Topic
ANKRD1
About: ANKRD1 is a research topic. Over the lifetime, 92 publications have been published within this topic receiving 6550 citations. The topic is also known as: ALRP & C-193.
Papers published on a yearly basis
Papers
TL;DR: In vivo analysis revealed that MLP-deficient mice reproduce the morphological and clinical picture of dilated cardiomyopathy and heart failure in humans, providing the first model for this condition in a genetically manipulatable organism.
864 citations
TL;DR: It is shown that MARP family members contain within their ankyrin repeat region a binding site for the myofibrillar elastic protein titin, which links titin-N2A-based myofibillar stress/strain signals to a MARP-based regulation of muscle gene expression.
359 citations
TL;DR: CARP abnormalities may be involved in the pathogenesis of HCM and functional abnormalities caused by the ANKRD1 mutations were examined at the cellular level in neonatal rat cardiomyocytes.
169 citations
TL;DR: The hypothesis that Ankrd2 may be involved in sensing stress signals and linking these to muscle gene regulation is strengthened by showing that it not only binds the tumor suppressor protein p53 both in vitro and in vivo but also enhances the up-regulation of the p21(WAFI/CIPI) promoter by p53.
155 citations
TL;DR: Combined inhibition of MuRF1/MuRF2 could provide a potent strategy to stimulate striated muscles anabolically and to protect muscles from sarcopenia during ageing.
Abstract: The muscle-specific RING finger proteins MuRF1 and MuRF2 have been proposed to regulate protein degradation and gene expression in muscle tissues. We have tested the in vivo roles of MuRF1 and MuRF2 for muscle metabolism by using knockout (KO) mouse models. Single MuRF1 and MuRF2 KO mice are healthy and have normal muscles. Double knockout (dKO) mice obtained by the inactivation of all four MuRF1 and MuRF2 alleles developed extreme cardiac and milder skeletal muscle hypertrophy. Muscle hypertrophy in dKO mice was maintained throughout the murine life span and was associated with chronically activated muscle protein synthesis. During ageing (months 4–18), skeletal muscle mass remained stable, whereas body fat content did not increase in dKO mice as compared with wild-type controls. Other catabolic factors such as MAFbox/atrogin1 were expressed at normal levels and did not respond to or prevent muscle hypertrophy in dKO mice. Thus, combined inhibition of MuRF1/MuRF2 could provide a potent strategy to stimulate striated muscles anabolically and to protect muscles from sarcopenia during ageing.
151 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2021 | 2 |
| 2020 | 4 |
| 2019 | 3 |
| 2018 | 1 |
| 2017 | 5 |
| 2016 | 5 |