 26, Revision de apoptosis intrinseca. Moreover, inhibition of caspases can have cytoprotective effects. Littlepage, Hong Liu, Celeste M. However, in tumors and tumor cell lines, they are overexpressed, and their silencing leads to restoration of efficient apoptosis via enhanced activation of DED caspases.

Cubre un vacio en el papel de la estromelisina en el cancer de mama. Ya tenemos primers de CARP1, que funcionan bien. Este articulo es interesante. Vilma Maldonado Lagunas Dr. Rac1b stimulates the production of highly reactive oxygen molecules, which promote cancer in two ways — by leading to tissue disorganization and by damaging genomic DNA.

Kroemer el de AIF Caspase activation has been frequently viewed appptosis synonymous with apoptotic cell death; however, caspases can also contribute to processes that do not culminate in cell demise. Changes in the cell skeleton induced by Rac1b trigger the formation of extremely reactive molecules known as reactive oxygen species, or ROS. En el caso del TIMP seria interesante analizar los niveles de ambas.

Here, we explore the contribution of caspases to cell death, either as upstream signals or as downstream effectors contributing to apoptotic morphology, as well as alternative strategies for cell death inhibition.

In addition, the induction of c-IAP2 transcription required nuclear factor- B activity. Furthermore, CARPs are rapidly cleaved during apoptosis.

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Papilomavirus induce la expresion de IAP Suppression of caspase and associated RING proteins results in sensitization to death ligands and inhibition of tumor cell growth. In a number of different models, caspase inhibition does not maintain cellular viability and instead shifts the morphology of death from apoptosis to nonapoptotic spoptosis.

Una nueva revision publicada en Nature Medicine 11- de G. Las CARP habian sido identificadas antes como RHF1, un gen que estaba sobreexpresado en cancer de esofago, pero para el que no tenian funcion esto no viene en el articulo.

Muerte celular programada en protozoarios: el caso de Giardia intestinalis.

Asimismo pueden utilizarlo para intriseca personales dentro del grupo, incluyendo fotos. Revision de checkpoint mitotico. Este es un articulo importante. Wednesday, July 27, Elemento faltante.

Friday, July 22, Caspase-independent cell death. Algunos pensaban que intrinweca modulacion era mediada solo por FLIP, una proteina parecida a c. In turn, the increased amount of ROS activates key genes that control the epithelial-mesenchymal transition — the first slippage in an avalanche of tissue disorganization.

H findings, including an elegant investigation in a recent issue of Cell Hao et al. E6 from HPV16 and 18 played a major role in the activation. Pueden realizar todo tipo de comentarios, avisos, quejas, etc.