描述：
CXCL5, also known as epithelial cellderived neutrophilactivating peptide (ENA-78), is an 8
kDa proinflammatory member of the CXC subfamily of chemokines. Its Glu-Leu-Arg (ELR)
motif confers angiogenic properties and distinguishes it from ELR-CXC chemokines which are
angiostatic. Human CXCL5 shares 57% amino acid (aa) sequence identity with mouse and rat
CXCL5. Among other human ELR+ chemokines, it shares 77% aa sequence identity with
CXCL6/GCP-2 and 35% 51% with CXCL1/GRO alpha, CXCL2/GRO beta, CXCL3/GRO gamma,
CXCL7/NAP-2, and CXCL8/IL8. Inflammatory stimulation upregulates CXCL5 production in
multiple hematopoietic cell types, fibroblasts, endothelial cells, and vascular smooth muscle
cells. In vivo, CXCL5 is elevated at sites of inflammation and pulmonary fibrosis where it
promotes neutrophil infiltration and activation as well as angiogenesis. Its upregulation
contributes to increased vascularization, tumor growth, and metastasis in many cancers. Full
length CXCL5 (78 aa) is trimmed at the Nterminus by cathepsin G and chymotrypsin to ENA-74
(74 aa) and ENA-70 (70 aa), with the shortened forms showing increased potency relative to
full length CXCL5. CXCL5 exerts its effects primarily through interactions with CXCR-2.
It also binds duffy antigen receptor for chemokines (DARC), which can limit CXCR2mediated
responses.
原厂资料：
CXCL5, also known as epithelial cellderived neutrophilactivating peptide (ENA-78), is an 8
kDa proinflammatory member of the CXC subfamily of chemokines. Its Glu-Leu-Arg (ELR)
motif confers angiogenic properties and distinguishes it from ELR-CXC chemokines which are
angiostatic. Human CXCL5 shares 57% amino acid (aa) sequence identity with mouse and rat
CXCL5. Among other human ELR+ chemokines, it shares 77% aa sequence identity with
CXCL6/GCP-2 and 35% 51% with CXCL1/GRO alpha, CXCL2/GRO beta, CXCL3/GRO gamma,
CXCL7/NAP-2, and CXCL8/IL8. Inflammatory stimulation upregulates CXCL5 production in
multiple hematopoietic cell types, fibroblasts, endothelial cells, and vascular smooth muscle
cells. In vivo, CXCL5 is elevated at sites of inflammation and pulmonary fibrosis where it
promotes neutrophil infiltration and activation as well as angiogenesis. Its upregulation
contributes to increased vascularization, tumor growth, and metastasis in many cancers. Full
length CXCL5 (78 aa) is trimmed at the Nterminus by cathepsin G and chymotrypsin to ENA-74
(74 aa) and ENA-70 (70 aa), with the shortened forms showing increased potency relative to
full length CXCL5. CXCL5 exerts its effects primarily through interactions with CXCR-2.
It also binds duffy antigen receptor for chemokines (DARC), which can limit CXCR2mediated
responses.
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