Pyk2 Amplifies Epidermal Growth Factor and c-Src-induced Stat3 Activation

Shi, Chong-Shan; Kehrl, John H.

doi:10.1074/jbc.m311875200

Cited by 48 publications

(32 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In some cases these genomic effects result from interacting with intermediate molecules such as cAMP response element-binding protein (CREB) or signal transducer and activator of transcription family members (STATs; see Fig. 4), resulting in transcriptional activation through DNA response elements different from those activated by PR binding to progestin response elements (Shi and Kehrl, 2004;Tung et al, 2011). As shown in Fig.…”

Section: Discussionmentioning

confidence: 98%

Src kinase signaling mediates estrous behavior induced by 5β-reduced progestins, GnRH, prostaglandin E2 and vaginocervical stimulation in estrogen-primed rats

Lima-Hernández

Beyer

Gómora‐Arrati

et al. 2012

Hormones and Behavior

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 98%

Src kinase signaling mediates estrous behavior induced by 5β-reduced progestins, GnRH, prostaglandin E2 and vaginocervical stimulation in estrogen-primed rats

Lima-Hernández

Beyer

Gómora‐Arrati

et al. 2012

Hormones and Behavior

View full text Add to dashboard Cite

“…These kinases are also involved in regulation of the cytoskeleton due to their ability to associate with various cytoskeletal proteins, including focal adhesion kinase (FAK). Pyk2 belongs to the FAK family, and is involved in cell proliferation and migration (39,53). Src and Pyk2 are activated by GPCRs, integrins, cytokines and growth factors, and appears to be indispensable for EGF-R activation (34).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of endothelin-1-induced MAP kinase activation in adrenal glomerulosa cells

Shah

Báukal

Chen

et al. 2006

The Journal of Steroid Biochemistry and Molecular Biology

View full text Add to dashboard Cite

G protein-coupled receptors (GPCRs) such as angiotensin II, bradykinin and endothelin-1 (ET-1) are critically involved in the regulation of adrenal function, including aldosterone production from zona glomerulosa cells. Whereas substantial data are available on the signaling mechanisms of ET-1 in cardiovascular tissues, such information in adrenal glomerulosa cells is lacking. Bovine adrenal glomerulosa (BAG) cells express receptors for endothelin-1 (ET-1) and their stimulation caused phosphorylation of Src (at Tyr416), proline-rich tyrosine kinase (Pyk2 at Tyr402), extracellularly regulated signal kinases (ERK1/2), and their dependent proteins, p90 ribosomal S6 kinase (RSK-1) and CREB. ET-1 elicited these responses predominantly through activation of a G i -linked cascade with a minor contribution from the G q /PKC pathway. Whereas selective inhibition of EGF-R kinase with AG1478 caused complete inhibition of EGF-induced ERK/ RSK-1/CREB activation, it caused only partial reduction (30-40%) of such ET-1-induced responses. Consistent with this, inhibition of matrix metalloproteinases (MMPs) with GM6001 reduced ERK1/2 activation by ET-1, consistent with partial involvement of the MMP-dependent EGF-R activation in this cascade. Activation of ERK/RSK-1/CREB by both ET-1 and EGF was abolished by inhibition of Src, indicating its central role in ET-1 signaling in BAG cells. Moreover, the signaling characteristics of ET-1 in cultured BAG cells closely resembled those observed in clonal adrenocortical H295R cells. The ET-1-induced proliferation of BAG and H295 R cells was much smaller than that induced by Ang II or FGF. These data demonstrate that ET-1 causes ERK/RSK-1/CREB phosphorylation predominantly through activation of G i and Src, with a minor contribution from MMP-dependent EGF-R transactivation.

show abstract

“…Several different studies have used both pharmacological inhibitors and dominant-negative forms of SFKs, and concluded that SFKs are required for both PDGF (Blake et al, 2000;Wang et al, 2000;Bowman et al, 2001;Simon et al, 2002) and EGF (Olayioye et al, 1999;Kazansky and Rosen, 2001;Guren et al, 2003;Kloth et al, 2003) stimulation of Stat tyrosine phosphorylation and activation. The nonreceptor tyrosine kinase Pyk2 is also involved in the SFKmediated activation of Stats in response to growth factors (Shi and Kehrl, 2004), although the mechanism by which this occurs is not clear. The block to PDGFstimulated DNA synthesis induced by a naturally occurring dominant-negative form of Stat3 (Stat3b) can be overcome by expressing Myc, potentially placing Stats in the PDGF-SFK-Myc pathway (Bowman et al, 2001).…”

Section: A Pathway Between Sfks and Mycmentioning

confidence: 99%

The interplay between Src family kinases and receptor tyrosine kinases

2004

View full text Add to dashboard Cite

Src family tyrosine kinases (SFKs) are involved in a diverse array of physiological processes, as highlighted in this review. An overview of how SFKs interact with, and participate in signaling from, receptor tyrosine kinases (RTKs) is discussed. And also, how SFKs are activated by RTKs, and how SFKs, in turn, can activate RTKs, as well as how SFKs can promote signaling from growth factor receptors in a number of ways including participation in signaling pathways required for DNA synthesis, control of receptor turnover, actin cytoskeleton rearrangements and motility, and survival are discussed.

show abstract

Pyk2 Amplifies Epidermal Growth Factor and c-Src-induced Stat3 Activation

Cited by 48 publications

References 64 publications

Src kinase signaling mediates estrous behavior induced by 5β-reduced progestins, GnRH, prostaglandin E2 and vaginocervical stimulation in estrogen-primed rats

Src kinase signaling mediates estrous behavior induced by 5β-reduced progestins, GnRH, prostaglandin E2 and vaginocervical stimulation in estrogen-primed rats

Mechanisms of endothelin-1-induced MAP kinase activation in adrenal glomerulosa cells

The interplay between Src family kinases and receptor tyrosine kinases

Contact Info

Product

Resources

About