Abstract:
:In Galpha(z)-deficient mice, survival of sympathetic neurons is significantly attenuated in the presence of pertussis toxin (PTX). This suggests that G(i/o) proteins may have distinct roles in neuronal survival. Here, we investigated the possible involvement of G(i/o) proteins in nerve growth factor (NGF)-induced pro-survival phosphatidylinositol-3-kinase (PI3K)/Akt signaling in rat pheochromocytoma PC12 cells. Treatment of PC12 cells with NGF increased the Akt phosphorylation level in a time- and dose-dependent manner. The NGF-dependent Akt activation was partially attenuated by PTX or overexpression of regulators of G protein signaling Z1 (RGSZ1) and Galpha-interacting protein (GAIP)), indicating the participation of G(i/o) proteins. In contrast, epidermal growth factor (EGF)-mediated Akt phosphorylation was unaffected by PTX or RGSZ1 and GAIP. Expression of PTX-resistant mutants of Galpha(i1), Galpha(i3), Galpha(oA), and Galpha(oB), but not Galpha(i2), abolished the inhibitory effect of PTX on NGF-induced Akt activation. The use of transducin as a Gbetagamma scavenger further revealed that Gbetagamma subunits rather than Galpha(i/o) acted as the signal transducer. The activation profiles of Akt-regulated downstream effectors such as Bad, IKK, and nuclear factor-kappaB (NFkappaB) were also examined. NGF-stimulated phosphorylation of Bad and IKK and transcriptional activity of NFkappaB were indeed sensitive to treatments with PTX. This is the first study that demonstrates the involvement of G(i/o) proteins in NGF-induced Akt signaling.
journal_name
Cell Signaljournal_title
Cellular signallingauthors
Wu EH,Wong YHdoi
10.1016/j.cellsig.2004.11.008subject
Has Abstractpub_date
2005-07-01 00:00:00pages
881-90issue
7eissn
0898-6568issn
1873-3913pii
S0898-6568(04)00247-5journal_volume
17pub_type
杂志文章abstract::Lysophosphatidic acid (LPA) plays a critical role in the pathophysiology of ovarian cancers. Previous studies have shown that LPA stimulates the proliferation of ovarian cancer cells via Gα12. The present study utilizing Protein/DNA array analyses of LPA-stimulated HeyA8 cells in which the expression of Gα12 was silen...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2013.08.012
更新日期:2014-01-01 00:00:00
abstract::Signal transducer and activator of transcription 1 (STAT1) is an important mediator for cytokine signal transduction, particularly IFN-γ. Following IFN-γ stimulation, STAT1 is activated through tyrosine phosphorylation. Little is known about the function and regulation of STAT1 dephosphorylation after activation. We s...
journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2011.04.003
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2007.12.007
更新日期:2008-04-01 00:00:00
abstract::Aurora B kinase forms the enzymatic core of the Chromosomal Passenger Complex (CPC) and is a master regulator of mitosis. Understanding the regulation of Aurora B is critical to illuminate its role in mitosis. INCENP, Survivin and Borealin have all been known to promote Aurora B activation. In this study, we have iden...
journal_title:Cellular signalling
pub_type: 杂志文章
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更新日期:2012-08-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2014.05.010
更新日期:2014-09-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2008.12.005
更新日期:2009-04-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
doi:10.1016/s0898-6568(99)00086-8
更新日期:2000-03-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/s0898-6568(99)00048-0
更新日期:1999-10-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2006.10.008
更新日期:2007-04-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/s0898-6568(03)00010-x
更新日期:2003-07-01 00:00:00
abstract::Bladder cancer (BC) is one of the most common tumours of the urinary system and is also known as a highly malignant tumour. In addition to conventional diagnosis and treatment methods, recent research has focused on studying the molecular mechanisms related to BC, in the hope that new, less toxic and effective targete...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2020.109886
更新日期:2021-03-01 00:00:00
abstract::Signal transducer and activator of transcription 6 (Stat6) is critical in Th2 polarization of immune cells and active Stat6 activity has been suggested in anti-tumor immunity in animal models. The present study aims at investigating the impact of natural Stat6 activity on tumor microenvironment in human colorectal can...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2011.11.005
更新日期:2012-03-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2016.06.010
更新日期:2016-09-01 00:00:00
abstract:BACKGROUND:Our previous study showed that human omental adipose-derived stem cells (ADSCs) promote ovarian cancer growth and metastasis. In this study, the role of autophagy in the ovarian cancer-promoting effects of omental ADSCs was further determined. METHODS:The growth and invasion of ovarian cancer cells were det...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2020.109549
更新日期:2020-05-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2007.02.009
更新日期:2007-07-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2004.01.006
更新日期:2004-08-01 00:00:00
abstract::This article has been withdrawn at the request of the Editors. The Publisher apologises for any inconvenience that this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy. ...
journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2008.05.011
更新日期:2009-03-27 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/0898-6568(90)90032-6
更新日期:1990-01-01 00:00:00
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journal_title:Cellular signalling
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doi:10.1016/j.cellsig.2014.11.023
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2008.10.021
更新日期:2009-02-01 00:00:00
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doi:10.1016/s0898-6568(02)00122-5
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2010.09.015
更新日期:2011-01-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章,评审
doi:10.1016/s0898-6568(01)00281-9
更新日期:2002-07-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/s0898-6568(03)00090-1
更新日期:2004-01-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/s0898-6568(96)00112-x
更新日期:1996-12-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2011.03.016
更新日期:2011-08-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/s0898-6568(00)00147-9
更新日期:2001-02-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2013.09.004
更新日期:2013-12-01 00:00:00
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journal_title:Cellular signalling
pub_type: 杂志文章
doi:10.1016/j.cellsig.2008.06.013
更新日期:2008-10-01 00:00:00