scholarly journals The CCN family of genes: a brief history

2001 ◽  
Vol 54 (2) ◽  
pp. 103-104 ◽  
Author(s):  
B Perbal
Keyword(s):  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Zhenghui Cheng ◽  
Yawen Zhang ◽  
Yinchao Tian ◽  
Yuhan Chen ◽  
Fei Ding ◽  
...  

Abstract Background Schwann cells (SCs) play a crucial role in the repair of peripheral nerves. This is due to their ability to proliferate, migrate, and provide trophic support to axon regrowth. During peripheral nerve injury, SCs de-differentiate and reprogram to gain the ability to repair nerves. Cysteine-rich 61 (Cyr61/CCN1) is a member of the CCN family of matrix cell proteins and have been reported to be abundant in the secretome of repair mediating SCs. In this study we investigate the function of Cyr61 in SCs. Results We observed Cyr61 was expressed both in vivo and in vitro. The promoting effect of Cyr61 on SC proliferation and migration was through autocrine and paracrine mechanisms. SCs expressed αvβ3 integrin and the effect of Cyr61 on SC proliferation and migration could be blocked via αvβ3 integrin. Cyr61 could influence c-Jun protein expression in cultured SCs. Conclusions In this study, we found that Cyr61 promotes SC proliferation and migration via αvβ3 integrin and regulates c-Jun expression. Our study contributes to the understanding of cellular and molecular mechanisms underlying SC’s function during nerve injury, and thus, may facilitate the regeneration of peripheral nerves after injury.


2018 ◽  
Vol 225 (3) ◽  
Author(s):  
Jin‐Feng Zhao ◽  
Hsiang‐Ying Chen ◽  
Jeng Wei ◽  
Shr‐Jeng Jim Leu ◽  
Tzong‐Shyuan Lee

2015 ◽  
Vol 9 (3) ◽  
pp. 267-278 ◽  
Author(s):  
J. E. Wells ◽  
M. Howlett ◽  
L. C. Cheung ◽  
Ursula R. Kees

Author(s):  
Harumi Kawaki ◽  
Satoshi Kubota ◽  
Masaharu Takigawa
Keyword(s):  

Author(s):  
Satoshi Kubota ◽  
Harumi Kawaki ◽  
Masaharu Takigawa
Keyword(s):  

Author(s):  
Taihao Quan ◽  
Sharon Shin ◽  
Zhaoping Qin ◽  
Gary J. Fisher

1998 ◽  
Vol 18 (10) ◽  
pp. 6131-6141 ◽  
Author(s):  
Rong Zhang ◽  
Lidia Averboukh ◽  
Weimin Zhu ◽  
Hong Zhang ◽  
Hakryul Jo ◽  
...  

ABSTRACT By using a model system for cell transformation mediated by the cooperation of the activated H-ras oncogene and the inactivated p53 tumor suppressor gene, rCop-1 was identified by mRNA differential display as a gene whose expression became lost after cell transformation. Homology analysis indicates that rCop-1 belongs to an emerging cysteine-rich growth regulator family called CCN, which includes connective-tissue growth factor, CYR61, CEF10 (v-src inducible), and the product of thenov proto-oncogene. Unlike the other members of the CCN gene family, rCop-1 is not an immediate-early gene, it lacks the conserved C-terminal domain which was shown to confer both growth-stimulating and heparin-binding activities, and its expression is lost in cells transformed by a variety of mechanisms. Ectopic expression of rCop-1 by retroviral gene transfers led to cell death in a transformation-specific manner. These results suggest that rCop-1 represents a new class of CCN family proteins that have functions opposing those of the previously identified members.


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