Stem cell factor (SCF)-Kit mediated phosphatidylinositol 3 (PI3) kinase signaling during mammalian oocyte growth and early follicular development

10.2741/1785 ◽  
2006 ◽  
Vol 11 (1) ◽  
pp. 126 ◽  
Author(s):  
Kui Liu
Keyword(s):  
Stem Cell ◽  
Stem Cell Factor ◽  
Follicular Development ◽  
Pi3 Kinase ◽  
Kinase Signaling ◽  
Oocyte Growth ◽  
Mammalian Oocyte ◽  
Phosphatidylinositol 3

scholarly journals Control of mammalian oocyte growth and early follicular development by the oocyte PI3 kinase pathway: New roles for an old timer

2006 ◽  
Vol 299 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Kui Liu ◽  
Singareddy Rajareddy ◽  
Lian Liu ◽  
Krishna Jagarlamudi ◽  
Karin Boman ◽  
...  
Keyword(s):  
Follicular Development ◽  
Pi3 Kinase ◽  
Oocyte Growth ◽  
Mammalian Oocyte ◽  
Pi3 Kinase Pathway ◽  
Kinase Pathway

Distinct functions of erythropoietin and stem cell factor are linked to activation of mTOR kinase signaling pathway in human erythroid progenitors

Cytokine ◽  
2013 ◽  
Vol 61 (1) ◽  
pp. 329-335 ◽  
Author(s):  
Renaud Geslain ◽  
Shahab Uddin ◽  
Hui Liu ◽  
Hongmei Jiang ◽  
Koen van Besien ◽  
...  
Keyword(s):  
Stem Cell ◽  
Signaling Pathway ◽  
Stem Cell Factor ◽  
Kinase Signaling ◽  
Erythroid Progenitors ◽  
Mtor Kinase ◽  
Kinase Signaling Pathway

Stem cell factor induces phosphatidylinositol 3′-kinase–dependent Lyn/Tec/Dok-1 complex formation in hematopoietic cells

Blood ◽  
2000 ◽  
Vol 96 (10) ◽  
pp. 3406-3413 ◽  
Author(s):  
Thamar B. van Dijk ◽  
Emile van den Akker ◽  
Martine Parren-van Amelsvoort ◽  
Hiroyuki Mano ◽  
Bob Löwenberg ◽  
...  
Keyword(s):  
Stem Cell ◽  
Tyrosine Kinase ◽  
Stem Cell Factor ◽  
Hematopoietic Cells ◽  
Sh2 Domain ◽  
Stable Complex ◽  
Phosphatidylinositol 3 Kinase ◽  
Sh2 Domains ◽  
And Migration ◽  
Phosphatidylinositol 3

Stem cell factor (SCF) has an important role in the proliferation, differentiation, survival, and migration of hematopoietic cells. SCF exerts its effects by binding to cKit, a receptor with intrinsic tyrosine kinase activity. Activation of phosphatidylinositol 3′-kinase (PI3-K) by cKit was previously shown to contribute to many SCF-induced cellular responses. Therefore, PI3-K-dependent signaling pathways activated by SCF were investigated. The PI3-K-dependent activation and phosphorylation of the tyrosine kinase Tec and the adapter molecule p62Dok-1 are reported. The study shows that Tec and Dok-1 form a stable complex with Lyn and 2 unidentified phosphoproteins of 56 and 140 kd. Both the Tec homology and the SH2 domain of Tec were identified as being required for the interaction with Dok-1, whereas 2 domains in Dok-1 appeared to mediate the association with Tec. In addition, Tec and Lyn were shown to phosphorylate Dok-1, whereas phosphorylated Dok-1 was demonstrated to bind to the SH2 domains of several signaling molecules activated by SCF, including Abl, CrkL, SHIP, and PLCγ-1, but not those of Vav and Shc. These findings suggest that p62Dok-1 may function as an important scaffold molecule in cKit-mediated signaling.

Kit/stem cell factor receptor-induced activation of phosphatidylinositol 3′-kinase is essential for male fertility

10.1038/72814 ◽  
2000 ◽  
Vol 24 (2) ◽  
pp. 157-162 ◽  
Author(s):  
Peter Blume-Jensen ◽  
Guoqiang Jiang ◽  
Robert Hyman ◽  
Kuo-Fen Lee ◽  
Stephen O'Gorman ◽  
...  
Keyword(s):  
Stem Cell ◽  
Male Fertility ◽  
Stem Cell Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

Stem cell factor induces phosphatidylinositol 3′-kinase–dependent Lyn/Tec/Dok-1 complex formation in hematopoietic cells

Blood ◽  
2000 ◽  
Vol 96 (10) ◽  
pp. 3406-3413 ◽  
Author(s):  
Thamar B. van Dijk ◽  
Emile van den Akker ◽  
Martine Parren-van Amelsvoort ◽  
Hiroyuki Mano ◽  
Bob Löwenberg ◽  
...  
Keyword(s):  
Stem Cell ◽  
Tyrosine Kinase ◽  
Stem Cell Factor ◽  
Hematopoietic Cells ◽  
Sh2 Domain ◽  
Stable Complex ◽  
Phosphatidylinositol 3 Kinase ◽  
Sh2 Domains ◽  
And Migration ◽  
Phosphatidylinositol 3

Abstract Stem cell factor (SCF) has an important role in the proliferation, differentiation, survival, and migration of hematopoietic cells. SCF exerts its effects by binding to cKit, a receptor with intrinsic tyrosine kinase activity. Activation of phosphatidylinositol 3′-kinase (PI3-K) by cKit was previously shown to contribute to many SCF-induced cellular responses. Therefore, PI3-K-dependent signaling pathways activated by SCF were investigated. The PI3-K-dependent activation and phosphorylation of the tyrosine kinase Tec and the adapter molecule p62Dok-1 are reported. The study shows that Tec and Dok-1 form a stable complex with Lyn and 2 unidentified phosphoproteins of 56 and 140 kd. Both the Tec homology and the SH2 domain of Tec were identified as being required for the interaction with Dok-1, whereas 2 domains in Dok-1 appeared to mediate the association with Tec. In addition, Tec and Lyn were shown to phosphorylate Dok-1, whereas phosphorylated Dok-1 was demonstrated to bind to the SH2 domains of several signaling molecules activated by SCF, including Abl, CrkL, SHIP, and PLCγ-1, but not those of Vav and Shc. These findings suggest that p62Dok-1 may function as an important scaffold molecule in cKit-mediated signaling.

Protein Kinase B (c-Akt), Phosphatidylinositol 3-Kinase, and STAT5 Are Activated by Erythropoietin (EPO) in HCD57 Erythroid Cells But Are Constitutively Active in an EPO-Independent, Apoptosis-Resistant Subclone (HCD57-SREI Cells)

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3757-3773 ◽  
Author(s):  
Haifeng Bao ◽  
Sarah M. Jacobs-Helber ◽  
Amy E. Lawson ◽  
Kalyani Penta ◽  
Amittha Wickrema ◽  
...  
Keyword(s):  
Stem Cell ◽  
Protein Kinase ◽  
Stem Cell Factor ◽  
Kinase Activity ◽  
Kinase Inhibitor ◽  
Protein Kinase B ◽  
Pi3 Kinase ◽  
Akt Pathway ◽  
Erythroid Cells ◽  
Phosphatidylinositol 3 Kinase

We found that erythropoietin (EPO) and stem cell factor (SCF) activated protein kinase B (PKB/Akt) in EPO-dependent HCD57 erythroid cells. To better understand signals controlling proliferation and viability, erythroid cells that resist apoptosis in the absence of EPO were subcloned and characterized (HCD57-SREI cells). Constitutive activations of PKB/Akt, STAT5a, and STAT5b were noted in these EPO-independent cells. PI3-kinase activity was an upstream activator of PKB/Akt because the PI3-kinase inhibitor LY294002 blocked both constitutive PKB/Akt and factor-dependent PKB/Akt activity. The LY294002 study showed that proliferation and viability of both HCD57-SREI and HCD57 cells correlated with the activity of PKB/Akt; however, PKB/Akt activity alone did not protect these cells from apoptosis. Treatment of HCD57 cells with SCF also activated PKB/Akt, but did not protect from apoptosis. This result suggested that PKB/PI3-kinase activity is necessary but not sufficient to promote viability and/or proliferation. Constitutive STAT5 activity, activated through an unknown pathway not including JAK2 or EPOR, may act in concert with the constitutive PI3-kinase/PKB/Akt pathway to protect the EPO-independent HCD57-SREI cells from apoptosis and promote limited proliferation.

Protein Kinase B (c-Akt), Phosphatidylinositol 3-Kinase, and STAT5 Are Activated by Erythropoietin (EPO) in HCD57 Erythroid Cells But Are Constitutively Active in an EPO-Independent, Apoptosis-Resistant Subclone (HCD57-SREI Cells)

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3757-3773 ◽  
Author(s):  
Haifeng Bao ◽  
Sarah M. Jacobs-Helber ◽  
Amy E. Lawson ◽  
Kalyani Penta ◽  
Amittha Wickrema ◽  
...  
Keyword(s):  
Stem Cell ◽  
Protein Kinase ◽  
Stem Cell Factor ◽  
Kinase Activity ◽  
Kinase Inhibitor ◽  
Protein Kinase B ◽  
Pi3 Kinase ◽  
Akt Pathway ◽  
Erythroid Cells ◽  
Phosphatidylinositol 3 Kinase

Abstract We found that erythropoietin (EPO) and stem cell factor (SCF) activated protein kinase B (PKB/Akt) in EPO-dependent HCD57 erythroid cells. To better understand signals controlling proliferation and viability, erythroid cells that resist apoptosis in the absence of EPO were subcloned and characterized (HCD57-SREI cells). Constitutive activations of PKB/Akt, STAT5a, and STAT5b were noted in these EPO-independent cells. PI3-kinase activity was an upstream activator of PKB/Akt because the PI3-kinase inhibitor LY294002 blocked both constitutive PKB/Akt and factor-dependent PKB/Akt activity. The LY294002 study showed that proliferation and viability of both HCD57-SREI and HCD57 cells correlated with the activity of PKB/Akt; however, PKB/Akt activity alone did not protect these cells from apoptosis. Treatment of HCD57 cells with SCF also activated PKB/Akt, but did not protect from apoptosis. This result suggested that PKB/PI3-kinase activity is necessary but not sufficient to promote viability and/or proliferation. Constitutive STAT5 activity, activated through an unknown pathway not including JAK2 or EPOR, may act in concert with the constitutive PI3-kinase/PKB/Akt pathway to protect the EPO-independent HCD57-SREI cells from apoptosis and promote limited proliferation.

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