期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 103, 期 5, 页码 1327-1343出版社
WILEY
DOI: 10.1002/jcb.21513
关键词
non-classical secretion; FGF1; IL1 alpha
资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR015569, P20RR015555] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL032348, R01HL035627] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R15DK070599] Funding Source: NIH RePORTER
- NCRR NIH HHS [P20 RR015569-01, P20 RR015555, RR15555, P20 RR015569, RR15569] Funding Source: Medline
- NHLBI NIH HHS [HL35627, R01 HL032348, HL32348, R01 HL035627] Funding Source: Medline
- NIDDK NIH HHS [R15DK070599, R15 DK070599] Funding Source: Medline
A growing number of proteins devoid of signal peptides have been demonstrated to be released through the non-classical pathways independent of endoplasmic reticulum and Golgi. Among them are two potent proangiogenic cytokines FGF1 and IL1 alpha. Stress-induced transmembrane translocation of these proteins requires the assembly of copper-dependent multiprotein release complexes. It involves the interaction of exported proteins with the acidic phospholipids of the inner leaflet of the cell membrane and membrane destabilization. Not only stress, but also thrombin treatment and inhibition of Notch signaling stimulate the export of FGF1. Non-classical release of FGF1 and IL1 alpha presents a promising target for treatment of cardiovascular, oncologic, and inflammatory disorders.
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