scholarly journals Cyclin G2 Suppresses Glomerulosclerosis by Regulating Canonical Wnt Signalling

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Chenyang Zhao ◽  
Jinlan Gao ◽  
Sen Li ◽  
Qi Liu ◽  
Xiaoyu Hou ◽  
...  

Recent data has shown that cyclin G2 (CCNG2) is an atypical cyclin that inhibits cell cycle progression and is often dysregulated in human cancers. The involvement of cyclin G2 in the occurrence and development of diabetic nephropathy (DN) has not been determined. In the present study, we conducted cyclin G2 knockout studies to determine whether this protein regulates glomerulosclerosis in DN mice. We found that cyclin G2 regulated the expression of renal glomerulosclerosis-related proteins via the canonical Wnt signalling pathway in glomerular mesangial cells. A cyclin G2 deficiency resulted in more severe renal injury in DN mice. These findings provided new insight into the pathogenesis of DN, revealing that cyclin G2 has a protective role in glomerulosclerosis and is a potential new target for the prevention and treatment of DN.

2019 ◽  
Vol 2019 ◽  
pp. 1-1
Author(s):  
Chenyang Zhao ◽  
Jinlan Gao ◽  
Sen Li ◽  
Qi Liu ◽  
Xiaoyu Hou ◽  
...  

2019 ◽  
Vol 20 (17) ◽  
pp. 4168 ◽  
Author(s):  
Mark Agostino ◽  
Sebastian Öther-Gee Pohl

Several proteins other than the frizzled receptors (Fzd) and the secreted Frizzled-related proteins (sFRP) contain Fzd-type cysteine-rich domains (CRD). We have termed these domains “putative Fzd-type CRDs”, as the relevance of Wnt signalling in the majority of these is unknown; the RORs, an exception to this, are well known for mediating non-canonical Wnt signalling. In this study, we have predicted the likely binding affinity of all Wnts for all putative Fzd-type CRDs. We applied both our previously determined Wnt‒Fzd CRD binding affinity prediction model, as well as a newly devised model wherein the lipid term was forced to contribute favourably to the predicted binding energy. The results obtained from our new model indicate that certain putative Fzd CRDs are much more likely to bind Wnts, in some cases exhibiting selectivity for specific Wnts. The results of this study inform the investigation of Wnt signalling modulation beyond Fzds and sFRPs.


Author(s):  
Hongyou Zhao ◽  
Bin Yi ◽  
Zhipin Liang ◽  
Ches’Nique Phillips ◽  
Hui-Yi Lin ◽  
...  

2020 ◽  
Vol 117 (35) ◽  
pp. 21609-21617
Author(s):  
Zhenxing Liu ◽  
Christopher P. Selby ◽  
Yanyan Yang ◽  
Laura A. Lindsey-Boltz ◽  
Xuemei Cao ◽  
...  

The circadian clock is a global regulatory mechanism that controls the expression of 50 to 80% of transcripts in mammals. Some of the genes controlled by the circadian clock are oncogenes or tumor suppressors. Among theseMychas been the focus of several studies which have investigated the effect of clock genes and proteins onMyctranscription and MYC protein stability. Other studies have focused on effects ofMycmutation or overproduction on the circadian clock in comparison to their effects on cell cycle progression and tumorigenesis. Here we have used mice with mutations in the essential clock genesBmal1,Cry1,andCry2to gain further insight into the effect of the circadian clock on this important oncogene/oncoprotein and tumorigenesis. We find that mutation of bothCry1andCry2, which abolishes the negative arm of the clock transcription–translation feedback loop (TTFL), causes down-regulation of c-MYC, and mutation ofBmal1,which abolishes the positive arm of TTFL, causes up-regulation of the c-MYC protein level in mouse spleen. These findings must be taken into account in models of the clock disruption–cancer connection.


2019 ◽  
Vol 61 ◽  
pp. 35-43
Author(s):  
Hongli Jiang ◽  
Jie Li ◽  
Xin He ◽  
Jinhong Xue ◽  
Shanshan Liang ◽  
...  

FEBS Letters ◽  
2011 ◽  
Vol 585 (3) ◽  
pp. 531-538 ◽  
Author(s):  
Brian Rooney ◽  
Helen O‧Donovan ◽  
Andrew Gaffney ◽  
Marie Browne ◽  
Noel Faherty ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0165438 ◽  
Author(s):  
Mei-Chi Chang ◽  
Yi-Ling Tsai ◽  
Eric Jein-Wein Liou ◽  
Chia-Mei Tang ◽  
Tong-Mei Wang ◽  
...  

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