PML Regulates Apoptosis at Endoplasmic Reticulum by Modulating Calcium Release | Zendy

Carlotta Giorgi | Zendy; Keisuke Ito | Zendy; HuiKuan Lin | Zendy; Clara Santangelo | Zendy; Mariusz R. Wiȩckowski | Zendy; Magdalena Lebiedzińska | Zendy; Angela Boi | Zendy; Massimo Bonora | Zendy; Jerzy Duszyński | Zendy; Rosa Bernardi | Zendy; Rosario Rizzuto | Zendy; Carlo Tacchetti | Zendy; Paolo Pinton | Zendy; Pier Paolo Pandolfi | Zendy

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PML Regulates Apoptosis at Endoplasmic Reticulum by Modulating Calcium Release

Author(s) -

Carlotta Giorgi,

Keisuke Ito,

HuiKuan Lin,

Clara Santangelo,

Mariusz R. Wiȩckowski,

Magdalena Lebiedzińska,

Angela Boi,

Massimo Bonora,

Jerzy Duszyński,

Rosa Bernardi,

Rosario Rizzuto,

Carlo Tacchetti,

Paolo Pinton,

Pier Paolo Pandolfi

Publication year - 2010

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.1189157

Subject(s) - endoplasmic reticulum , microbiology and biotechnology , phosphorylation , protein kinase b , inositol , protein phosphatase 2 , apoptosis , calcium signaling , mitochondrion , phosphatase , signal transduction , biology , kinase , chemistry , receptor , biochemistry

Promoting Apoptosis During acute disease, the promyelocytic leukemia (PML) protein becomes fused to another protein as a result of a chromosomal translocation. This protein appears to have multiple and varied functions, including the ability to form distinctive complexes in the nucleus that suppress tumorigenesis and promote apoptotic cell death.Giorgiet al. (p.1247 , published online 28 October; see the Perspective byCuljkovic-Kraljacic and Borden ) have proposed a mechanism by which PML influences the cellular signals that promote apoptosis. The protein was localized at sites of contact between the endoplasmic reticulum and mitochondria, where it associated with a calcium channel, a protein kinase, and a protein phosphatase, to regulate calcium mobilization into the mitochondrion, which then triggers the cell death program.

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