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. Author manuscript; available in PMC: 2010 Feb 16.
Published in final edited form as: Curr Mol Med. 2009 Jun;9(5):527. doi: 10.2174/156652409788488784

Table 3.

Cell Culture and Animal Studies Examining the Role of Gαq/11 in Apoptosis

No. G Protein Model System Cell Type Apoptotic Stimulus Phenotype Pathway Comments Ref.
1 Gαq/11 Endogenous
Carbachol activation (M3)
Chinese Hamster Ovary (CHO cells) etoposide Inhibited PLC-independent
Increased Bcl-2 expression
Activation of ERK1/2, JNK
M3 receptor truncation caused loss of anti-apoptotic activity [93,94]
2 Gαq/11 Endogenous
Carbachol activation (M3)
CHO Cells NONE Stimulated Downstream Rac-1 activation Cells overexpressing Rac1 [95]
3 Gαq/11 Endogenous
Adenosine activation (P2Y1)
Human Astrocytoma (1231N1 cells) Serum starvation Stimulated PKC activation
PI3K, ERK1/2 activation
[96]
4 Gα11 Overexpression HeLa Cells NONE Stimulated Activation of ROCK Blocked by overexpression of Bcl-2 [97,98]
5 Gα11 Endogenous
M1 activation
HeLa Cells NONE Stimulated Activation of ROCK Blocked by overexpression of Bcl-2 [97,98]
6 R183C-Gαq Overexpression COS-7 Cells, CHO Cells NONE Stimulated PKC activation Blocked by overexpression of Bcl-2 [99]
7 Gαq Overexpression Rat Ventricular Myocytes Low-glucose Inhibited Activation of PI3K, EGFR, and Src kinases [100]
8 Gαq Endogenous
P. multocida toxin activation
Rat Ventricular Myocytes H2O2 Stimulated Activation of PLC
Inhibition of Akt
[101]
9 Q209L-Gαq Overexpression Rat Ventricular Myocytes NONE Stimulated Depletion of PIP2
Reduced Akt phosphorylation
Inhibited by overexpression of myristoylated Akt [102-104]