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Validated All-in-One™ qPCR Primer for TRIM63(NM_032588.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene encodes a member of the RING zinc finger protein family found in striated muscle and iris. The product of this gene is localized to the Z-line and M-line lattices of myofibrils, where titin's N-terminal and C-terminal regions respectively bind to the sarcomere. In vitro binding studies have shown that this protein also binds directly to titin near the region of titin containing kinase activity. Another member of this protein family binds to microtubules. Since these family members can form heterodimers, this suggests that these proteins may serve as a link between titin kinase and microtubule-dependent signal pathways in muscle.
Gene References into function
- interacts with titin to regulate sarcomeric M-line and thick filament structure and may have nuclear functions via its interaction with glucocorticoid modulatory element binding protein-1.
- MURF2 associates transiently with microtubules, myosin and titin during sarcomere assembly.
- MuRF1 functions as a ubiquitin ligase to catalyze ubiquitylation of troponin I through a RING finger-dependent mechanism
- MuRF1 mRNA expression was significantly increased in quadriceps of patients with COPD; transcriptional regulation of atrogin-1 and MuRF1 may occur via FoxO-1, but independently of AKT
- Expression of mRNA for MuRF-1 increased approximately 3-fold at 10 days without changes in MAFbx or tripeptidyl peptidase II mRNA, but all decreased between 10 and 21 days of muscle disuse.
- MuRF-1 and MAFbx, are differently affected by the exercise as well as by repeated exercise
- Results showed upregulation of MuRf1 and MAFbx in atrophied muscle and support their role as regulatory peptides in various conditions which lead to muscle atrophy.
- MuRF1 expression in skeletal muscle re-directs glycogen synthesis to the liver and stimulates pancreatic insulin secretion, providing a feedback loop that connects skeletal muscle metabolism with the liver and the pancreas during metabolic stress.
- These findings present new insights into the role of the glucocorticoid receptor and FOXO family of transcription factors in the transcriptional regulation of the MuRF1 gene
- Findings aid the future exploration of the cellular function and therapeutic potential of MuRF1.
