Activation of the Interleukin-4/Signal Transducer and Activator of Transcription 6 Signaling Pathway and Homeodomain-Interacting Protein Kinase 2 Production by Tonsillar Mononuclear Cells in IgA Nephropathy

2013 ◽  
Vol 38 (4) ◽  
pp. 321-332 ◽  
Author(s):  
Liyu He ◽  
Youming Peng ◽  
Hong Liu ◽  
Wenqing Yin ◽  
Xian Chen ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Iga Nephropathy ◽  
Signaling Pathway ◽  
Mononuclear Cells ◽  
Interleukin 4 ◽  
Signal Transducer ◽  
Interacting Protein

Dependence of the content of individual molecules in agranucocytes of whole blood at coronary heart disease from the level of phosphorylation of protein kinase r 38 in terms of low intensity microwave radiation

2016 ◽  
Vol 10 (1) ◽  
pp. 0-0 ◽  
Author(s):  
Логаткина ◽  
A. Logatkina ◽  
Бондарь ◽  
S. Bondar ◽  
Терехов ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Protein Kinase ◽  
Signaling Pathway ◽  
Microwave Radiation ◽  
Whole Blood ◽  
Mononuclear Cells ◽  
Protein Kinase R ◽  
Low Intensity ◽  
Mononuclear Leucocytes

Molecular indicators reflecting the states of stress-limiting systems of mononuclear leucocytes in the blood, as well as the effects of low-intensive microwave radiation in patients with coronary artery disease were studied. The work it was evaluated the content in mononuclear leucocytes whole blood of components PI3P/AKT/mTOR/p70S6K1 of signaling pathway, heat shock proteins (HSP27, HSP70, HSP90), the concentra-tion of antioxidants and peroxides depending on the level of phosphorylation of the terminal protein kinase MAPK/SAPK of signaling pathway – p38. The results of the study. It was revealed the dependence of a level of studied factors from the degree of phosphorylation p38 in patients with coronary heart disease. It was defined the 38 p sensitivity to the effects of low-intensity microwave radiation, it is manifested by increased level of phosphorylation in the irradiated cul-tures. This study revealed the sensitivity to low-intensity microwave irradiation of content in the mononuclear cells phosphorylated forms of the protein kinases AMPK, AKT1, p70S6K1, as well as the antioxidant status and protein of p53-dependent initial content in the cell phosphorylated form p38. It was shown a possibility of microwave radiation to reduce the content in the cells of the protein kinase and p70 ACT more pronounced at high levels of phosphorylation p38.

Genetic control of interleukin-4–induced activation of the human signal transducer and activator of transcription 6 signaling pathway

2003 ◽  
Vol 64 (4) ◽  
pp. 402-415 ◽  
Author(s):  
Wen Jie Zhang ◽  
Walter A Koltun ◽  
Anna F Tilberg ◽  
Jennifer L Thompson ◽  
Michael J Chorney
Keyword(s):  
Genetic Control ◽  
Signaling Pathway ◽  
Interleukin 4 ◽  
Signal Transducer ◽  
Human Signal

scholarly journals Cyclic AMP Stimulates SF-1-Dependent CYP11A1 Expression through Homeodomain-Interacting Protein Kinase 3-Mediated Jun N-Terminal Kinase and c-Jun Phosphorylation

2007 ◽  
Vol 27 (6) ◽  
pp. 2027-2036 ◽  
Author(s):  
Hsin-Chieh Lan ◽  
Hua-Jung Li ◽  
Guang Lin ◽  
Pao-Yen Lai ◽  
Bon-chu Chung
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
Cyclic Amp ◽  
Signaling Pathway ◽  
Camp Signaling ◽  
Functional Interaction ◽  
Interacting Protein ◽  
Surface Receptors ◽  
Camp Signaling Pathway ◽  
Camp Stimulation

ABSTRACT Steroids are synthesized in adrenal glands and gonads under the control of pituitary peptides. These peptides bind to cell surface receptors to activate the cyclic AMP (cAMP) signaling pathway leading to an increase of steroidogenic gene expression. Exactly how cAMP activates steroidogenic gene expression is not clear, except for the knowledge that transcription factor SF-1 plays a key role. Investigating the factors participating in SF-1 action, we found that c-Jun and homeodomain-interacting protein kinase 3 (HIPK3) were required for basal and cAMP-stimulated expression of one major steroidogenic gene, CYP11A1. HIPK3 enhanced SF-1 activity, and c-Jun was required for the functional interaction of HIPK3 with SF-1. Furthermore, after cAMP stimulation, both c-Jun and Jun N-terminal kinase (JNK) were phosphorylated through HIPK3. These phosphorylations were important for SF-1 activity and CYP11A1 expression. Thus, we have defined HIPK3-mediated JNK activity and c-Jun phosphorylation as important events that increase SF-1 activity for CYP11A1 transcription in response to cAMP. This finding has linked three common factors, HIPK3, JNK, and c-Jun, to the cAMP signaling pathway leading to increased steroidogenic gene expression.

scholarly journals microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Ya Peng ◽  
Xiangsheng Li ◽  
Huowang Liu ◽  
Xiaowen Deng ◽  
Chang She ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
Transforming Growth Factor Beta ◽  
Mononuclear Cells ◽  
Transforming Growth Factor ◽  
Interleukin 4 ◽  
M2 Macrophages ◽  
Peripheral Blood Mononuclear ◽  
Cell Progression

Abstract Objectives Nasopharyngeal carcinoma (NPC) is a type of nasopharyngeal disease with high metastasis and invasion properties. Tumor-associated alternative activated (M2) macrophages are evidenced to connect with NPC. Based on this, this study purposes to explore the mechanism and participation of microRNA-18a (miR-18a) from M2 macrophages in NPC. Methods Peripheral blood mononuclear cells were differentiated to macrophages and macrophages were polarized to M2 type by interleukin-4. SUNE-1 and CNE2 cells were transfected with restored or depleted miR-18a or transforming growth factor-beta III receptor (TGFBR3) to explore their roles in NPC progression with the involvement of the TGF-β signaling pathway. Next, SUNE-1 and CNE2 cells were co-cultured with M2 macrophages that had been treated with restored or depleted miR-18a or TGFBR3 to comprehend their combined roles in NPC with the involvement of the TGF-β signaling pathway. Results MiR-18a was highly expressed and TGFBR3 was lowly expressed in NPC cells. MiR-18a restoration, TGFBR3 knockdown or co-culture with miR-18a mimics, or si-TGFBR3-transfected M2 macrophages promoted SUNE-1 cell progression, tumor growth in mice, decreased p-Smad1/t-Smad1, and elevated p-Smad3/t-Smad3. miR-18a downregulation, TGFBR3 overexpression, or co-culture with miR-18a inhibitors or OE-TGFBR3-transfected M2 macrophages depressed CNE2 cell progression, tumor growth in mice, increased p-Smad1/t-Smad1, and decreased p-Smad3/t-Smad3. Conclusion Our study elucidates that miR-18a from M2 macrophages results in promoted NPC cell progression and tumor growth in nude mice via TGFBR3 repression, along with the Smad1 inactivation and Smad3 activation.

Protein kinase C‐mediated calcium entry dependent upon dihydropyridine‐sensitive channels: a T‐cell receptor‐coupled signaling pathway involved in interleukin 4 synthesis

2001 ◽  
Vol 15 (9) ◽  
pp. 1577-1579 ◽  
Author(s):  
Magali Savignac ◽  
Abdallah Badou ◽  
Marc Moreau ◽  
Catherine Leclerc ◽  
Jean-Charles Guéry ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
T Cell ◽  
Protein Kinase ◽  
Signaling Pathway ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Calcium Entry ◽  
Interleukin 4 ◽  
Kinase C
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