-
TFAM overexpression normalizes pathological hypertrophic factor NFAT4 in the presence of oxidative stress.
-
results suggest a nucleation-cooperativity-based mechanism for sensitive detection of mitochondrial DNA and pathogen genomes, and identify HMGB/TFAM proteins as DNA-structuring host factors; they provide an explanation for the peculiar cGAS dimer structure and suggest that cGAS preferentially binds incomplete nucleoid-like structures or bent DNA
-
TFAM is essential for transcription, replication and packaging of mtDNA into nucleoids. Tfam knockout mice display embryonic lethality secondary to severe mtDNA depletion. In this report, for the first time, we associate a homozygous variant in TFAM with a novel mtDNA depletion syndrome.
-
Perturbation of mitochondrial complex function by ablation of the mitochondrial transcription factor A (Tfam) reproduces multiple hallmarks of aging in hippocampal neurogenesis.
-
During muscle differentiation, Tfam protein levels are regulated by the availability of Tfam mRNA, which is controlled by both transcription and mRNA stability.
-
TFAM binds to RNA-containing 4-way junctions but does not bind appreciably to RNA hairpins, internal loops, or linear RNA:DNA hybrids.
-
Data show that mitochondrial transcription factor A (TFAM) packages single mitochondrial DNA (mtDNA) molecules.
-
There was upregulation of mtDNA and TFAM in 6-wk diabetic mice, suggesting that TFAM activation could be a therapeutic strategy to treat peripheral neuropathy.
-
This study demonistrated that Tfam gene inactive patkinsin disease cause dopamine loss and circadian rhythm disorder.
-
Mitochondrial transcription factor A, an endogenous danger signal, promotes TNFalpha release via RAGE- and TLR9-responsive plasmacytoid dendritic cells.
-
overexpression of TFAM can restore mitochondrial function to normal levels in NYGGF4-overexpressing adipocytes
-
Acute exercise induces tumour suppressor protein p53 translocation to the mitochondria and promotes a p53-Tfam-mitochondrial DNA complex in skeletal muscle.
-
Data indicate that TFAM-deficient keratinocytes failed to generate mitochondria-derived reactive oxygen species, and prevented the transmission of Notch and beta-catenin signals for epidermal differentiation and hair follicle development.
-
The reduction of mitochondrial transcription factor A (TFAM) in adipose tissue increases mitochondria oxidation capacity due to complex I deficiency and greater uncoupling.
-
Data suggest that microRNA 494 regulates mitochondrial biogenesis by down-regulating mtTFA (mitochondrial transcription factor A) and Foxj3 (forkhead box J3 protein) during myocyte differentiation and skeletal muscle adaptation to physical exercise.
-
disruption of mitochondrial function by selective deletion of the Tfam gene in midbrain DA neurons results in physiological changes in the nigrostriatal circuitry that occur before the onset of locomotor impairments of Parkinson disease.
-
TFAM overexpression can reduce mitochondrial permeability transition and ameliorate delayed neuronal death in the hippocampus after transient forebrain ischemia
-
The MitoPark mouse, in which the mitochondrial transcription factor Tfam is selectively removed in midbrain dopamine (DA) neurons, is a genetic model for Parkinson's disease and response to levodopa.
-
TFAM induces a structural change of the promoter that is required for POLRMT-dependent promoter recognition
-
Accumulation of TFAM protein after H2O2 stress contributes to the regeneration of the mtDNA pool but that other mechanisms, independent from the TFAM protein amount have to be postulated to explain the proliferation of the mtDNA pool after GSH depletion.