The &lt;i&gt;c-fgr&lt;/i&gt;Proto-Oncogene: Expression in Epstein-Barr-Virus-Infected B Lymphocytes and in Cells of the Myelomonocytic and Granulocytic Lineages

Patel, Mukesh R.; Faulkner, Lee; Katz, David R.; Brickell, Paul M.

doi:10.1159/000163665

Cited by 4 publications

(3 citation statements)

References 12 publications

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“…Blr1 (CXCR‐5), CXCR3, and IL‐8R (CXCR‐2) are chemokine receptors, and after binding to their ligands, they have been shown to elicit signals leading to migration of B‐lymphocytes, T‐lymphocytes, and phagocytes, respectively. Similarly, C‐Fgr, a member of the Src gene family kinases, has been shown to stimulate chemotaxis by phagocytes [13]. Moreover, Pim‐2 is a serine/threonine kinase that phosphorylates different signaling molecules, most of which have been reported to promote the proliferation and survival of lymphocytes and phagocytes [14].…”

Section: Resultsmentioning

confidence: 99%

Chronic lung inflammation in aging mice

Aoshiba

Nagai

2007

FEBS Letters

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To determine whether aging is associated with a pro-inflammatory shift in the lung, inflammation and inflammation-related gene expression in the lungs of 12-week-old and 24-month-old Balb/c mice were studied. cDNA microarray and quantitative reverse transcription-polymerase chain reaction analyses showed that eight inflammation-related genes, including CD20, Burkitt lymphoma receptor 1, CXCR-3, provirus integration site for Moloney murine leukemia virus-2, CD72, IL-8RB, C-Fgr, and CD8b, were upregulated in the aged mice. Immunohistochemistry showed that the lungs of the aged mice contained increased numbers of CD4 cells, CD8 cells, B cells and macrophages. These results suggest that a pro-inflammatory shift occurs in the lungs of mice with aging.

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Section: Resultsmentioning

confidence: 99%

Chronic lung inflammation in aging mice

Aoshiba

Nagai

2007

FEBS Letters

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“…FGR is a member of the protein tyrosine kinases (PTKs) family. FGR gene expression has been shown to be restricted to peripheral blood granulocytes and monocytes, and tissue macrophages [ 37 ]. It further contributes to the regulation of immune responses, including neutrophils, monocytes, macrophages, mast cells, phagocytosis, cell adhesion, and migration [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Immune-associated biomarkers identification for diagnosing carotid plaque progression with uremia through systematical bioinformatics and machine learning analysis

et al. 2023

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Background Uremia is one of the most challenging problems in medicine and an increasing public health issue worldwide. Patients with uremia suffer from accelerated atherosclerosis, and atherosclerosis progression may trigger plaque instability and clinical events. As a result, cardiovascular and cerebrovascular complications are more likely to occur. This study aimed to identify diagnostic biomarkers in uremic patients with unstable carotid plaques (USCPs). Methods Four microarray datasets (GSE37171, GSE41571, GSE163154, and GSE28829) were downloaded from the NCBI Gene Expression Omnibus database. The Limma package was used to identify differentially expressed genes (DEGs) in uremia and USCP. Weighted gene co-expression network analysis (WGCNA) was used to determine the respective significant module genes associated with uremia and USCP. Moreover, a protein–protein interaction (PPI) network and three machine learning algorithms were applied to detect potential diagnostic genes. Subsequently, a nomogram and a receiver operating characteristic curve (ROC) were plotted to diagnose USCP with uremia. Finally, immune cell infiltrations were further analyzed. Results Using the Limma package and WGCNA, the intersection of 2795 uremia-related DEGs and 1127 USCP-related DEGs yielded 99 uremia-related DEGs in USCP. 20 genes were selected as candidate hub genes via PPI network construction. Based on the intersection of genes from the three machine learning algorithms, three hub genes (FGR, LCP1, and C5AR1) were identified and used to establish a nomogram that displayed a high diagnostic performance (AUC: 0.989, 95% CI 0.971–1.000). Dysregulated immune cell infiltrations were observed in USCP, showing positive correlations with the three hub genes. Conclusion The current study systematically identified three candidate hub genes (FGR, LCP1, and C5AR1) and established a nomogram to assist in diagnosing USCP with uremia using various bioinformatic analyses and machine learning algorithms. Herein, the findings provide a foothold for future studies on potential diagnostic candidate genes for USCP in uremic patients. Additionally, immune cell infiltration analysis revealed that the dysregulated immune cell proportions were identified, and macrophages could have a critical role in USCP pathogenesis.

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“…Since superoxide production in response to external stimuli has recently been reported in fibroblasts (4), mesangial cells (7), tonsilar B lymphocytes (9), and in lymphocytes immortalized by EBV (5, 6, 10) and since some ofthe membrane components of the phagocyte NADPH oxidase have been found to be present in these cells (4, 9), we postulated that the cytosolic components of the enzyme might be present as well. In addition, transformed B lymphoblasts demonstrate enhanced expression of surface adhesion molecules such as CD2, CD48, and LFA-3 as well as expression of the granulocyte-specificfgr oncogene (34)(35)(36). Therefore, these B lymphoblasts have a GT deletion at base 75 and normal sequence at base 502.…”

Section: Discussionmentioning

confidence: 99%

In vitro molecular reconstitution of the respiratory burst in B lymphoblasts from p47-phox-deficient chronic granulomatous disease.

Volpp¹,

Lin²

1993

J. Clin. Invest.

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Epstein-Barr virus-transformed lymphocytes generate superoxide in response to various agonists in an enzymatic reaction similar to that which occurs in stimulated phagocytes. We generated transformed B lymphoblast cell lines from controls, from four patients with p47-phox-deficient chronic granulomatous disease, and from three parents. The cells from controls and from the parents generated 7.0-35 nmol of O°/107 cells per 30 min in response to phorbol myristate acetate. None of the patient cell lines generated any detectable superoxide. Both p47-phox and p67-phox were detected by immunoblot in the cytosol of control and parent cell lines and, as in neutrophils, these proteins had affinity for GTP-agarose. The patients' cell lines contained no detectable p47-phox by immunoblot. mRNA for both cytosolic proteins was detected in all cell lines. We generated cDNA and obtained multiple clones from two patients by polymerase chain reaction. One patient was a compound heterozygote with each allele resulting in an early stop codon. Clones derived from the other patient demonstrated only a GT deletion at base 75. The cDNA for p47-phox was inserted into an EBV-expression vector and stably transfected cell lines were obtained using hygromycin B selection. Transfected cell lines from a p47-phox-deficient patient generated normal levels of superoxide and had readily detectable cytosolic p47-phox. Thus, B lymphoblasts provide an excellent model system for studies of the NADPH oxidase, for expression of functional recombinant forms ofoxidase components, and for initial experimental approaches to genetic reconstitution in CGD. (J. Clin. Invest. 1993.91:201-207.)

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The <i>c-fgr</i>Proto-Oncogene: Expression in Epstein-Barr-Virus-Infected B Lymphocytes and in Cells of the Myelomonocytic and Granulocytic Lineages

Cited by 4 publications

References 12 publications

Chronic lung inflammation in aging mice

Chronic lung inflammation in aging mice

Immune-associated biomarkers identification for diagnosing carotid plaque progression with uremia through systematical bioinformatics and machine learning analysis

In vitro molecular reconstitution of the respiratory burst in B lymphoblasts from p47-phox-deficient chronic granulomatous disease.

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