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Caveolae-associated protein 2 or Cavin-2 is a protein that in humans is encoded by the CAVIN2gene (previously SDPR).[5][6][7] Cavin-2 is highly expressed in a variety of human endothelial cells.[8]
This gene has a calcium-independent phospholipid-binding protein whose expression increases in serum-starved cells. This protein has also been shown to be a substrate for protein kinase C (PKC) phosphorylation.[7]
Cavin-2 is required for blood vessel formation (angiogenesis) in humans and zebrafish and required also for the endothelial cell proliferation, migration and invasion in humans.[8] Cavin-2 plays an important role in endothelial cell maintenance by regulating eNOS activity.[8] Cavin-2 controls the generation of nitric oxide (NO) in human endothelial cells by controlling the activity and stability of the protein endothelial nitric-oxide synthase (eNOS).[8]
Cavin-2 is highly secreted from human endothelial cells (HUVEC), they are secreted through endothelial microparticles (EMPs) but not exosomes and is required for EMP biogenesis.[8]
Cavin-2/SDPR is shown to act as a metastasis suppressor by xenograft studies utilizing breast cancer cell lines.[9]
Cavin-2 may elicit its metastasis suppressor function by directly interacting with ERK and limiting its pro-survival role.[9] Moreover, it is suggested that cavin-2 is silenced during breast cancer progression by promoterDNA methylation.[9] Metastasis suppressor role of cavin-2 may go beyond breast cancer since tumor samples from bladder, colorectal, lung, pancreatic, and ovarian cancers as well as sarcomas also exhibited loss of cavin-2 expression.[9]
↑"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
↑"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
↑Gustincich S, Vatta P, Goruppi S, Wolf M, Saccone S, Della Valle G, etal. (April 1999). "The human serum deprivation response gene (SDPR) maps to 2q32-q33 and codes for a phosphatidylserine-binding protein". Genomics. 57 (1): 120–9. doi:10.1006/geno.1998.5733. PMID10191091.
↑Gustincich S, Schneider C (September 1993). "Serum deprivation response gene is induced by serum starvation but not by contact inhibition". Cell Growth & Differentiation. 4 (9): 753–60. PMID8241023.
Cross SH, Charlton JA, Nan X, Bird AP (March 1994). "Purification of CpG islands using a methylated DNA binding column". Nature Genetics. 6 (3): 236–44. doi:10.1038/ng0394-236. PMID8012384. S2CID12847618.
Gevaert K, Goethals M, Martens L, Van Damme J, Staes A, Thomas GR, Vandekerckhove J (May 2003). "Exploring proteomes and analyzing protein processing by mass spectrometric identification of sorted N-terminal peptides". Nature Biotechnology. 21 (5): 566–9. doi:10.1038/nbt810. PMID12665801. S2CID23783563.
Brandenberger R, Wei H, Zhang S, Lei S, Murage J, Fisk GJ, etal. (June 2004). "Transcriptome characterization elucidates signaling networks that control human ES cell growth and differentiation". Nature Biotechnology. 22 (6): 707–16. doi:10.1038/nbt971. PMID15146197. S2CID27764390.
