scholarly journals Tyrosine Phosphorylation-Mediated Signaling Pathways in Dictyostelium

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Tong Sun ◽  
Leung Kim
Keyword(s):  
Cell Proliferation ◽  
Cell Differentiation ◽  
Tyrosine Kinase ◽  
Signaling Pathways ◽  
Tyrosine Phosphorylation ◽  
Cellular Responses ◽  
Model Systems ◽  
Cytokine Signaling ◽  
Tyrosine Kinase Signaling ◽  
Metazoan Cell

While studies on metazoan cell proliferation, cell differentiation, and cytokine signaling laid the foundation of the current paradigms of tyrosine kinase signaling, similar studies using lower eukaryotes have provided invaluable insight for the understanding of mammalian pathways, such as Wnt and STAT pathways. Dictyostelium is one of the leading lower eukaryotic model systems where stress-induced cellular responses, Wnt-like pathways, and STAT-mediated pathways are well investigated. These Dictyostelium pathways will be reviewed together with their mammalian counterparts to facilitate the comparative understanding of these variant and noncanonical pathways.

scholarly journals Dual inhibition of HDAC and tyrosine kinase signaling pathways with CUDC-907 attenuates TGFβ1 induced lung and tumor fibrosis

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Wentian Zhang ◽  
Yajie Zhang ◽  
Tian Tu ◽  
Sabastian Schmull ◽  
Yu Han ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tyrosine Kinase ◽  
Signaling Pathways ◽  
Lung Fibrosis ◽  
Single Agent ◽  
Dependent Manner ◽  
Kinase Signaling ◽  
Dual Inhibitor ◽  
Tyrosine Kinase Signaling ◽  
Dual Inhibition

Abstract TGFβ1 signaling is a critical driver of collagen accumulation in pulmonary fibrotic diseases and a well-characterized regulator of cancer associated fibroblasts (CAF) activation in lung cancer. Myofibroblasts induced by TGFβ1 and other factors are key players in the pathogenesis of lung fibrosis and tumor. Tremendous attention has been gained to targeting myofibroblasts in order to inhibit the progression of fibrosis and myofibroblast-induced tumor progression and metastasis. Here we determined the therapeutic efficacy of simultaneously targeting PI3K and HDAC pathways in lung myofibroblasts and CAF with a single agent and to evaluate biomarkers of treatment response. CUDC-907 is a first-in-class compound, functioning as a dual inhibitor of HDACs and PI3K/AKT pathway. We investigated its effects in counteracting the activity of TGFβ1-induced myofibroblasts/CAF in regard to cell proliferation, migration, invasion, apoptosis in vitro antifibrosis efficiency in vivo. We found that CUDC-907 inhibited myofibroblasts/CAF cell proliferation, migration and apoptosis in a dose-dependent manner and caused cell cycle arrest at G1-S phase. CUDC-907 not only inhibited myofibroblasts markers expression, but also significantly inhibited the phosphorylation level of AKT, mTOR, Smad2/3, and promoted acetylation of histones. Furthermore, the observed inhibitory effect was also confirmed in bleomycin-induced mice lung fibrosis and nude mouse transplanted tumor model. Overall, these data suggest that dual inhibition of HDAC and the tyrosine kinase signaling pathways with CUDC-907 is a promising treatment strategy for TGFβ1-induced lung and tumor fibrosis.

scholarly journals How Protein Kinase A Activates Canonical Tyrosine Kinase Signaling Pathways To Promote Granulosa Cell Differentiation

Endocrinology ◽  
2017 ◽  
Vol 158 (7) ◽  
pp. 2043-2051 ◽  
Author(s):  
Nathan C. Law ◽  
Elyse M. Donaubauer ◽  
Anthony J. Zeleznik ◽  
Mary Hunzicker-Dunn
Keyword(s):  
Cell Differentiation ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Protein Kinase A ◽  
Signaling Pathways ◽  
Granulosa Cell ◽  
Kinase Signaling ◽  
Tyrosine Kinase Signaling ◽  
Kinase A

Attenuation of serum inducibility of immediate early genes by oncoproteins in tyrosine kinase signaling pathways

1993 ◽  
Vol 13 (4) ◽  
pp. 2011-2019
Author(s):  
C L Yu ◽  
E V Prochownik ◽  
M J Imperiale ◽  
R Jove
Keyword(s):  
Tyrosine Kinase ◽  
Signaling Pathways ◽  
Immediate Early Genes ◽  
Immediate Early ◽  
Transformed Cells ◽  
Kinase Signaling ◽  
Tyrosine Kinase Signaling ◽  
Early Genes ◽  
Serum Stimulation ◽  
Stimulation Of

Immediate early genes involved in controlling cell proliferation are rapidly and transiently induced following stimulation of susceptible cells with serum. To study how oncoproteins regulate immediate early genes, we examined serum inducibility of these genes in cells transformed by various oncoproteins. We found that induction of the immediate early gene, c-fos, by serum stimulation was markedly attenuated in four independent cell lines stably transformed by the v-Src tyrosine kinase. Cells chronically transformed by other oncoproteins implicated in tyrosine kinase signaling pathways, including v-Sis, v-Ras, and v-Raf, showed the same pattern of attenuation. In contrast, serum inducibility of c-fos was not attenuated in cells transformed by simian virus 40, which is thought to transform cells through a different pathway. Cell cycle analyses showed that proliferation of these transformed cell lines could be arrested effectively in 0.1% serum, demonstrating that the attenuation was not simply due to continuous cycling of transformed cells after serum deprivation. Moreover, serum inducibility of other immediate early genes, including c-jun, junB, egr-1, and NGFI-B, also was strikingly attenuated by these same oncoproteins. Nuclear run-on transcription assays established that this attenuation of serum inducibility occurred at the transcriptional level. Finally, flow cytometric analysis demonstrated that serum-starved v-Src-transformed cells were viable and able to progress into S phase of the cell cycle after serum stimulation, even though the induction of immediate early genes was greatly attenuated in these cells. Our results suggest that activation of immediate early genes is repressed by chronic stimulation of tyrosine kinase signaling pathways in transformed cells.

scholarly journals Dual Inhibition of HDAC and Tyrosine Kinase Signaling Pathways with CUDC-907 Inhibits Thyroid Cancer Growth and Metastases

2017 ◽  
Vol 23 (17) ◽  
pp. 5044-5054 ◽  
Author(s):  
Shweta Kotian ◽  
Lisa Zhang ◽  
Myriem Boufraqech ◽  
Kelli Gaskins ◽  
Sudheer Kumar Gara ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Tyrosine Kinase ◽  
Signaling Pathways ◽  
Cancer Growth ◽  
Kinase Signaling ◽  
Tyrosine Kinase Signaling ◽  
Dual Inhibition
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