Rap1, a small GTP-binding protein is upregulated during arrest of proliferation in human keratinocytes
dc.contributor.author | D'Silva, Nisha J. | en_US |
dc.contributor.author | Mitra, R. S. | en_US |
dc.contributor.author | Zhang, Z. | en_US |
dc.contributor.author | Kurnit, David M. | en_US |
dc.contributor.author | Babcock, C. R. | en_US |
dc.contributor.author | Polverini, Peter J. | en_US |
dc.contributor.author | Carey, Thomas E. | en_US |
dc.date.accessioned | 2006-04-19T13:34:38Z | |
dc.date.available | 2006-04-19T13:34:38Z | |
dc.date.issued | 2003-09 | en_US |
dc.identifier.citation | D'Silva, N.J.; Mitra, R.S.; Zhang, Z.; Kurnit, D.M.; Babcock, C.R.; Polverini, P.J.; Carey, T.E. (2003)."Rap1, a small GTP-binding protein is upregulated during arrest of proliferation in human keratinocytes." Journal of Cellular Physiology 196(3): 532-540. <http://hdl.handle.net/2027.42/34444> | en_US |
dc.identifier.issn | 0021-9541 | en_US |
dc.identifier.issn | 1097-4652 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/34444 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=12891710&dopt=citation | en_US |
dc.description.abstract | Rap1 is a small GTP-binding protein (SMG) that exists in two 95% homologous isoforms, rap1A and rap1B. The functions of the rap1 proteins are not well understood. In this report we examined expression and function of rap1 in primary (HOKs) and immortalized (IHOKs) human oral keratinocytes under different growth conditions. In HOKs, rap1 increased with passage number, suggesting a role in differentiation and arrest of proliferation. Similarly, when inhibition of proliferation and differentiation were induced in HOKs by 1.2 mM CaCl 2 , both rap1 and involucrin increased with increasing concentrations of CaCl 2 . However, when similar experiments were done with IHOKs, which continue to proliferate in the presence of 1.2 mM CaCl 2 , the increase in involucrin expression was similar to HOKs but there was no substantial increase in rap1, suggesting that increased expression of rap1 is linked to inhibition of proliferation rather than differentiation of keratinocytes. Upon transfection of immortalized keratinocytes with rapGAP, which inactivates both isoforms of endogenous active rap1, enhanced proliferation was observed. Thus, we conclude that rap1 inhibits proliferation in keratinocytes. J. Cell. Physiol. 196: 532–540, 2003. © 2003 Wiley-Liss, Inc. | en_US |
dc.format.extent | 330194 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Cell & Developmental Biology | en_US |
dc.title | Rap1, a small GTP-binding protein is upregulated during arrest of proliferation in human keratinocytes | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Kinesiology and Sports | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Oral Medicine, Pathology and Oncology, University of Michigan School of Dentistry, Ann Arbor, Michigan ; Department of Oral Medicine, Pathology and Oncology, University of Michigan, School of Dentistry, 1011 N. University Ave, Rm 5217, Ann Arbor, MI 48109-1078. | en_US |
dc.contributor.affiliationum | Department of Oral Medicine, Pathology and Oncology, University of Michigan School of Dentistry, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Oral Medicine, Pathology and Oncology, University of Michigan School of Dentistry, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Departments of Pediatrics and Human Genetics, University of Michigan Medical Center, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Oral Medicine, Pathology and Oncology, University of Michigan School of Dentistry, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Oral Medicine, Pathology and Oncology, University of Michigan School of Dentistry, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Otolaryngology, Laboratory of Head and Neck Cancer Biology, The University of Michigan Medical School and the Comprehensive Cancer Center, Ann Arbor, Michigan | en_US |
dc.identifier.pmid | 12891710 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/34444/1/10331_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/jcp.10331 | en_US |
dc.identifier.source | Journal of Cellular Physiology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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