Activation of STAT3 by Gαs Distinctively Requires Protein Kinase A, JNK, and Phosphatidylinositol 3-Kinase

Liu, Andrew M.F.; Lo, Rico K.H.; Wong, Cecilia S.S.; Morris, Christina; Wise, Helen; Wong, Yung Hou

doi:10.1074/jbc.m605288200

Cited by 48 publications

(38 citation statements)

References 70 publications

(72 reference statements)

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“…STAT3 is typically activated through phosphorylation at tyrosine 705 by intrinsic tyrosine kinase activity of activated growth factor receptors or cytokine receptor-associated Janus kinase, but GasPCR/adenylyl cyclase/cAMP/PKA signaling can also activate STAT3. [124][125][126][127] For example, G-protein a-subunit-activating mutations in sporadic benign and malignant liver tumors are characterized by an inflammatory phenotype associated with STAT3 activation. 126 The…”

Section: Interstitial Inflammation and Fibrosismentioning

confidence: 99%

Strategies Targeting cAMP Signaling in the Treatment of Polycystic Kidney Disease

Torres

Harris

2014

Journal of the American Society of Nephrology

243

218

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Polycystic kidney disease (PKD) is a leading cause of ESRD worldwide. In PKD, excessive cell proliferation and fluid secretion, pathogenic interactions of mutated epithelial cells with an abnormal extracellular matrix and alternatively activated interstitial macrophages, and the disruption of mechanisms controlling tubular diameter contribute to cyst formation. Studies with animal models suggest that several diverse pathophysiologic mechanisms, including dysregulation of intracellular calcium levels and cAMP signaling, mediate these cystogenic mechanisms. This article reviews the evidence implicating calcium and cAMP as central players in a network of signaling pathways underlying the pathogenesis of PKD and considers the therapeutic relevance of treatment strategies targeting cAMP signaling.

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Section: Interstitial Inflammation and Fibrosismentioning

confidence: 99%

Strategies Targeting cAMP Signaling in the Treatment of Polycystic Kidney Disease

Torres

Harris

2014

Journal of the American Society of Nephrology

243

218

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“…This intriguing observation points to additional regulatory control of hIP-activated STAT3 activity since Tyr 705 phosphorylation is required for STAT3 transcriptional activity (Darnell, 1997 (Liu et al, 2006). In this present study, we tested the hypothesis that activation of G s and G q by hIP confers upon the receptor an alternative pathway to stimulate STAT3.…”

Section: Stat3 Can Be Activated By Several Gα Subunits Including Pertmentioning

confidence: 92%

“…The inability of MEK1/2 to inhibit cicaprost-induced STAT3 Tyr 705 phosphorylation in HEL cells suggests that hIP may employ signaling pathways different from those of the C5aR (Lo et al, 2003) (Liu et al, 2006;Lo et al, 2003). The expression level of total STAT3 was unaffected by these kinase inhibitors (Fig.…”

Section: Involvement Of Src/jaks and Pi3k Signaling Pathways In Cicapmentioning

confidence: 97%

“…Gα o and Gα i2 (Ram et al, 2000) and PTX-insensitive Gα s (Liu et al, 2006), Gα 16 (Lo et al, 2003), and Gα 14 (Lo and Wong, 2004). In HEL cells, the G 16 -coupled complement C5a receptor (C5aR) activates STAT3 through multiple pathways including the PLCβ/PKC/Raf-1/MEK/ERK axis (Lo et al, 2003).…”

Section: Stat3 Can Be Activated By Several Gα Subunits Including Pertmentioning

confidence: 99%

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Prostacyclin receptor-induced STAT3 phosphorylation in human erythroleukemia cells is mediated via Gαs and Gα16 hybrid signaling

Liu

Wise

et al. 2008

Cellular Signalling

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“…It is therefore necessary to demonstrate the nuclear accumulation of PY-STAT3 when studying PY-STAT3-dependent gene expression. Stimulation of heart tissue with β-adrenergic agonists leads to STAT3 phosphorylation [18,31] and increased transcriptional activity [31]. Intravenous infusion with the β-adrenergic agonist dobutamine in swine resulted in a significant increase in heart rate (from 121±10 before Data are mean±SE from four independent experiments.…”

Section: Nuclear Appearance Of Py-stat3mentioning

confidence: 99%

Nuclear protein extraction from frozen porcine myocardium

et al. 2010

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Protocols for the extraction of nuclear proteins have been developed for cultured cells and fresh tissue, but sometimes only frozen tissue is available. We have optimized the homogenization procedure and subsequent fractionation protocol for the preparation of nuclear protein extracts from frozen porcine left ventricular (LV) tissue. This method gave a highly reproducible protein yield (6.5±0.7% of total protein; mean±SE, n=9) and a 6-fold enrichment of the nuclear marker protein B23. The nuclear protein extracts were essentially devoid of cytosolic, myofilament, and histone proteins. Compared to nuclear extracts from fresh LV tissue, some loss of nuclear proteins to the cytosolic fraction was observed. Using this method, we studied the distribution of tyrosinephosphorylated signal transducer and activator of transcription 3 (PY-STAT3) in LV tissue of animals treated with the β-agonist dobutamine. Upon treatment, PY-STAT3 increased 30.2±8.5-fold in total homogenates, but only 6.9±2.1-fold (n=4, P=0.03) in nuclear protein extracts. Of all PY-STAT3 formed, only a minor fraction appeared in the nuclear fraction. This simple and reproducible protocol yielded nuclear protein extracts that were highly enriched in nuclear proteins with almost complete removal of cytosolic and myofilament proteins. This nuclear protein extraction protocol is therefore well-suited for nuclear proteome analysis of frozen heart tissue collected in biobanks.

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Activation of STAT3 by Gαs Distinctively Requires Protein Kinase A, JNK, and Phosphatidylinositol 3-Kinase

Cited by 48 publications

References 70 publications

Strategies Targeting cAMP Signaling in the Treatment of Polycystic Kidney Disease

Strategies Targeting cAMP Signaling in the Treatment of Polycystic Kidney Disease

Prostacyclin receptor-induced STAT3 phosphorylation in human erythroleukemia cells is mediated via Gαs and Gα16 hybrid signaling

Nuclear protein extraction from frozen porcine myocardium

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