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The mitochondrial transcription factor TFAM in neurodegeneration: emerging evidence and mechanisms.
Study shows that the human mitochondrial transcription factor A (TFAM) is a versatile G-quadruplex (G4s) binding protein. These TFAM-G4 interactions suggest functional recognition of G4s in the mitochondria.
CTGF can reduce glycolysis and mitochondrial OXPHOS pathways by increasing mtTFA protein degradation and in turn reduces cancer migration and invasion in oral squamous cell carcinoma (OSCC).
radiation stimulated the levels of TFAM mRNA and protein.
Two tag SNPs of TFAM and POLG were associated with multibacillary leprosy in Han Chinese from Southwest China.
Data revealed that TFAM expression level was regulated by TP73-AS1/miR-200a axis in breast cancer cells.
Study clearly shows that hTFAM efficiently breaks the mitochondria-mediated vicious cycle in both Alzheimer's disease (AD) model neurons and mouse brains, resulting in an effective improvement of the AD pathophysiology including Abeta accumulation and cognitive dysfunction.
these findings establish a new link between HIF-2alpha and MAPK-signaling that mediates the adaptive regulation of mitochondrial gene expression under low oxygen tension.
the results presented in this study obviously provided the evidence that TFAM was upregulated in glioma cell line and glioma tissue specimens. Therefore TFAM may be a novel diagnostic marker and therapeutic target for glioma and other cancer.
Biotinylated TMP interacts with TFAM.
TFAM polymorphisms (rs1937, rs1049432, and rs11006132) as well as their haplotypes did not show significant association with aggressiveness of prostate cancer in overweight or obese men.
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
p53 might incrase mtDNA copy number through its regulation on TFAM expression via TFAMpromoter.
TFAM is a gene regulator that acts to mitigate calcium mishandling and ROS production by wrapping around mitochondrial DNA complexes. TFAM's regulatory functions over serca2a, NFAT, and Lon protease contribute to cardiomyocyte stability. [review]
The results suggest that a high mtTFA expression is a useful marker for tumor progression and a poor prognosis in left-sided colorectal cancer patients.
Study reports crystal structures of human mitochondrial transcription initiation complexes assembled on both light and heavy strand promoters. The structures reveal how transcription factors TFAM and TFB2M assist mitochondrial RNA polymerase to achieve promoter-dependent initiation.
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.
Tissue microarray (TMA) data showed that elevated expression of TFAM was related to the histological grade and TNM stage of NSCLC patients.
The authors did not find statistically significant differences in the genotype frequencies for the TFAM +35G/C polymorphism between women with polycystic ovary syndrome and controls and found that mtDNA copy number is not associated with TFAM+35G/C SNP in polycystic ovary syndrome patients.
Alleles in mitochondrial transcription factor A (TFAM) and AP endonuclease 1 (APE1) are associated with reduced cognitive performance.
TFAM may exert a critical role in porcine gametogenesis and preimplantation embryo development.
Our results suggest that TFAM plays an important role in lipid metabolism and may be a strong candidate gene for obesity in mammals.
de novo mtTFA expression associated with mitochondrial biogenesis activation & high levels of nuclear respiratory factor-1 mRNA from oocyte stage onwards argue for essential function of these factors during the first steps of bovine embryogenesis.
TFAM overexpression normalizes pathological hypertrophic factor NFAT4 in the presence of oxidative stress.
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.
This gene encodes a key mitochondrial transcription factor containing two high mobility group motifs. The encoded protein also functions in mitochondrial DNA replication and repair. Sequence polymorphisms in this gene are associated with Alzheimer's and Parkinson's diseases. There are pseudogenes for this gene on chromosomes 6, 7, and 11. Alternative splicing results in multiple transcript variants.
transcription factor A, mitochondrial
, HMG box mitochondrial transcription factor
, mitochondrial transcription factor 1
, mitochondrial transcription factor A
, transcription factor 6
, transcription factor 6-like 1
, transcription factor 6-like 2 (mitochondrial transcription factor)
, transcription factor 6-like 3
, transcription factor 6-like 2
, testis-specific HMG-box protein m-tsHMG
, testis-specific high mobility group protein