|
Hypertrophic Cardiomyopathy
|
0.640 |
GeneticVariation
|
disease |
BEFREE |
TRIM63 mutations, identified in patients with HCM, impart loss-of-function effects on E3 ligase activity and are probably causal mutations in HCM.
|
22821932 |
2012 |
|
Hypertrophic Cardiomyopathy
|
0.640 |
GeneticVariation
|
disease |
BEFREE |
The p.Q247X variant in TRIM63 is not likely to be a highly penetrant variant causing hypertrophic cardiomyopathy.
|
24436435 |
2014 |
|
Hypertrophic Cardiomyopathy
|
0.640 |
Biomarker
|
disease |
BEFREE |
These findings implicate an impaired interaction between titin and MURF1 as a novel mechanism underlying the pathogenesis of HCM.
|
31628103 |
2019 |
|
Hypertrophic Cardiomyopathy
|
0.640 |
GeneticVariation
|
disease |
BEFREE |
These data strongly supported that rare variants in MuRF1 and MuRF2 are associated with higher penetrance and more severe clinical manifestations of HCM.
|
24865491 |
2014 |
|
Diabetes Mellitus
|
0.040 |
Biomarker
|
group |
BEFREE |
Consequently, we confirmed reduced activity of mTOR signaling components and higher expression of atrophy-related markers typified by FoxO1/atrogin-1/MuRF1 and myostatin-Smad2/3 signaling during the course of diabetes.
|
30510624 |
2018 |
|
Diabetes Mellitus
|
0.040 |
GeneticVariation
|
group |
BEFREE |
Under various pathophysiological muscle-wasting conditions, such as diabetes and starvation, a family of ubiquitin ligases, including muscle-specific RING-finger protein 1 (MuRF1), are induced to target muscle proteins for degradation via ubiquitination.
|
18468620 |
2008 |
|
Diabetes Mellitus
|
0.040 |
Biomarker
|
group |
BEFREE |
The aim of this study was to evaluate the changes in biomarkers of skeletal muscle proteolysis (atrogin-1, muscle RING finger-1 protein [MuRF-1]) and inflammation (nuclear factor kappa-B) in skeletal muscles of rats under two catabolic conditions, diabetes mellitus (DM) and acute joint inflammation, and the effects of insulin therapy.
|
29497304 |
2018 |
|
Diabetes Mellitus
|
0.040 |
Biomarker
|
group |
BEFREE |
The present study investigated the effect of diabetes and acute muscle contraction upon the TRIM63 and FBXO32 expression as well as the potential involvement of some miRNAs.
|
28000044 |
2017 |
|
Diabetes
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
Under various pathophysiological muscle-wasting conditions, such as diabetes and starvation, a family of ubiquitin ligases, including muscle-specific RING-finger protein 1 (MuRF1), are induced to target muscle proteins for degradation via ubiquitination.
|
18468620 |
2008 |
|
Diabetes
|
0.030 |
Biomarker
|
disease |
BEFREE |
Consequently, we confirmed reduced activity of mTOR signaling components and higher expression of atrophy-related markers typified by FoxO1/atrogin-1/MuRF1 and myostatin-Smad2/3 signaling during the course of diabetes.
|
30510624 |
2018 |
|
Diabetes
|
0.030 |
Biomarker
|
disease |
BEFREE |
The present study investigated the effect of diabetes and acute muscle contraction upon the TRIM63 and FBXO32 expression as well as the potential involvement of some miRNAs.
|
28000044 |
2017 |
|
Multiple Myeloma
|
0.030 |
PosttranslationalModification
|
disease |
BEFREE |
The objective of this study was to investigate expression of the interferon regulatory factor family (IRF1-9) and the potential role of DNA methylation in silencing IRF genes in MM cell lines and purified MM cells from patients.
|
18922617 |
2008 |
|
Multiple Myeloma
|
0.030 |
Biomarker
|
disease |
BEFREE |
Consistent expression of both the viral homologues of IRF and IL-8R in myeloma suggests a possible role for these transforming viral genes in the pathogenesis of this disease.
|
10626142 |
1999 |
|
Multiple Myeloma
|
0.030 |
Biomarker
|
disease |
BEFREE |
The cellular interferon regulatory factor-4 (IRF-4), which is a member of IRF family, is involved in the development of multiple myeloma and Epstein-Barr virus (EBV)-mediated transformation of B lymphocytes.
|
21454650 |
2011 |
|
Myopathy
|
0.030 |
Biomarker
|
group |
BEFREE |
In this study, we aimed to assess the efficacy of a recently discovered small-molecule inhibitor of MuRF1 in treating CHF-induced diaphragm myopathy and loss of contractile function.
|
31140761 |
2019 |
|
Myopathy
|
0.030 |
GeneticVariation
|
group |
BEFREE |
MuRF1 gene point mutations have been found to generate protein aggregate myopathies defined as muscle disorder characterized by protein accumulation in muscle fibers.
|
29868881 |
2019 |
|
Myopathy
|
0.030 |
GeneticVariation
|
group |
BEFREE |
New cardiac and skeletal protein aggregate myopathy associated with combined MuRF1 and MuRF3 mutations.
|
25801283 |
2015 |
|
Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
TRIM 63 glutathione S-transferase A1 and alanyl aminopeptidase are the main differentially expressed genes for this group of tumors.
|
18344867 |
2008 |
|
Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
LOH of p53, p16 and IRF were detected in 16 of 50 (32%), 5 of 38 (13%) and 5 of 48 (10%) tumors, respectively.
|
21165583 |
2011 |
|
Neoplasms
|
0.030 |
GeneticVariation
|
group |
BEFREE |
These cells grew slowly and were expanded over a period of 3 years and have maintained characteristics consistent with those of both the original ASPS tumor from the patient and the xenograft tumor including (1) presence of the alveolar soft part locus-transcription factor E3 type 1 fusion transcript and nuclear expression of the alveolar soft part locus-transcription factor E3 type 1 fusion protein; (2) maintenance of the t(X;17)(p11;q25) translocation characteristic of ASPS; and (3) expression of upregulated ASPS transcripts involved in angiogenesis (ANGPTL2, HIF-1-α, MDK, c-MET, VEGF, and TIMP-2), cell proliferation (PRL, PCSK1), metastasis (ADAM9), as well as the transcription factor BHLHB3 and the muscle-specific transcripts TRIM63 and ITGβ1BP3.
|
21552147 |
2011 |
|
Atrophy, Disuse
|
0.030 |
Biomarker
|
disease |
BEFREE |
Transcript expression of these genes and Fboxo32 (MAFbx), because of its previously identified role in disuse atrophy together with Trim63 (MuRF1), were confirmed by real-time quantitative RT-PCR, and DNA methylation of their promoter regions was analyzed by PCR and pyrosequencing.
|
28821632 |
2017 |
|
Atrophy, Disuse
|
0.030 |
AlteredExpression
|
disease |
BEFREE |
The results reveal that irrespectively of age, mRNA expression levels of MuRF-1 and Atrogin-1 increased in the very initial phase (2-4 days) of human disuse-muscle atrophy along with a marked reduction in PGC-1α and PGC-1β (1-4 days) and a ~10% decrease in myofiber size (4 days).
|
23284670 |
2012 |
|
Atrophy, Disuse
|
0.030 |
Biomarker
|
disease |
BEFREE |
These proceedings focus on 1) the role of insulin resistance in mediating disuse-induced changes in muscle protein synthesis (MPS) and breakdown (MPB), as well as cross-talk between carbohydrate and protein metabolism; 2) the relative importance of MPS/MPB in mediating involuntary muscle loss in humans and animals; 3) interpretative limitations associated with MPS/MPB "markers," e.g., MuRF1/MAFbx mRNA; and finally, 4) how OMIC technologies can be leveraged to identify molecular pathways (e.g., ATF4, p53, p21) mediating disuse atrophy.
|
27382036 |
2016 |
|
Chronic Kidney Diseases
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Knockdown of SCP4 significantly suppressed FoxO1/3a-mediated expression of Atrogin-1 and MuRF-1 and prevented muscle wasting in mice with CKD.
|
28506762 |
2017 |
|
Chronic Kidney Diseases
|
0.030 |
AlteredExpression
|
group |
BEFREE |
Here, we showed that resveratrol prevented an increase in MuRF1 expression and attenuated muscle atrophy in vivo model of CKD.
|
28392400 |
2017 |