Tripartite Motif Containing 72 Proteins (TRIM72)

Human Tripartite Motif Containing 72 (TRIM72) interaction partners

1. serum TRIM72 may be a potential biomarker for the diagnosis and the prognosis of colon cancer.

2. MG53 is an effective biomarker of myocardial injury and dysfunction in murine hearts. However, MG53 is not expressed in human heart and therefore does not hold utility as a clinical biomarker of myocardial injury

3. MG53 is a facilitator of rapid injury repair, a mediator of cell migration, and a modulator of myofibroblast differentiation during wound healing

4. Zn(2+) interacts with MG53 in protection against injury to the cell membrane

5. MG53 induces FAK (show PTK2 Proteins) ubiquitination with the aid of UBE2H (show UBE2H Proteins) during skeletal myogenesis.

6. MG53/TRIM72 protein can be directly applied as a therapeutic agent to increase membrane repair capacity of many cell types.

7. data reveal NM-IIA as a key cytoskeleton motor protein that facilitates vesicle trafficking during MG53-mediated cell membrane repair

8. membrane-delimited interaction between MG53 and PTRF (show PTRF Proteins) contributes to initiation of cell membrane repair

9. MG53, annexin A1, and dysferlin localize to the t-tubule network and show enriched labeling at longitudinal tubules of the t-system in overstretch

10. Crystal structure of PRY-SPRY domain of human TRIM72.

Mouse (Murine) Tripartite Motif Containing 72 (TRIM72) interaction partners

1. Results show that MG53 binds to Orai1 (show TMEM132A Proteins) via its PRY-SPRY region and co-localizes with Orai1 (show TMEM132A Proteins) in the plasma membrane in skeletal muscle which enhances extracellular Ca2 (show CA2 Proteins)+ entry via Orai1 (show TMEM132A Proteins) by store-operated Ca(2 (show CA2 Proteins)+) entry mechanism.

2. MG53 is essential to preserve T-tubule integrity and thereby Ca(2 (show CA2 Proteins)+) handling properties and cardiac function under pathological cardiac stress.

3. MG53 is an effective biomarker of myocardial injury and dysfunction in murine hearts. However, MG53 is not expressed in human heart and therefore does not hold utility as a clinical biomarker of myocardial injury

4. TRIM72 directly and indirectly modulates caveolar endocytosis

5. MG53 protein is expressed in lung tissue.

6. Findings indicate that the manifestation of metabolic syndrome alters MG53 activity by reducing its extracellular expression in the serum and causing it to aggregate around mitochondria within striated (show NSDHL Proteins) muscle cells.

7. MG53 is a facilitator of rapid injury repair, a mediator of cell migration, and a modulator of myofibroblast differentiation during wound healing

8. MG53 is a vital component of reno-protection, and targeting MG53-mediated repair of renal proximal tubular epithelium cells represents a potential approach to prevention and treatment of acute kidney injury

9. Zn(2+) interacts with MG53 in protection against injury to the cell membrane

10. MG53-deficient hearts downregulated PPARalpha (show PPARA Proteins) target genes. MG53 plays a novel role in transcriptional upregulation of PPARalpha (show PPARA Proteins) and its target genes, resulting in lipid accumulation and lipid toxicity, thereby contributing to diabetic cardiomyopathy.