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10.1161/CIRCRESAHA.116.305421 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.116.305421 C4443748!4443748!25999420     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circ+Res 2015 ; 116 (11): 1800-9 Nephropedia Template TP {{tp|p=25999420|t=2015. Regulated necrotic cell death: The passive aggressive side of Bax and Bak |pdf=|usr=}}{{25999420}} gab.com Text Regulated necrotic cell death: The passive aggressive side of Bax and Bak JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25999420 #FOAvip While the molecular effectors of apoptotic cell death have been largely annotated over the past 30 years, leading to a strong biologic understanding of this process and its importance in cell biology, cell death through necrosis has only recently been accepted as a similarly regulated process with definable molecular effectors. The mitochondria are important and central mediators of both apoptosis and regulated necrosis. In apoptosis the Bcl-2 family members Bax and Bak undergo oligomerization in the outer mitochondrial membrane resulting in the release of apoptosis inducing substrates and the activation of caspases and nucleases. In contrast, during necrosis the mitochondria become dysfunctional and maladaptive in conjunction with reactive oxygen species production and the loss of ATP production, in part through opening of the mitochondrial permeability transition pore. While regulated necrosis is caspase independent, recent evidence has shown that it still requires the apoptotic regulators Bax and Bak, which can regulate the permeability characteristics of the outer mitochondrial membrane in their non-oligomerized state. Here we review the non-apoptotic side of Bcl-2 family, specifically the role of Bax and Bak in regulated necrotic cell death. We will also discuss how these Bcl-2 family member effectors could be part of a larger integrated network that ultimately decides the fate of a given cell somewhere within a molecular continuum between apoptosis and regulated necrosis. Twit Text FOAVip Regulated necrotic cell death: The passive aggressive side of Bax and Bak ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25999420 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25999420 #FOAvip English Wikipedia <ref>{{Cite pmid|25999420}}</ref> Regulated necrotic cell death: The passive aggressive side of Bax and Bak #MMPMID25999420 Karch J; Molkentin JD Circ Res 2015[May]; 116 (11): 1800-9 PMID25999420show ga While the molecular effectors of apoptotic cell death have been largely annotated over the past 30 years, leading to a strong biologic understanding of this process and its importance in cell biology, cell death through necrosis has only recently been accepted as a similarly regulated process with definable molecular effectors. The mitochondria are important and central mediators of both apoptosis and regulated necrosis. In apoptosis the Bcl-2 family members Bax and Bak undergo oligomerization in the outer mitochondrial membrane resulting in the release of apoptosis inducing substrates and the activation of caspases and nucleases. In contrast, during necrosis the mitochondria become dysfunctional and maladaptive in conjunction with reactive oxygen species production and the loss of ATP production, in part through opening of the mitochondrial permeability transition pore. While regulated necrosis is caspase independent, recent evidence has shown that it still requires the apoptotic regulators Bax and Bak, which can regulate the permeability characteristics of the outer mitochondrial membrane in their non-oligomerized state. Here we review the non-apoptotic side of Bcl-2 family, specifically the role of Bax and Bak in regulated necrotic cell death. We will also discuss how these Bcl-2 family member effectors could be part of a larger integrated network that ultimately decides the fate of a given cell somewhere within a molecular continuum between apoptosis and regulated necrosis. äRegulated necrotic cell death: The passive aggressive side of Bax and (epmc).pdf DeepDyve Pubget Overpricing