Antiproliferative activity of CCN3: Involvement of the C-terminal module and post-translational regulation A.M. Bleau and N. Planque contributed equally to this work.
dc.contributor.author | Bleau, A. M. | en_US |
dc.contributor.author | Planque, N. | en_US |
dc.contributor.author | Lazar, N. | en_US |
dc.contributor.author | Zambelli, D. | en_US |
dc.contributor.author | Ori, A. | en_US |
dc.contributor.author | Quan, T. | en_US |
dc.contributor.author | Fisher, G. J. | en_US |
dc.contributor.author | Scotlandi, K. | en_US |
dc.contributor.author | Perbal, Bernard | en_US |
dc.date.accessioned | 2007-09-20T19:04:31Z | |
dc.date.available | 2008-09-08T14:25:14Z | en_US |
dc.date.issued | 2007-08-15 | en_US |
dc.identifier.citation | Bleau, A.M.; Planque, N.; Lazar, N.; Zambelli, D.; Ori, A.; Quan, T.; Fisher, G.; Scotlandi, K.; Perbal, B. (2007)."Antiproliferative activity of CCN3: Involvement of the C-terminal module and post-translational regulation A.M. Bleau and N. Planque contributed equally to this work. ." Journal of Cellular Biochemistry 101(6): 1475-1491. <http://hdl.handle.net/2027.42/56135> | en_US |
dc.identifier.issn | 0730-2312 | en_US |
dc.identifier.issn | 1097-4644 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/56135 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17340618&dopt=citation | en_US |
dc.description.abstract | Previous work had suggested that recombinant CCN3 was partially inhibiting cell proliferation. Here we show that native CCN3 protein secreted into the conditioned medium of glioma transfected cells indeed induces a reduction in cell proliferation. Large amounts of CCN3 are shown to accumulate both cytoplasmically and extracellularly as cells reach high density, therefore highlighting new aspects on how cell growth may be regulated by CCN proteins. Evidence is presented establishing that the amount of CCN3 secreted into cell culture medium is regulated by post-translational proteolysis. As a consequence, the production of CCN3 varies throughout the cell cycle and CCN3 accumulates at the G2/M transition of the cycle. We also show that CCN3-induced inhibition of cell growth can be partially reversed by specific antibodies raised against a C-terminal peptide of CCN3. The use of several clones expressing various portions of CCN3 established that the CT module of CCN3 is sufficient to induce cell growth inhibition. J. Cell. Biochem. 101: 1475–1491, 2007. © 2007 Wiley-Liss, Inc. | en_US |
dc.format.extent | 347132 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
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 | Antiproliferative activity of CCN3: Involvement of the C-terminal module and post-translational regulation A.M. Bleau and N. Planque contributed equally to this work. | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Genetics | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | 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 Dermatology, University of Michigan Medical School, 1150 W. Medical Center Dr., Medical Science I, Room 6447, Ann Arbor, Michigan 48109-0609 | en_US |
dc.contributor.affiliationum | Department of Dermatology, University of Michigan Medical School, 1150 W. Medical Center Dr., Medical Science I, Room 6447, Ann Arbor, Michigan 48109-0609 | en_US |
dc.contributor.affiliationother | UniversitÉ Paris7-D. Diderot, UFR de Biochimie, Laboratoire d'Oncologie Virale et MolÉculaire, 2 place Jussieu, 75005 Paris, France | en_US |
dc.contributor.affiliationother | UniversitÉ Paris7-D. Diderot, UFR de Biochimie, Laboratoire d'Oncologie Virale et MolÉculaire, 2 place Jussieu, 75005 Paris, France | en_US |
dc.contributor.affiliationother | UniversitÉ Paris7-D. Diderot, UFR de Biochimie, Laboratoire d'Oncologie Virale et MolÉculaire, 2 place Jussieu, 75005 Paris, France | en_US |
dc.contributor.affiliationother | Laboratorio di Ricerca Oncologica, Istituti Ortopedici Rizzoli, Via Di Barbiano 1/10, 40136 Bologna, Italy | en_US |
dc.contributor.affiliationother | UniversitÉ Paris7-D. Diderot, UFR de Biochimie, Laboratoire d'Oncologie Virale et MolÉculaire, 2 place Jussieu, 75005 Paris, France ; Laboratorio di Ricerca Oncologica, Istituti Ortopedici Rizzoli, Via Di Barbiano 1/10, 40136 Bologna, Italy | en_US |
dc.contributor.affiliationother | Laboratorio di Ricerca Oncologica, Istituti Ortopedici Rizzoli, Via Di Barbiano 1/10, 40136 Bologna, Italy | en_US |
dc.contributor.affiliationother | UniversitÉ Paris7-D. Diderot, UFR de Biochimie, Laboratoire d'Oncologie Virale et MolÉculaire, 2 place Jussieu, 75005 Paris, France ; UniversitÉ Paris7-D. Diderot, UFR de Biochimie, Laboratoire d'Oncologie Virale et MolÉculaire, 2 place Jussieu, Case 7048, 75005 Paris, France. | en_US |
dc.identifier.pmid | 17340618 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/56135/1/21262_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/jcb.21262 | en_US |
dc.identifier.source | Journal of Cellular Biochemistry | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.