| Calcium signaling in apoptotic mammalian cells | |
Abstract/OtherAbstract
:
|
Thesis (Ph.D.)--Hong Kong University of Science and Technology, 2008, xx, 169 leaves : ill. (some col.) ; 30 cm, HKUST Call Number: Thesis BIOL 2008 Lao, The calcium ion (Ca2+), as an important second messenger, is known to be involved in many cellular functions. The present study is aimed at investigating the roles of Ca2+ signaling in regulating apoptosis of mammalian cells. We tried to answer the following questions: (1) Is the mitochondrial Ca2+ signal involved in the early stage to drive the progression of apoptosis? (2) What are the characteristics and transportation mechanisms of the mitochondrial Ca2+ signal in apoptosis? (3) What are the mechanisms by which the Bcl-2 family proteins such as Bcl-2 and Bax regulate the Ca2+ mobilization from endoplasmic reticulum (ER) to cytosol and mitochondria during apoptosis? (4) Are there any other regulators such as Bcl-2 family proteins binding partners affecting the Ca2+ signals? Using single living cell Ca2+ imaging techniques, we found that mitochondrial Ca2+ signal plays a positive role in the early stage of UV- or TNFα- induced apoptosis in HeLa cells. The transient mitochondrial Ca2+ spikes are synchronous with the cytosolic Ca2+ changes. Our results suggested that the Ca2+ release from ER plays an important role on regulating the apoptotic process since the cytosolic Ca2+ elevation during ATP treatment and TNFα-induced apoptosis are highly correlated. We then investigated the mechanisms by which Bcl-2 family proteins affect the IP3 dependent Ca2+ mobilization. We found that pro-apoptotic protein Bax can counteract with anti-apoptotic Bcl-2 to facilitate the ER Ca2+ release by interacting with IP3 receptor. Our results suggested that Bax could sensitize the IP3 receptor, while Bcl-2 could inhibit IP3 receptor during apoptosis. Finally, we examined the effect of other Bcl-2 family proteins and their binding partners on Ca2+ signaling. Our results indicated that the Bcl-2 family proteins may regulate the apoptotic process through modulating the Ca2+ mobilization from ER to cytosol and mitochondria. |
Authors
:
|
Lao, Yuanzhi |
Related Documents
:
|
8202864 - Lsd1 complex controls cell type terminal differentiation during mammalian organogenesis 9496874 - Inhibition of interleukin 1β-converting enzyme-mediated apoptosis of mammalian cells b... 9637764 - Whole-cell kinetics of trichloroethylene degradation by phenol hydroxylase in a ralston... 10025424 - Effects of lead on the lipid compusition of micrococcus luteus cells |
Contributors
:
|
- |
Publication Detail
:
|
Publisher : - Type : Thesis Format : 339 bytes, text/html |
Date Detail
:
|
2009-02-16, 2009-02-16, 2008 |
Subject
:
|
Apoptosis, Calcium channels, Cellular signal transduction |
Coverage
:
|
- |
Relation
:
|
- |
Source
:
|
- |
Copyright Information
:
|
- |
Other Details
:
|
Languages : en_US |
Export Citation
:
|
APA/MLA Format Download EndNote Download BibTex |
Previous Document: The Hydrology and Biology of Cypress Creek (Hays County), a Subtropical Karstic Stream in South Cent...
Next Document: MAB-30 functions to maintain cell identity of sensory ray in C. elegans