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Epidermal growth factor receptor tyrosine kinase inhibitor reverses mesenchymal to epithelial phenotype and inhibits metastasis in inflammatory breast cancer.

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OBJECTIVE Inflammatory breast cancer (IBC) is a rare but aggressive type of advanced breast cancer. Epidermal growth factor receptor (EGFR) expression is an independent poor prognostic factor in IBC. The purpose of this study was to determine the effect on IBC tumorigenicity and metastasis of

Mechanism of Mer receptor tyrosine kinase inhibition of glomerular endothelial cell inflammation.

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Endotoxin induces a variety of proinflammatory mediators and plays a crucial role in kidney inflammation. The receptor tyrosine kinase, Mer, diminishes renal inflammation by attenuating inflammatory responses. We previously reported that Mer is predominantly expressed on glomerular endothelial cells

Roles of macrophage stimulating protein and tyrosine kinase receptor RON in smoke-induced airway inflammation of rats.

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OBJECTIVE To investigate the roles of macrophage stimulating protein (MSP) and its tyrosine kinase receptor RON in smoke-induced airway inflammation of rats. METHODS Inhalation of combustion smoke was administered in rats to induce airway inflammation. Alveolar macrophages (AM) of healthy and

Linking tyrosine kinase inhibitor-mediated inflammation with normal epithelial cell homeostasis and tumor therapeutic responses.

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Receptor tyrosine kinases (RTKs) bearing oncogenic mutations in EGFR, ALK and ROS1 occur in a significant subset of lung adenocarcinomas. Tyrosine kinase inhibitors (TKIs) targeting tumor cells dependent on these oncogenic RTKs yield tumor shrinkage, but also a variety of adverse events. Skin

RON receptor tyrosine kinase, a negative regulator of inflammation, is decreased during simian immunodeficiency virus-associated central nervous system disease.

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Expressed on tissue-resident macrophages, the receptor tyrosine kinase, recepteur d'orgine nantais (RON), functions to maintain inflammation homeostasis by activating genes that promote wound repair and resolve inflammation while repressing genes that perpetuate tissue damage and cell death. Chronic

Enhanced efferocytosis of apoptotic cardiomyocytes through myeloid-epithelial-reproductive tyrosine kinase links acute inflammation resolution to cardiac repair after infarction.

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BACKGROUND Efficient clearance of apoptotic cells (efferocytosis) is a prerequisite for inflammation resolution and tissue repair. After myocardial infarction, phagocytes are recruited to the heart and promote clearance of dying cardiomyocytes. The molecular mechanisms of efferocytosis of

The oral spleen tyrosine kinase inhibitor fostamatinib attenuates inflammation and atherogenesis in low-density lipoprotein receptor-deficient mice.

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OBJECTIVE Spleen tyrosine kinase (SYK) has come into focus as a potential therapeutic target in chronic inflammatory diseases, such as rheumatoid arthritis and asthma, as well as in B-cell lymphomas. SYK has also been involved in the signaling of immunoreceptors, cytokine receptors, and integrins.

Tyrosine kinases in inflammatory dermatologic disease.

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Tyrosine kinases (TKs) are enzymes that catalyze the phosphorylation of tyrosine residues on protein substrates. They are key components of signaling pathways that drive an array of cellular responses including proliferation, differentiation, migration, and survival. Specific TKs have recently been

The Role of Tyrosine Phosphorylation of Protein Kinase C Delta in Infection and Inflammation.

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Protein Kinase C (PKC) is a family composed of phospholipid-dependent serine/threonine kinases that are master regulators of inflammatory signaling. The activity of different PKCs is context-sensitive and these kinases can be positive or negative regulators of signaling pathways. The delta isoform

Small molecule tyrosine kinase inhibitors for the treatment of intestinal inflammation.

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BACKGROUND We developed a series of dendritic cell autoimmune modulators (DCAMs) based on small molecule Flt3 receptor tyrosine kinase inhibitors (TKIs) for the inhibition of intestinal inflammation and oral delivery. METHODS DCAMs were administered orally during and after induction of dextran

A case of inflammatory nonscarring alopecia associated with the tyrosine kinase inhibitor nilotinib.

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OBJECTIVE Nilotinib, a recently approved multitargeted tyrosine kinase inhibitor targeting the BCR-Abl translocation involved in chronic myelogenous leukemia, reportedly produces alopecia according to the package insert, but clinical and histologic descriptions of the alopecia are lacking. METHODS A

Spleen tyrosine kinase inhibition blocks airway constriction and protects from Th2-induced airway inflammation and remodeling.

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BACKGROUND Spleen tyrosine kinase (Syk) is an intracellular nonreceptor tyrosine kinase, which has been implicated as central immune modulator promoting allergic airway inflammation. Syk inhibition has been proposed as a new therapeutic approach in asthma. However, the direct effects of Syk

Oxidative stress triggers tyrosine phosphorylation in B cells through a redox- and inflammatory cytokine-sensitive mechanism.

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Exposure to oxidants such as hydrogen peroxide (H2O2) and gamma-ray irradiation has been recently shown to trigger tyrosine phosphorylation in B cells as does cross-linking surface immunoglobulin (sIg) by antigens or anti-immunoglobulins. We studied the mechanism by which H2O2 induced tyrosine

The tyrosine kinase inhibitor tyrphostin AG126 reduces the development of acute and chronic inflammation.

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Protein tyrosine kinases help to regulate the expression of many genes that play important roles in inflammation. Here we investigate the effects of the tyrosine kinase inhibitor tyrphostin AG126 in two animal models of acute and chronic inflammation, carrageenan-induced pleurisy and

Protection against peroxynitrite dependent tyrosine nitration and alpha 1-antiproteinase inactivation by some anti-inflammatory drugs and by the antibiotic tetracycline.

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OBJECTIVE To examine in vitro the ability of several drugs to protect against deleterious effects of peroxynitrite, a cytotoxic agent formed by reaction of nitric oxide with superoxide radical, that may be generated in the rheumatoid joint and could cause joint damage. METHODS The ability of several

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