Involvement of Insulin-like Growth Factor Type 1 Receptor and Protein Kinase Cδ in Bis(maltolato)oxovanadium(IV)-Induced Phosphorylation of Protein Kinase B in HepG2 Cells†

Biochemistry ◽  
2006 ◽  
Vol 45 (38) ◽  
pp. 11605-11615 ◽  
Author(s):  
Mohamad Z. Mehdi ◽  
George Vardatsikos ◽  
Sanjay K. Pandey ◽  
Ashok K. Srivastava
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Hepg2 Cells ◽  
Protein Kinase B ◽  
Insulin Like Growth Factor ◽  
Factor Type ◽  
Protein Kinase Cδ

Insulin-like growth factor type-1 receptor transactivation in vasoactive peptide and oxidant-induced signaling pathways in vascular smooth muscle cellsThis paper is one of a selection of papers published in this Special Issue, entitled Young Investigators' Forum.

2007 ◽  
Vol 85 (1) ◽  
pp. 105-111 ◽  
Author(s):  
Zeina M. Azar ◽  
Mohamad Z. Mehdi ◽  
Ashok K. Srivastava
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Signaling Pathways ◽  
Growth Factor Receptor ◽  
Insulin Like Growth Factor ◽  
Ang Ii ◽  
Factor Type

Transactivation of epidermal growth factor receptor (EGFR) is a well-documented mechanism by which vasoactive peptides and H2O2 elicit their cellular responses. However, a role for the insulin-like growth factor type-1 receptor (IGF-1R) transactivation in mediating the effects of angiotensin II (Ang II) and H2O2 in vascular smooth muscle cells from different artery types have also been recently recognized. By using a series of pharmacological inhibitors of various growth factor receptor tyrosine kinases and a direct analysis of the phosphorylation status of the β-subunit of IGF-1R, a requirement of this growth factor receptor in Ang II and H2O2 response has been demonstrated. This review discusses some of the studies that highlight the importance of IGF-1R transactivation in mediating Ang II- and H2O2-induced mitogen-activated protein kinase and protein kinase B signaling pathways.

Production and Characterization of Monoclonal Antibodies Against Insulin-Like Growth Factor Type 1 Receptor

Hybridoma ◽  
2006 ◽  
Vol 25 (4) ◽  
pp. 230-237 ◽  
Author(s):  
Mehrnaz Keyhanfar ◽  
Briony E. Forbes ◽  
Leah J. Cosgrove ◽  
John C. Wallace ◽  
Grant W. Booker
Keyword(s):  
Monoclonal Antibodies ◽  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Factor Type

Insulin-like growth factor type 1 receptor (IGF-1R) exclusive nuclear staining: A predictive biomarker for IGF-1R monoclonal antibody (Ab) therapy in sarcomas

2012 ◽  
Vol 48 (16) ◽  
pp. 3027-3035 ◽  
Author(s):  
Irène Asmane ◽  
Emmanuel Watkin ◽  
Laurent Alberti ◽  
Adeline Duc ◽  
Perrine Marec-Berard ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Growth Factor ◽  
Predictive Biomarker ◽  
Nuclear Staining ◽  
Insulin Like Growth Factor ◽  
Factor Type

Expression of Insulin-like Growth Factor Type 1 Receptor is Linked to Inflammation in Adamantinomatous Craniopharyngioma

2021 ◽  
Author(s):  
Lang Yang ◽  
Kai Li ◽  
Weizhao Li ◽  
Chaohu Wang ◽  
Yi Liu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Growth Factor ◽  
High Expression ◽  
Inflammatory Factors ◽  
Insulin Like Growth Factor ◽  
Factor Type ◽  
Adamantinomatous Craniopharyngioma ◽  
The Relationship ◽  
Igf1r Expression

Introduction Insulin-like growth factor type 1 receptor (IGF1R) is overexpressed in various malignant tumors, which relates to their transformation and recurrence. Craniopharyngioma is a benign tumor with malignant results, often accompanied by a severe inflammatory reaction. However, the relationship between IGF1R expression and the inflammatory response of craniopharyngioma is unclear. Methods We enrolled 85 patients with adamantinomatous craniopharyngioma (ACP) in a study to explore the relationship between IGF1R expression and clinical features of this disease. Results Patients in the IGF1R high expression group had a significantly higher incidence of hypopituitarism, higher recurrence rate and lower progression-free survival. Beta-catenin can further regulate expression of the stem cell marker, CD44, by regulating IGF1R. Using immunofluorescence, we found that tumor stem cell–like cells did not express phosphorylated (p)-ERK, although p-ERK activation was evident in the surrounding cells. Picropodophyllin, a specific inhibitor of IGF1R, increased the expression of p-ERK protein, and decreased the transcription level of interleukin-6. Conclusions High expression of IGF1R might promote inflammation of ACP, which might be an unfavorable factor for pituitary function and prognosis. The high expression of IGF1R in tumor cell stem-like cells might inhibit the expression of p-ERK and promote the generation of inflammatory factors. Insulin-like growth factor type 1 receptor plays a stemness maintenance role in ACP and regulates the production of inflammatory factors through a p-ERK pathway, which suggests that targeting IGF1R and p-ERK might provide a new direction for alleviating tumor inflammation.

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