Journal of Leukocyte Biology | |
CXC chemokines in angiogenesis | |
Jan E. Ehlert2  Marie D. Burdick1  Christina L. Addison2  John A. Belperio2  Robert M. Strieter1  Douglas A. Arenberg2  Michael P. Keane2  | |
[1] Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Los Angeles School of Medicine; and Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Los Angeles School of Medicine; and Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Los Angeles School of Medicine; and;Department of Internal Medicine, Division of Pulmonary and Critical Medicine, The University of Michigan Medical School, Ann Arbor Department of Internal Medicine, Division of Pulmonary and Critical Medicine, The University of Michigan Medical School, Ann Arbor Department of Internal Medicine, Division of Pulmonary and Critical Medicine, The University of Michigan Medical School, Ann Arbor | |
关键词: cytokines; neovascularization; wound repair; tumorigenesis; tumor metastasis; | |
DOI : | |
学科分类:生理学 | |
来源: Federation of American Societies for Experimental Biology | |
【 摘 要 】
A variety of factors have been identified that regulate angiogenesis, including the CXC chemokine family. The CXC chemokines are a unique family of cytokines for their ability to behave in a disparate manner in the regulation of angiogenesis. CXC chemokines have four highly conserved cysteine amino acid residues, with the first two cysteine amino acid residues separated by one non-conserved amino acid residue (i.e., CXC). A second structural domain within this family determines their angiogenic potential. The NH2 terminus of the majority of the CXC chemokines contains three amino acid residues (Glu-Leu-Arg: the ELR motif), which precedes the first cysteine amino acid residue of the primary structure of these cytokines. Members that contain the ELR motif (ELR+) are potent promoters of angiogenesis. In contrast, members that are inducible by interferons and lack the ELR motif (ELR−) are potent inhibitors of angiogenesis. This difference in angiogenic activity may impact on the pathogenesis of a variety of disorders.
【 授权许可】
Unknown
【 预 览 】
Files | Size | Format | View |
---|---|---|---|
RO201912010181937ZK.pdf | 40KB | download |