APOPTOSIS VA INTRINSECA Y EXTRINSECA PDF

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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In addition, the induction of c-IAP2 transcription required nuclear factor- B activity. Friday, July 22, Caspase-independent cell death. Kroemer el de AIF Caspase activation has been frequently viewed as synonymous with apoptotic cell death; however, caspases can also contribute to processes that do not culminate in cell demise.

APOPTOSIS by Alejandra Chávez on Prezi

E6 from HPV16 and 18 played a major role in the activation. Moreover, inhibition of caspases can have cytoprotective effects. Furthermore, CARPs are rapidly cleaved during apoptosis.

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. Algunos pensaban que la modulacion era mediada solo por FLIP, una proteina parecida a c. Tuesday, July 26, Revision de apoptosis intrinseca. Este es nuestro blog. 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.

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.

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Ya tenemos primers de CARP1, que funcionan bien. Here, we explore the contribution of caspases to cell death, either as upstream signals or as downstream effectors contributing to apoptotic morphology, as etxrinseca as alternative strategies for cell death inhibition.

In a number of different models, caspase inhibition does not maintain cellular viability and instead shifts the apooptosis of death from apoptosis to nonapoptotic pathways. Cubre un vacio en el papel de la estromelisina en el cancer de mama. Papilomavirus induce la expresion de IAP Vilma Maldonado Lagunas Dr. 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.

Asimismo pueden utilizarlo para actividades personales dentro del grupo, incluyendo fotos. Long-term inhibition of CARP expression results in suppression of cancer cell growth, highlighting their importance in tumor cell survival.

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

For more than a decade, it has been apparent that apoptosis and other forms of cell death are often controlled at one or more crucial steps involving the mitochondria. Recent findings, including an elegant investigation in a recent issue of Cell Hao et al.

Este es el corte de p65 por caspasa 3. Wednesday, July 27, Elemento faltante. Suppression of caspase and associated RING proteins results in sensitization u death ligands and inhibition of tumor cell growth. Sin embargo no existian las contrapartes de las caspasas de la via extrinseca. Bissell, appears in the 7 July issue of Nature. Una nueva revision publicada en Nature Medicine 11- de G.

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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. Podria ser un marcador? Changes in the cell skeleton induced by Rac1b trigger the formation of extremely reactive molecules known as reactive oxygen species, or ROS. Fata, Devin Leake, Elizabeth L. Este es un articulo importante. Esto coincide con papers previos en los que los niveles relativos de IKK1 y 2 extrinsecaa la activacion de NFkB y un articulo previo de IKK1 como inhibidor en macrofagos.

Me gustaria que todos lo leyeran, sobre extrinsecw por nuestro resultados de smac y lo que planeo hacer fa continuacion. En el caso del TIMP seria interesante analizar los niveles de ambas. Interesante por el hecho de que la modificacion externa, mediada por el estroma, puede incidir en la progresion del cancer.

Este articulo es interesante. Revision de checkpoint mitotico. 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.

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