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Updated: May 7, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles
08:35

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Published on: October 5, 2012

ERのストレスは,BH3のみのタンパク質Bimを活性化することで,アポトーシスを引き起こす

Hamsa Puthalakath1, Lorraine A O'Reilly, Priscilla Gunn

  • 1The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia.

Cell
|July 3, 2007
PubMed
まとめ

エンドプラズマ網膜 (ER) のストレスは,Bimタンパク質を活性化することによって細胞死を誘発する. デフォスフォリレーションとトランスクリプション誘導を含む新しい経路は,ERのストレス誘発のアポトーシスメカニズムを明らかにします.

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Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

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Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

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