Gingival epithelial cells support osteoclastogenesis by producing receptor activator of nuclear factor kappa B ligand via protein kinase A signaling

2015 ◽  
Vol 51 (4) ◽  
pp. 462-470 ◽  
Author(s):  
M. Usui ◽  
T. Sato ◽  
G. Yamamoto ◽  
Y. Okamatsu ◽  
T. Hanatani ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Epithelial Cells ◽  
Protein Kinase A ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Gingival Epithelial Cells ◽  
Receptor Activator ◽  
Kinase A

Epithelial Cells Secrete Interferon-γ Which Suppresses Expression of Receptor Activator of Nuclear Factor Kappa-B Ligand in Human Mandibular Osteoblast-Like Cells

2017 ◽  
Vol 88 (3) ◽  
pp. e65-e74 ◽  
Author(s):  
Pakchisa Khonsuphap ◽  
Prasit Pavasant ◽  
Rizky Aditya Irwandi ◽  
Chidchanok Leethanakul ◽  
Anjalee Vacharaksa
Keyword(s):  
Epithelial Cells ◽  
Nuclear Factor Kappa B ◽  
Interferon Γ ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Receptor Activator

Osteoprotegerin (OPG) levels, total soluble receptor activator of nuclear factor-Kappa B ligand (total sRANKL) , and RANKL/OPG ratio in patients with rheumatoid arteritis

2017 ◽  
Vol 2 (1) ◽  
pp. 23-29
Author(s):  
Sousan Kolahi ◽  
Amir Ghorbanihaghjo ◽  
Nadereh Rashtchizadeh ◽  
Alireza Khabbazi ◽  
Mehrzad Hajialilo ◽  
...  
Keyword(s):  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Soluble Receptor ◽  
Nuclear Factor Kappa ◽  
Receptor Activator

scholarly journals A Distal Region Involving Hepatocyte Nuclear Factor 4α and CAAT/Enhancer Binding Protein Markedly Potentiates the Protein Kinase A Stimulation of the Glucose-6-Phosphatase Promoter

2005 ◽  
Vol 19 (1) ◽  
pp. 163-174 ◽  
Author(s):  
Amandine Gautier-Stein ◽  
Gilles Mithieux ◽  
Fabienne Rajas
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Binding Sites ◽  
Binding Protein ◽  
Distal Region ◽  
Proximal Region ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Enhancer Binding Protein ◽  
Kinase A

Abstract Glucose-6-phosphatase (Glc6Pase) is the last enzyme of gluconeogenesis and is only expressed in the liver, kidney, and small intestine. In these tissues, the mRNA and its activity are increased when cAMP levels increased (e.g. in fasting or diabetes). We first report that a proximal region (within −200 bp relative to the transcription start site) and a distal region (−694/−500 bp) are both required for a potent cAMP and a protein kinase A (PKA) responsiveness of the Glc6Pase promoter. Using different molecular approaches, we demonstrate that hepatocyte nuclear factor (HNF4α), CAAT/ enhancer-binding protein-α (C/EBPα), C/EBPβ, and cAMP response element-binding protein (CREB) are involved in the potentiated PKA responsiveness: in the distal region, via one HNF4α- and one C/EBP-binding sites, and in the proximal region, via two HNF4α and two CREB-binding sites. We also show that HNF4α, C/EBPα, and C/EBPβ are constitutively bound to the endogenous Glc6Pase gene, whereas CREB and CREB-binding protein (CBP) will be bound to the gene upon stimulation by cAMP. These data strongly suggest that the cAMP responsiveness of the Glc6Pase promoter requires a tight cooperation between a proximal and a distal region, which depends on the presence of several HNF4α-, C/EBP-, and CREB-binding sites, therefore involving an intricate association of hepatic and ubiquitous transcription factors.

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