Journal
BIOCHEMICAL SOCIETY TRANSACTIONS
Volume 40, Issue -, Pages 831-835Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BST20120051
Keywords
age-related macular degeneration; diabetic nephropathy; hepatitis C virus; serine-arginine protein kinase 1 (SRPK1); serine/arginine-rich splicing factor 1 (SRSF1); vascular endothelial growth factor (VEGF)
Categories
Funding
- Medical Research Council
- Diabetes UK [11/0004192]
- British Heart Foundation [PG 11/20/28792]
- Academy of Medical Sciences Clinician Scientist Fellowship [G0802829]
- Diabetes UK [11/0004192] Funding Source: researchfish
- Kidney Research UK [RP18/2010] Funding Source: researchfish
- Medical Research Council [G0802829] Funding Source: researchfish
- BBSRC [BB/J007293/1] Funding Source: UKRI
- MRC [G0802829] Funding Source: UKRI
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SRPK1 (serine-arginine protein kinase 1) is a protein kinase that specifically phosphorylates proteins containing serine-arginine-rich domains. Its substrates include a family of SR proteins that are key regulators of mRNA AS (alternative splicing). VEGF (vascular endothelial growth factor), a principal angiogenesis factor contains an alternative 3' splice site in the terminal exon that defines a family of isoforms with a different amino acid sequence at the C-terminal end, resulting in anti-angiogenic activity in the context of VEGF(165)-driven neovascularization. It has been shown recently in our laboratories that SRPK1 regulates the choice of this splice site through phosphorylation of the splicing factor SRSF1 (serine/arginine-rich splicing factor 1). The present review summarizes progress that has been made to understand how SRPK1 inhibition may be used to manipulate the balance of pro- and anti-angiogenic VEGF isoforms in animal models in vivo and therefore control abnormal angiogenesis and other pathophysiological processes in multiple disease states.
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