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Validated All-in-One™ qPCR Primer for TFAM(NM_003201.2) 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 mitochondrial transcription factor that is a key activator of mitochondrial transcription as well as a participant in mitochondrial genome replication. Studies in mice have demonstrated that this gene product is required to regulate the mitochondrial genome copy number and is essential for embryonic development. A mouse model for Kearns-Sayre syndrome was produced when expression of this gene was eliminated by targeted disruption in heart and muscle cells. [provided by RefSeq].
Gene References into function
- the effects of mitochondrial transcription factor A (TFAM) and single-stranded DNA-binding protein (mtSSB) on D-loops
- mtTFA plays an important role in the recognition of oxidative DNA damage.
- both the mitochondrial transcription factor TFAM and mitochondrial single-stranded DNA-binding protein colocalize with Twinkle in intramitochondrial foci
- This protein interacts with p53 protein and helps regulate DNA damage.
- TFB1 interacts with the C-terminal activation region of h-mtTFA and stimulates transcription independently of its RNA methyltransferase activity
- This study describe a family with autosomal dominant progressive external ophthalmoplegia caused by a novel heterozygous A to C transversion at nucleotide 956 of the Twinkle gene.
- There was an association of genotype rs1937G/G with Alzheimer disease in females and an association of a TFAM haplotype with Alzheimer disease both in the whole sample and in females.
- mtDNA amount is finely correlated with the amount of TFAM but not with the transcription level
- TFAM induces a structural change of the promoter that is required for POLRMT-dependent promoter recognition
- Overexpression of mitochondrial transcription factor A (TFAM) stimulates mitochondrial DNA transcription, but is not sufficient to stimulate mitochondrial DNA replication.
- Overexpression of TFAM in transgenic mice inhibited left ventricular remodeling after myocardial infarct and may provide a novel therapeutic strategy of cardiac failure.
- we have determined its chromosomal localization, suggesting that its locus is highly conserved; we have searched for the presence of the delta5 isoform, demonstrating that it is present only in hominids
- These results suggest that PGC-1alpha variants with Gly/Gly at 482nd amino acid may impair the Tfam transcription, a regulatory function of mitochondrial biogenesis, resulting in dysfunctional mtDNA replication.
- the C-terminal tail of TFAM is important for the strong general binding to mtDNA; this strong DNA-binding conferred by the C-tail may play an important role in the nucleoid structure
- We have determined whether POLG and TFAM have functional roles in post-ejaculatory sperm mtDNA.
- Three polymorphisms in the TFAM gene rs1937, rs2306604 and rs1049432 do not predict endurance capacity/trainability in Chinese males.
- rs2306604 A-allele of mitochondrial transcription factor A could be a moderate risk factor for Alzheimer's diseae
- Transcription factor ZNF143 is required for expression of TFAM gene.
- Data suggested that the mitochondrial targeting sequence of hTFAM may extend beyond the cleavable presequence.
- TFAM-variants did not contribute to the risk of developing Parkinson disease
- PHB1 maintains the organization and copy number of the mtDNA through both TFAM-independent and -dependent pathways.
- The nigral dopamine neurons of MitoPark mice show respiratory chain dysfunction, accompanied by the development of intraneuronal inclusions and cell death. In early adulthood, the mice show progressing loss of motor function.
- Overexpression of TFAM is therefore considered to ameliorate age-dependent impairment of the brain functions through the prevention of oxidative stress and mitochondrial dysfunctions in microglia.
- determined the variation in the TFAM, TFB1M, and TFB2M genes in cardiac hypertrophy
