Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
6
0

Year Published

2020
2020
2022
2022

Publication Types

Select...
4

Relationship

3
1

Authors

Journals

citations
Cited by 7 publications
(6 citation statements)
references
References 7 publications
(7 reference statements)
0
6
0
Order By: Relevance
“…VCP expression was also found to be progressively decreased in the mouse hearts, along with persistent pressure overload [16]. Reciprocally, cardiac-specific overexpression of VCP attenuated the pressure overload-induced cardiac pathogenesis [19]. These phenomena are linked to the inhibitory effects of VCP on the transduction of the AKT/mTOC1R/S6K signaling pathway [16].…”
Section: Vcp Represents a New Regulator In Cardiac Er And Mitochondria Functions And Is Involved In Various Heart Diseasesmentioning
confidence: 93%
See 1 more Smart Citation
“…VCP expression was also found to be progressively decreased in the mouse hearts, along with persistent pressure overload [16]. Reciprocally, cardiac-specific overexpression of VCP attenuated the pressure overload-induced cardiac pathogenesis [19]. These phenomena are linked to the inhibitory effects of VCP on the transduction of the AKT/mTOC1R/S6K signaling pathway [16].…”
Section: Vcp Represents a New Regulator In Cardiac Er And Mitochondria Functions And Is Involved In Various Heart Diseasesmentioning
confidence: 93%
“…In addition, the VCP expression level was also shown to be upregulated in some cancers, mainly in response to the increased burden of protein degradation, indicating that VCP inhibition could be a promising therapeutic approach to cancer management [13][14][15]. Furthermore, recent studies also found that VCP participates in cardiomyocyte growth and survival, and plays a protective role against the stress-induced pathogenesis in heart diseases by attenuating mitochondrial and ER stress through regulating calcium homeostasis [16][17][18][19].…”
Section: Introductionmentioning
confidence: 99%
“…Elevated levels of phosphorylated RPS6 are correlated with increased activity of the mTORC1 (mechanistic target of rapamycin complex 1) pathway. Under physiological conditions, Vcp is known to inhibit mTORC1 signaling [ 28 , 29 , 30 ]. Interestingly, we found significant upregulation of phosphorylated RPS6 (pRPS6) ( Figure 4 B,E) (N = 4; p = 0.0286) in vcp ex3/ex3 mutant embryos compared to controls, whereas total RPS6 protein levels were unchanged in vcp ex3/ex3 mutant embryos ( Figure 4 B,D) (N = 4; p = 0.3143), suggesting activated mTOR signaling and thereby the repression of autophagy [ 31 ].…”
Section: Resultsmentioning
confidence: 99%
“…Pressure overload suppresses the expression of VCP/p97 which activated mTORC2 and attenuates the inhibitive effect of VCP/p97 on mTORC1 signaling, subsequently promotes the protein synthesis pathway ( Figure 2 ). While VCP/p97 overexpression restores the pressure overload-suppressed VCP/p97 and represses the pressure overload-induced activation of mTORC1, protects the heart against pressure overload-induced cardiac hypertrophy [ 65 ] ( Figure 2 ).…”
Section: Vcp/p97 and Ischemia/reperfusion Injurymentioning
confidence: 99%