From Wikipedia, the free encyclopedia
Prader-Willi/Angelman region-1, also known as PAR1, is a human gene.[1]
[edit] References
[edit] Further reading
- Sutcliffe JS, Nakao M, Christian S, et al. (1995). "Deletions of a differentially methylated CpG island at the SNRPN gene define a putative imprinting control region.". Nat. Genet. 8 (1): 52–8. doi:10.1038/ng0994-52. PMID 7987392.
- Schulze A, Hansen C, Skakkebaek NE, et al. (1996). "Exclusion of SNRPN as a major determinant of Prader-Willi syndrome by a translocation breakpoint.". Nat. Genet. 12 (4): 452–4. doi:10.1038/ng0496-452. PMID 8630505.
- Christian SL, Bhatt NK, Martin SA, et al. (1998). "Integrated YAC contig map of the Prader-Willi/Angelman region on chromosome 15q11-q13 with average STS spacing of 35 kb.". Genome Res. 8 (2): 146–57. PMID 9477342.
- Wirth J, Back E, Hüttenhofer A, et al. (2001). "A translocation breakpoint cluster disrupts the newly defined 3' end of the SNURF-SNRPN transcription unit on chromosome 15.". Hum. Mol. Genet. 10 (3): 201–10. PMID 11159938.
- Dorsam RT, Tuluc M, Kunapuli SP (2005). "Role of protease-activated and ADP receptor subtypes in thrombin generation on human platelets.". J. Thromb. Haemost. 2 (5): 804–12. doi:10.1111/j.1538-7836.2004.00692.x. PMID 15099288.
- Nakayama T, Hirano K, Hirano M, et al. (2004). "Inactivation of protease-activated receptor-1 by proteolytic removal of the ligand region in vascular endothelial cells.". Biochem. Pharmacol. 68 (1): 23–32. doi:10.1016/j.bcp.2004.03.005. PMID 15183114.
- Shi X, Gangadharan B, Brass LF, et al. (2005). "Protease-activated receptors (PAR1 and PAR2) contribute to tumor cell motility and metastasis.". Mol. Cancer Res. 2 (7): 395–402. PMID 15280447.
- Heider I, Schulze B, Oswald E, et al. (2005). "PAR1-type thrombin receptor stimulates migration and matrix adhesion of human colon carcinoma cells by a PKCepsilon-dependent mechanism.". Oncol. Res. 14 (10): 475–82. PMID 15559761.
- Tantivejkul K, Loberg RD, Mawocha SC, et al. (2005). "PAR1-mediated NFkappaB activation promotes survival of prostate cancer cells through a Bcl-xL-dependent mechanism.". J. Cell. Biochem. 96 (3): 641–52. doi:10.1002/jcb.20533. PMID 16052512.
