Investigation of Cytokine—Receptor Interactions by Isotope-Edited FTIR Spectroscopy

1999 ◽  
pp. 167-182 ◽  
Author(s):  
Tiansheng Li ◽  
Tsutomu Arakawa ◽  
Thomas P. Horan ◽  
Byeong Chang
Keyword(s):  
Ftir Spectroscopy ◽  
Cytokine Receptor ◽  
Receptor Interactions

scholarly journals Insights into Cytokine–Receptor Interactions from Cytokine Engineering

2015 ◽  
Vol 33 (1) ◽  
pp. 139-167 ◽  
Author(s):  
Jamie B. Spangler ◽  
Ignacio Moraga ◽  
Juan L. Mendoza ◽  
K. Christopher Garcia
Keyword(s):  
Cytokine Receptor ◽  
Receptor Interactions

scholarly journals Upregulated CDKN2A expression may be an independent protective factor in Luminal-like breast cancer

2020 ◽  
Author(s):  
Yier Qiu ◽  
Guowen Lu ◽  
Yingjie Wu
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Mrna Expression ◽  
Protective Factor ◽  
Killer Cell ◽  
Cytokine Receptor ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
Receptor Interactions ◽  
Cancer Tissues

Abstract Background: Previous studies revealed that CDKN2A (cyclin-dependent kinase inhibitor 2A) functioned as a tumour suppressor in various types of malignant tumours. The aim of the study was to clarify the value of CDKN2A expression in the prognosis of breast cancer.Method: Using the Cancer Genome Atlas (TCGA) database, we compared CDKN2A mRNA levels between breast cancer tissues and normal tissues and analyzed the relationship between clinical features and CDKN2A expression with the Wilcox test and the Kruskal-Wallis test. Kaplan-Meier and Cox analyses were performed to determine the correlation between CDKN2A expression and breast cancer prognosis. Gene set enrichment analysis (GSEA) was performed using the TCGA data set.Results: We first found that CDKN2A expression was markedly higher in breast cancer tissues than in normal tissues using the TCGA database (P=0.000). In addition, CDKN2A mRNA expression in breast cancer was positively correlated with age (P=0.018), histological types (P=0.028), ER status (P=0.000), PR status (P=0.000) and molecular subtypes (P=0.000). Kaplan-Meier analysis showed that increased CDKN2A expression was associated with increased survival time in breast cancer patients (P=0.000), especially in Luminal-like subtype. Univariate and multivariate Cox analyses indicated that CDKN2A expression was an independent prognostic biomarker for breast cancer (P=0.037). GSEA suggested that pathways involving cell adhesion molecules (CAMs), cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity were differentially enriched in the CDKN2A-high expression group.Conclusion: Our research demonstrated that high CDKN2A mRNA expression may be an independent protective factor for improved prognosis in Luminal-like breast cancer. Additionally, the signaling pathways related to CAMs, cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity regulated by CDKN2A mRNA expression should be further studied.

scholarly journals Upregulated CDKN2A expression may be an independent protective factor in Luminal-like breast cancer

2020 ◽  
Author(s):  
Yier Qiu ◽  
Guowen Lu ◽  
Yingjie Wu
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Mrna Expression ◽  
Protective Factor ◽  
Killer Cell ◽  
Cytokine Receptor ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
Receptor Interactions ◽  
Cancer Tissues

Abstract Background: Previous studies revealed that CDKN2A (cyclin-dependent kinase inhibitor 2A) functioned as a tumour suppressor in various types of malignant tumours. The aim of the study was to clarify the value of CDKN2A expression in the prognosis of breast cancer.Method: Using the Cancer Genome Atlas (TCGA) database, we compared CDKN2A mRNA levels between breast cancer tissues and normal tissues and analyzed the relationship between clinical features and CDKN2A expression with the Wilcox test and the Kruskal-Wallis test. Kaplan-Meier and Cox analyses were performed to determine the correlation between CDKN2A expression and breast cancer prognosis. Gene set enrichment analysis (GSEA) was performed using the TCGA data set.Results: We first found that CDKN2A expression was markedly higher in breast cancer tissues than in normal tissues using the TCGA database (P=0.000). In addition, CDKN2A mRNA expression in breast cancer was positively correlated with age (P=0.018), histological types (P=0.028), ER status (P=0.000), PR status (P=0.000) and molecular subtypes (P=0.000). Kaplan-Meier analysis showed that increased CDKN2A expression was associated with increased survival time in breast cancer patients (P=0.000), especially in Luminal-like subtype. Univariate and multivariate Cox analyses indicated that CDKN2A expression was an independent prognostic biomarker for breast cancer (P=0.037). GSEA suggested that pathways involving cell adhesion molecules (CAMs), cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity were differentially enriched in the CDKN2A-high expression group.Conclusion: Our research demonstrated that high CDKN2A mRNA expression was an independent protective factor for improved prognosis in Luminal-like breast cancer. Additionally, the signaling pathways related to CAMs, cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity regulated by CDKN2A mRNA expression should be further studied.

Synergy Between Kit Ligand (KL) and IL-4 In Mast Cells Is Mediated by Cross-Receptor Interactions In Lipid Rafts.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1564-1564
Author(s):  
Maheswaran Mani ◽  
Shivkumar Venkatasubrahmanyam ◽  
Yujun Yang ◽  
Mark Krampf ◽  
Jing Huang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mast Cells ◽  
Tyrosine Phosphorylation ◽  
Lipid Raft ◽  
Cytokine Receptor ◽  
General Mechanism ◽  
Membrane Microdomains ◽  
Type I ◽  
Receptor Interactions ◽  
Restricted Type

Abstract Abstract 1564 Studies of erythroid and thymic differentiation have shown that cross-receptor interactions between the stem cell factor receptor Kit, a receptor tyrosine kinase (RTK), and tissue-restricted Type I cytokine receptors (EpoR and IL-7R, respectively) are necessary for normal development of each lineage. To determine whether these Kit-Type I cytokine receptor interactions are a ubiquitous phenomena in Kit (+) hematopoietic cells, we studied murine bone marrow derived mast cells (BMMC), which express Kit and IL-4R, and are responsive to both cognate ligands. Both KL and IL-4 were individually mitogenic; combinations of KL and IL-4 synergistically promoted BMMC proliferation, even at suboptimal concentrations of each ligand (Synergy Index 2.7 for SCF 20ng/ml + IL-4 5ng/ml). Similar to the results seen previously with Kit and EpoR or IL-7R, activation of Kit by KL resulted in cross-receptor tyrosine phosphorylation of the IL-4Rα and γc subunits of IL-4R, even in the absence of their cognate ligand, IL-4. Each subunit of the IL-4R was independently phosphorylated by activated Kit, in the absence of Jak3. Furthermore, in the malignant mast cell line HMC-1, inhibition of oncogenic Kit by imatinib also reversed constitutive phosphorylation of IL-4R. Previous studies have shown that STAT 1α, STAT 5A, and STAT 5B, but not Stat6, are bound to and directly phosphorylated by activated Kit. In contrast, STAT6 is activated by engagement of IL-4R by its cognate ligand. Cross-receptor phosphorylation of IL-4R by activated Kit in BMMC induced STAT6 phosphorylation, with the same apparent pI as after activation of IL-4R by cognate ligand. Subcellular fractionation showed that activated Kit, γc, Jak3, and STATs were localized in lipid raft fractions upon KL stimulation. Inhibition of lipid raft formation by MβCD resulted in loss of both cross-receptor tyrosine phosphorylation of IL-4R by Kit and synergistic proliferation, but not proliferation induced by each cognate ligand. Gene expression analyses of KL stimulated BMMC from wt and IL-4Rα/γc deficient mice demonstrated that over 30% of the Kit gene signature was dependent on the presence of the IL-4R. Together, the data indicate that the synergy of KL and IL-4 in BMMC is mediated by cross-receptor interactions between Kit and IL-4R in raft membrane microdomains. The Kit-IL-4R interaction is the third cross-receptor interaction described between the Kit RTK and a tissue-restricted Type I cytokine receptor. Besides RBC, thymocytes, and mast cells, such cross-receptor interactions are likely to be a general mechanism for synergistic and tissue-specific pleiotropic signaling by Kit in hematopoiesis and possibly other cell types, e.g., various Kit (+) stem cell populations and cancers. Disclosures: No relevant conflicts of interest to declare.

Studies of cytokine-cytokine receptor interactions: Influence of ligand dimerization

1995 ◽  
pp. 417-425 ◽  
Author(s):  
Larry D. Ward ◽  
Geoffrey J. Howlett ◽  
Robert L. Moritz ◽  
Annet Hammacher ◽  
Kiyoshi Yasukawa ◽  
...  
Keyword(s):  
Cytokine Receptor ◽  
Receptor Interactions

scholarly journals Cytokine–receptor interactions as drug targets

2010 ◽  
Vol 14 (4) ◽  
pp. 511-519 ◽  
Author(s):  
Gideon Schreiber ◽  
Mark R Walter
Keyword(s):  
Drug Targets ◽  
Cytokine Receptor ◽  
Receptor Interactions

scholarly journals Upregulated CDKN2A expression may be an independent protective factor in Luminal-like breast cancer

2020 ◽  
Author(s):  
Yier Qiu ◽  
Guowen Lu ◽  
Yingjie Wu
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Mrna Expression ◽  
Protective Factor ◽  
Killer Cell ◽  
Cytokine Receptor ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
Receptor Interactions ◽  
Cancer Tissues

Abstract Background Previous studies revealed that CDKN2A (cyclin-dependent kinase inhibitor 2A) functioned as a tumour suppressor in various types of malignant tumours. The aim of the study was to clarify the value of CDKN2A expression in the prognosis of breast cancer. Method Using the Cancer Genome Atlas (TCGA) database, we compared CDKN2A mRNA levels between breast cancer tissues and normal tissues and analyzed the relationship between clinical features and CDKN2A expression with the Wilcox test and the Kruskal-Wallis test. Kaplan-Meier and Cox analyses were performed to determine the correlation between CDKN2A expression and breast cancer prognosis. Gene set enrichment analysis (GSEA) was performed using the TCGA data set. Results We first found that CDKN2A expression was markedly higher in breast cancer tissues than in normal tissues using the TCGA database (P=0.000). In addition, CDKN2A mRNA expression in breast cancer was positively correlated with age (P=0.018), histological types (P=0.028), ER status (P=0.000), PR status (P=0.000) and molecular subtypes (P=0.000). Kaplan-Meier analysis showed that increased CDKN2A expression was associated with increased survival time in breast cancer patients (P=0.000), especially in Luminal-like subtype. Univariate and multivariate Cox analyses indicated that CDKN2A expression was an independent prognostic biomarker for breast cancer (P=0.037). GSEA suggested that pathways involving cell adhesion molecules (CAMs), cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity were differentially enriched in the CDKN2A-high expression group. Conclusion Our research demonstrated that high CDKN2A mRNA expression was an independent protective factor for improved prognosis in Luminal-like breast cancer. Additionally, the signaling pathways related to CAMs, cytokine-receptor interactions, cytosolic DNA sensing, the cell cycle, and killer cell-mediated cytotoxicity regulated by CDKN2A mRNA expression should be further studied.

The receptor–receptor interactions within the cytokine receptor superfamily. Role in neuroinflammation and beyond

2014 ◽  
Vol 20 (1) ◽  
pp. 6-7
Author(s):  
D.O. Borroto-Escuela ◽  
W. Romero-Fernandez ◽  
I. Brito ◽  
A.O. Tarakanov ◽  
D. Guidolin ◽  
...  
Keyword(s):  
Cytokine Receptor ◽  
Receptor Interactions
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