Journal
NATURE COMMUNICATIONS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms8920
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Funding
- European Research Council
- British Heart Foundation
- Leducq Foundation
- Medical Research Council
- Department of Health via the National Institute for Health Research Comprehensive Biomedical Research Centre
- Intermediate British Heart Foundation [FS/14/1/30551]
- German Research Foundation (DFG) [815]
- MRC [G0600785, G1000458, G0700320, MR/L009684/1, MR/K003232/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/C503646/1] Funding Source: researchfish
- British Heart Foundation [PG/10/98/28655, PG/15/26/31373, RG/12/12/29872, FS/14/57/31138, FS/14/1/30551, RG/13/11/30384, PG/13/13/30018, FS/11/45/28859] Funding Source: researchfish
- Cancer Research UK [16463] Funding Source: researchfish
- Medical Research Council [998501, G0600785, G1000458, MR/L009684/1, G0700320, MR/K003232/1] Funding Source: researchfish
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Angiogenesis is essential for tissue development, wound healing and tissue perfusion, with its dysregulation linked to tumorigenesis, rheumatoid arthritis and heart disease. Here we show that pro-angiogenic stimuli couple to NADPH oxidase-dependent generation of oxidants that catalyse an activating intermolecular-disulphide between regulatory-RI alpha subunits of protein kinase A (PKA), which stimulates PKA-dependent ERK signalling. This is crucial to blood vessel growth as 'redox-dead' Cys17Ser RI alpha knock-in mice fully resistant to PKA disulphide-activation have deficient angiogenesis in models of hind limb ischaemia and tumour-implant growth. Disulphide-activation of PKA represents a new therapeutic target in diseases with aberrant angiogenesis.
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