The prenylflavonoid Icaritin enhances osteoblast proliferation and function by signal transducer and activator of transcription factor 3 (STAT-3) regulation of C-X-C chemokine receptor type 4 (CXCR4) expression

Bone ◽  
2017 ◽  
Vol 105 ◽  
pp. 122-133 ◽  
Author(s):  
RZL Lim ◽  
L. Li ◽  
N. Chew ◽  
E.L. Yong
Keyword(s):  
Transcription Factor ◽  
Chemokine Receptor ◽  
Cxcr4 Expression ◽  
Receptor Type ◽  
Signal Transducer ◽  
Osteoblast Proliferation ◽  
And Function ◽  
Transcription Factor 3

scholarly journals Analytical and Biological Considerations in the Measurement of Cell-Associated CCR5 and CXCR4 mRNA and Protein

2010 ◽  
Vol 17 (7) ◽  
pp. 1148-1154 ◽  
Author(s):  
D. E. Campbell ◽  
J. P. Lai ◽  
N. B. Tustin ◽  
E. Riedel ◽  
R. Tustin ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
Highly Active Antiretroviral Therapy ◽  
Cxcr4 Expression ◽  
Receptor Type ◽  
Blood Collection ◽  
T Helper ◽  
Ccr5 Expression ◽  
Highly Active ◽  
Cxcr4 Mrna ◽  
Separation Media

ABSTRACT The accurate measurement of T cell-associated CC chemokine receptor type 5 (CCR5) and CXC chemokine receptor type 4 (CXCR4) expression, including expression of CCR5 and CXCR4 mRNA as an immune measure of immunologic response to highly active antiretroviral therapy (HAART) and newer agents, including entry inhibitors, is essential. Previous studies have reported alterations in lymphocyte cell membrane CCR5 expression that were related to blood collection and cell separation media. Clinical trials often require the transport of specimens to central laboratories for evaluation, resulting in significant time delays between specimen procurement and analysis. This study shows that CCR5 expression on naïve and memory T cells is influenced by blood collection media and specimen age. Peripheral blood collected in Streck Vacutainer tubes containing a cell stabilizer and fixative was found to improve detection of CCR5 expression compared to specimens collected in K2 EDTA anticoagulant. The selection of flow cytometry gating strategies for the identification of naïve and memory T-helper cells can also significantly influence the sensitivity of detection of CCR5 expression. Procedural methods are described that allow for the optimal measurement of naïve and memory T-helper cell CCR5 and CXCR4 expression as well as the quantitation of CCR5 and CXCR4 mRNA.

Inhibition of Signal Transducer and Activator Transcription Factor 3 in Rats with Acute Hepatic Failure

2000 ◽  
Vol 273 (1) ◽  
pp. 129-135 ◽  
Author(s):  
Yukio Kamohara ◽  
Nozomu Sugiyama ◽  
Toru Mizuguchi ◽  
Daniel Inderbitzin ◽  
Helene Lilja ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Hepatic Failure ◽  
Acute Hepatic Failure ◽  
Signal Transducer ◽  
Transcription Factor 3

Butein downregulates chemokine receptor CXCR4 expression and function through suppression of NF-κB activation in breast and pancreatic tumor cells

2010 ◽  
Vol 80 (10) ◽  
pp. 1553-1562 ◽  
Author(s):  
Angeline Wei Ling Chua ◽  
Hui Sin Hay ◽  
Peramaiyan Rajendran ◽  
Muthu K. Shanmugam ◽  
Feng Li ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Chemokine Receptor ◽  
Pancreatic Tumor ◽  
Cxcr4 Expression ◽  
Chemokine Receptor Cxcr4 ◽  
And Function

scholarly journals Relationship between Expression of EMT Transcription Factor of ZEB1 and CXCR4 Chemokine Receptor

2017 ◽  
Vol 3 ◽  
pp. 55
Author(s):  
Naghmeh Ahmadiankia
Keyword(s):  
Transcription Factor ◽  
Cause Of Death ◽  
Chemokine Receptor ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Critical Role ◽  
Cxcr4 Expression ◽  
Mesenchymal Transition

Metastasis is one the most leading cause of death from cancer and the chemokine receptor of CXCR4 has a critical role in cancer metastasis. Moreover, metastasis is always correlated with epithelial-mesenchymal transition (EMT). In this study, the correlation between expression of EMT-TF of ZEB1 and CXCR4 has been examined. The results revealed that in ZEB1 knocked out cells, the expression of CXCR4 decreased significantly. This indicated that ZEB1 might be one of the regulators of CXCR4 expression.

scholarly journals Atf3 links loss of epithelial polarity to defects in cell differentiation and cytoarchitecture

2017 ◽  
Author(s):  
Colin D. Donohoe ◽  
Gábor Csordás ◽  
Andreia Correia ◽  
Marek Jindra ◽  
Corinna Klein ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Cell Polarity ◽  
Target Genes ◽  
Asymmetric Distribution ◽  
Activating Transcription Factor 3 ◽  
Epithelial Polarity ◽  
Activating Transcription Factor ◽  
And Function ◽  
Transcription Factor 3

AbstractInterplay between apicobasal cell polarity modules and the cytoskeleton is critical for differentiation and integrity of epithelia. However, this coordination is poorly understood at the level of gene regulation by transcription factors. Here, we establish the Drosophila activating transcription factor 3 (atf3) as a cell polarity response gene acting downstream of the membrane-associated Scribble polarity complex. Loss of the tumor suppressors Scribble or Dlg1 induces atf3 expression via aPKC but independent of Jun-N-terminal kinase (JNK) signaling. Strikingly, removal of Atf3 from Dlg1 deficient cells restores polarized cytoarchitecture, levels and distribution of endosomal trafficking machinery, and differentiation. Conversely, excess Atf3 alters microtubule network, vesicular trafficking and the partition of polarity proteins along the apicobasal axis. Genomic and genetic approaches implicate Atf3 as a regulator of cytoskeleton organization and function, and identify Lamin C as one of its bona fide target genes. By affecting structural features and cell morphology, Atf3 functions in a manner distinct from other transcription factors operating downstream of disrupted cell polarity.Author summaryEpithelial cells form sheets and line both the outside and inside of our body. Their proper development and function require the asymmetric distribution of cellular components from the top to the bottom, known as apicobasal polarization. As loss of polarity hallmarks a majority of cancers in humans understanding how epithelia respond to a collapse of the apicobasal axis is of great interest. Here, we show that in the fruit fly Drosophila melanogaster, the breakdown of epithelial polarity engages Activating transcription factor 3 (Atf3), a protein that directly binds the DNA and regulates gene expression. We demonstrate that many of the pathological consequences of disturbed polarity require Atf3, as its loss in this context results in normalization of cellular architecture, vesicle trafficking and differentiation. Using unbiased genome-wide approaches we identify the genetic program controlled by Atf3 and experimentally verify select candidates. Given the evolutionary conservation of Atf3 between flies and man, we believe that our findings in the Drosophila model will contribute to a better understanding of diseases stemming from compromised epithelial polarity.

scholarly journals The roles of signal transducer and activator of transcription factor 3 in tumor angiogenesis

Oncotarget ◽  
2017 ◽  
Vol 8 (40) ◽  
pp. 69139-69161 ◽  
Author(s):  
Peng Gao ◽  
Na Niu ◽  
Tianshu Wei ◽  
Hideto Tozawa ◽  
Xiaocui Chen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Tumor Angiogenesis ◽  
Signal Transducer ◽  
Transcription Factor 3

Temporal Expression of Cytokines and Signal Transducer and Activator of Transcription Factor 3 Activation after Neonatal Hypoxia/Ischemia in Mice

2013 ◽  
Vol 35 (2-3) ◽  
pp. 212-225 ◽  
Author(s):  
K. Shrivastava ◽  
G. Llovera ◽  
M. Recasens ◽  
M. Chertoff ◽  
L. Giménez-Llort ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Signal Transducer ◽  
Temporal Expression ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia ◽  
Transcription Factor 3
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