Suppressing mitochondrial inner membrane protein (IMMT) inhibits the proliferation of breast cancer cells through mitochondrial remodeling and metabolic regulation.
Study demonstrated that high-IMMT expression is related to some clinicopathological parameters of patients with lung adenocarcinoma and that its expression is an independent prognostic predictor of poorer survival.
It analyses revealed that Trak1 interacts and colocalizes with mitofusins on the outer mitochondrial membrane and functions with mitofusins to promote mitochondrial tethering and fusion.
Mitofilin-knockdown cells showed decreased mitochondrial membrane potential (DeltaPsim) and intracellular ATP content which were minimally affected in CHCHD6-knockout cells.
Mic60 interacted with mtDNA and was involved in the architecture of mtDNA D-loop region. Taken together our findings reveal a previously unrecognized important role of Mic60 in mtDNA transcription.
Transgenic overexpression of mitofilin preserves mitochondrial structure leading to restoration of mitochondrial function and attenuation of cardiac contractile dysfunction in the diabetic heart.
Mitofilin a mitochondria protein is shown to be related to cardiac hypertrophy for the first time which enhances our understanding of the role of mitochondria in cardiac hypertrophy.
A protein encoded by this locus was found to be differentially expressed in postmortem brains from patients with atypical frontotemporal lobar degeneration.
The mitochondrial dysfunction induced by DISC1 deficiency was partially reversed by coexpression of Mitofilin confirming a functional link between DISC1 and Mitofilin for the normal mitochondrial function.
role in protein import related to maintenance of mitochondrial structure is suggested; mitofilin helps regulate mitochondrial morphology and four of the associated proteins (metaxins 1 and 2 SAM50 and CHCHD3) have been implicated in protein import
Data show that the nuclear matrix protein matrin 3 cytoskeletal motor protein HMP and the circadian clock protein lark were significantly decreased in fetal Down syndrome brain.
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