TRIM52 Protects Against Doxorubicin-Induced Cardiac Inflammation, Oxidative Stress and Cardiac Injury. [PDF]
ABSTRACT Tripartite motif 52 (TRIM52) has been identified as a key regulator of inflammatory responses. However, its involvement in doxorubicin (DOX)‐induced cardiotoxicity (DIC) and the underlying molecular mechanisms remain poorly understood. To investigate the functional role of TRIM52, we employed an adeno‐associated virus serotype 9 (AAV9 ...
Zhang Z +8 more
europepmc +2 more sources
Functional and Adaptive Significance of Promoter Mutations That Affect Divergent Myocardial Expressions of TRIM72 in Primates [PDF]
Cis-regulatory elements play important roles in tissue-specific gene expression and in the evolution of various phenotypes, and mutations in promoters and enhancers may be responsible for adaptations of species to environments.
Yuanqing Feng, Jian Lu, Chuan-Yun Li
exaly +4 more sources
Gait analysis for functional evaluation in a surgical hindlimb suspension model of muscle atrophy. [PDF]
Abstract figure legend Gait analysis reveals neuromuscular dysfunction following hindlimb suspension and partial recovery after reloading. Schematic overview of the experimental design and principal findings. Mice underwent 14 days of hindlimb suspension (HLS), resulting in muscle atrophy marked by reduced fiber size, satellite cell loss, and decreased
Xu Y +13 more
europepmc +2 more sources
TRIM72 is a membrane repair protein that protects against ischemia reperfusion (I/R) injury. We previously identified Cys144 (C144) on TRIM72 as a site of S-nitrosylation. To study the importance of C144, we generated a knock-in mouse with C144 mutated to a serine (TRIM72 C144S). We subjected ex vivo perfused mouse hearts to 20 min of ischemia followed
Elizabeth Murphy +2 more
exaly +4 more sources
MG53 suppresses interferon-β and inflammation via regulation of ryanodine receptor-mediated intracellular calcium signaling [PDF]
TRIM proteins are known to play critical roles in the context of viral infection. Here the authors establish MG53 (TRIM72) suppresses IFN and inflammation by modulation of ryanodine receptor related intracellular calcium induction.
Matthew Sermersheim +11 more
doaj +2 more sources
Recombinant TRIM72/MG53 protein enhances plasma membrane repair and reduces neurotoxicity in models of Alzheimer’s Disease [PDF]
Abstract Background Amyloid beta (Aβ) is one of the earliest hallmarks in Alzheimer’s Disease (AD) that has been shown to localize with the plasma membrane, decrease membrane integrity, elevate intracellular calcium concentrations, increase oxidative stress and directly induce membrane damage.
Bulgart H +5 more
europepmc +2 more sources
Deficient Sarcolemma Repair in ALS: A Novel Mechanism with Therapeutic Potential [PDF]
The plasma membrane (sarcolemma) of skeletal muscle myofibers is susceptible to injury caused by physical and chemical stresses during normal daily movement and/or under disease conditions. These acute plasma membrane disruptions are normally compensated
Ang Li +6 more
doaj +2 more sources
Swimming Exercise Alleviated Insulin Resistance by Regulating Tripartite Motif Family Protein 72 Expression and AKT Signal Pathway in Sprague-Dawley Rats Fed with High-Fat Diet [PDF]
We aimed to investigate whether swimming exercise could improve insulin resistance (IR) by regulating tripartite motif family protein 72 (TRIM72) expression and AKT signal pathway in rats fed with high-fat diet.
Jie Qi +4 more
doaj +2 more sources
TRIM72 mediates lung epithelial cell death upon hyperoxia exposure [PDF]
Background: Premature infants often require oxygen (O2) therapy for respiratory distress syndrome; however, excessive use of O2 can cause clinical conditions such as bronchopulmonary dysplasia. Although many treatment methods are currently available, they are not effective in preventing bronchopulmonary dysplasia.
Huang, Liang-Ti +2 more
openaire +5 more sources
Autoantibodies targeting TRIM72 compromise membrane repair and contribute to inflammatory myopathy [PDF]
Idiopathic inflammatory myopathies (IIM) involve chronic inflammation of skeletal muscle and subsequent muscle degeneration due to an uncontrolled autoimmune response; however, the mechanisms leading to pathogenesis are not well understood. A compromised sarcolemmal repair process could promote an aberrant exposure of intramuscular antigens with the ...
Kevin E. McElhanon +13 more
openaire +4 more sources

