Literature DB >> 9529608

The Bcl-2 family and cell death regulation.

K Newton1, A Strasser.   

Abstract

Members of the Bcl-2 protein family fall into two categories on the basis of their ability to either promote or suppress apoptosis. Recent findings have linked these proteins to caspases, the cysteine proteases that effect the collapse of the cell via binding to CED-4. It seems that Bcl-2 proteins influence cell survival by regulating the activation of key caspases.

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Year:  1998        PMID： 9529608     DOI： 10.1016/s0959-437x(98)80064-6

Source DB:  PubMed          Journal:  Curr Opin Genet Dev        ISSN： 0959-437X            Impact factor:   5.578


  12 in total

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4.  Pharmacological inhibition of protein kinase C activity could induce apoptosis in gastric cancer cells by differential regulation of apoptosis-related genes.

Authors:  G H Zhu; B C Wong; M C Eggo; S T Yuen; K C Lai; S K Lam
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5.  Nerve growth factor signaling through p75 induces apoptosis in Schwann cells via a Bcl-2-independent pathway.

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6.  IL-7Ralpha and E47: independent pathways required for development of multipotent lymphoid progenitors.

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7.  Transforming growth factor beta (TGFbeta) mediates Schwann cell death in vitro and in vivo: examination of c-Jun activation, interactions with survival signals, and the relationship of TGFbeta-mediated death to Schwann cell differentiation.

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Review 8.  Oxidative stress by targeted agents promotes cytotoxicity in hematologic malignancies.

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9.  Regulated overexpression of the survival factor bcl-2 in CHO cells increases viable cell density in batch culture and decreases DNA release in extended fixed-bed cultivation.

Authors:  M Fussenegger; D Fassnacht; R Schwartz; J A Zanghi; M Graf; J E Bailey; R Pörtner
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10.  Aquatic birnavirus-induced ER stress-mediated death signaling contribute to downregulation of Bcl-2 family proteins in salmon embryo cells.

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