Sandbox Reserved 1122: Difference between revisions

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=== Cell cycle control ===

Bcl-2 is able to exert an anti-proliferative activity which is completely independant from its anti-apoptotic activity. In quiescent cells, Bcl-2 is responsible for faster G0/G1 arrest and for slower G0-G1/S transition. Posttranslational phosphorylations are very important for Bcl-2 anti-proliferative activity, for example, phosphorylation at Thr 56 by CDK1 delays G2/M exit. <scene name='71/719863/Scenelucas/2'>BH4</scene> and unstructured loop between <scene name='71/719863/Scenebh3/3'>BH3</scene> and <scene name='71/719863/Scenelucas/2'>BH4</scene> are crucial for this cell cycle control activity. Tyr28 is critical for anti-proliferative activity, a point mutation reduces the ability of Bcl-2 to block the re-entry of quiescent cells. Inhibition of G0-G1/S is a consequence of increased levels of p130 and p27 which are regulated by Bcl-2. Bcl-2 also inhibits Raf-1 which normally activates ERK. ERK then inhibits Rb and this allows cell to pass the restriction point which leads to G1. Bcl-2 anti-proliferatif activity together with prevention of starvation-induced autophagy allow cells to survive in poor conditions. <ref> [http://www.sciencedirect.com/science/article/pii/S0167488903001824 Control of proliferation by Bcl-2 family members] </ref>

Bcl-2 is able to exert an anti-proliferative activity which is completely independant from its anti-apoptotic activity. In quiescent cells, Bcl-2 is responsible for faster G0/G1 arrest and for slower G0-G1/S transition. Posttranslational phosphorylations are very important for Bcl-2 anti-proliferative activity, for example, phosphorylation at Thr 56 by CDK1 delays G2/M exit. <scene name='71/719863/Scenelucas/2'>BH4</scene> and unstructured loop between <scene name='71/719863/Scenebh3/3'>BH3</scene> and <scene name='71/719863/Scenelucas/2'>BH4</scene> are crucial for this cell cycle control activity. <scene name='71/719863/Scenetr28/1'>Tyr28</scene> is critical for anti-proliferative activity, a point mutation reduces the ability of Bcl-2 to block the re-entry of quiescent cells. Inhibition of G0-G1/S is a consequence of increased levels of p130 and p27 which are regulated by Bcl-2. Bcl-2 also inhibits Raf-1 which normally activates ERK. ERK then inhibits Rb and this allows cell to pass the restriction point which leads to G1. Bcl-2 anti-proliferatif activity together with prevention of starvation-induced autophagy allow cells to survive in poor conditions. <ref> [http://www.sciencedirect.com/science/article/pii/S0167488903001824 Control of proliferation by Bcl-2 family members] </ref>

== Diseases ==

Sandbox Reserved 1122: Difference between revisions

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 === Cell cycle control ===
-Bcl-2 is able to exert an anti-proliferative activity which is completely independant from its anti-apoptotic activity. In quiescent cells, Bcl-2 is responsible for faster G0/G1 arrest and for slower G0-G1/S transition. Posttranslational phosphorylations are very important for Bcl-2 anti-proliferative activity, for example, phosphorylation at Thr 56 by CDK1 delays G2/M exit. <scene name='71/719863/Scenelucas/2'>BH4</scene>  and unstructured loop between <scene name='71/719863/Scenebh3/3'>BH3</scene> and <scene name='71/719863/Scenelucas/2'>BH4</scene> are crucial for this cell cycle control activity. Tyr28 is critical for anti-proliferative activity, a point mutation reduces the ability of Bcl-2 to block the re-entry of quiescent cells. Inhibition of G0-G1/S is a consequence of increased levels of p130 and p27 which are regulated by Bcl-2. Bcl-2 also inhibits Raf-1 which normally activates ERK. ERK then inhibits Rb and this allows cell to pass the restriction point which leads to G1. Bcl-2 anti-proliferatif activity together with prevention of starvation-induced autophagy allow cells to survive in poor conditions. <ref> [http://www.sciencedirect.com/science/article/pii/S0167488903001824 Control of proliferation by Bcl-2 family members] </ref>
+Bcl-2 is able to exert an anti-proliferative activity which is completely independant from its anti-apoptotic activity. In quiescent cells, Bcl-2 is responsible for faster G0/G1 arrest and for slower G0-G1/S transition. Posttranslational phosphorylations are very important for Bcl-2 anti-proliferative activity, for example, phosphorylation at Thr 56 by CDK1 delays G2/M exit. <scene name='71/719863/Scenelucas/2'>BH4</scene>  and unstructured loop between <scene name='71/719863/Scenebh3/3'>BH3</scene> and <scene name='71/719863/Scenelucas/2'>BH4</scene> are crucial for this cell cycle control activity. <scene name='71/719863/Scenetr28/1'>Tyr28</scene> is critical for anti-proliferative activity, a point mutation reduces the ability of Bcl-2 to block the re-entry of quiescent cells. Inhibition of G0-G1/S is a consequence of increased levels of p130 and p27 which are regulated by Bcl-2. Bcl-2 also inhibits Raf-1 which normally activates ERK. ERK then inhibits Rb and this allows cell to pass the restriction point which leads to G1. Bcl-2 anti-proliferatif activity together with prevention of starvation-induced autophagy allow cells to survive in poor conditions. <ref> [http://www.sciencedirect.com/science/article/pii/S0167488903001824 Control of proliferation by Bcl-2 family members] </ref>
 == Diseases ==