Khandaker, M H

CXCR1 and CXCR2 are rapidly down-modulated by bacterial endotoxin through a unique agonist-independent, tyrosine kinase-dependent mechanism. [electronic resource] - Journal of immunology (Baltimore, Md. : 1950) Aug 1998 - 1930-8 p. digital

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

0022-1767


Antigens, CD--biosynthesis
Benzoquinones
Down-Regulation--drug effects
Enzyme Inhibitors--pharmacology
Enzyme Precursors--metabolism
GTP-Binding Proteins--physiology
Genistein--pharmacology
Humans
Interleukin-1--metabolism
Interleukin-8--metabolism
Intracellular Signaling Peptides and Proteins
Lactams, Macrocyclic
Lipopolysaccharides--pharmacology
Molecular Weight
Neutrophil Activation--immunology
Neutrophils--enzymology
Phosphorylation
Protein-Tyrosine Kinases--antagonists & inhibitors
Quinones--pharmacology
Receptors, Chemokine--agonists
Receptors, Interleukin--agonists
Receptors, Interleukin-8A
Receptors, Interleukin-8B
Rifabutin--analogs & derivatives
Signal Transduction--drug effects
Syk Kinase
Time Factors
Tumor Necrosis Factor-alpha--metabolism
Tyrosine--metabolism