NOV story: the way to CCN3
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BioMed Central
Open Access
Review
NOV story: the way to CCN3 Bernard Perbal* Address: Laboratoire d'Oncologie Virale et Moléculaire, Case 7048, UFR de Biochimie, Université Paris 7 – D. Diderot, 2 place Jussieu, 75005 ParisFrance Email: Bernard Perbal* - [email protected] * Corresponding author
Published: 20 February 2006 Cell Communication and Signaling2006, 4:3
doi:10.1186/1478-811X-4-3
Received: 10 February 2006 Accepted: 20 February 2006
This article is available from: http://www.biosignaling.com/content/4/1/3 © 2006Perbal; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract The principal aim of this historical review- the first in a new series- is to present the basic concepts that led to the discovery of NOV and to show how our ideas evolved regarding the role and functions of this new class of proteins. It should prove particularly useful to the new comers and to students who are engaged in this exciting field. It is also a good opportunity to acknowledge the input of those who participated in the development of this scientific endeavour
Introduction In this manuscript I am presenting milestones in our discovery of NOV (CCN3), a founding member the CCN family of regulatory proteins [1], now known to be composed of six members that play critical roles in normal fundamental biological processes including angiogenesis, wound repair, regulation of cell spreading proliferation and survival [2,3]. Alterations in the expression of CCN genes are also associated with cancerogenesis [4,5]. The past In my opinion, the « nov story » finds its roots in 1982 with the molecular cloning of a MAV-1(N) (myeloblastosis associated virus type 1) proviral genome that was shown to specifically induce nephroblastomas when injected into day-old chickens [6,7]. As a fellow on leave from the CNRS at UCLA in the laboratory of Pr. M. Baluda, I had cloned both the v-myb oncogene [8] and c-myb proto-oncogene [9] and I became interested in the molecular basis for MAV-induced nephroblastomas, which resemble the Wilms' tumors [10]. The MAV strains that were used at this time were inducing nephroblastomas, lymphoid leukosis and osteopetrosis [11]. Because these
strains were at best, plaque purified, it was not easy to assess the biological properties of MAV. Back at that time, the idea prevailed that retroviruses induced tumors by inserting in the vicinity of cellular proto-oncogenes. Pioneer work of Hayward, Astrin and collaborators had opened the road for my interest in identifying the integration sites of MAV. After my return to France, M. Brisac who was a student in my laboratory was given the task to characterize the MAV junction fragments in tumor DNA, with the help of Dr. G. Dambrine at the INRA who provided animal facilities and expertise in chicken pathology. Severa
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