TFAM Antibodies

Transcription factor A, mitochondrial (TFAM)

Binds to the mitochondrial light strand promoter and works in mitochondrial transcription regulation (PubMed:29445193). Required for accurate and effective promoter recognition by the mitochondrial RNA polymerase.

Promotes transcription initiation from the HSP1 and the light strand promoter by binding immediately upstream of transcriptional start sites. Can unwind DNA.

Gene Information

Human
Gene Name:	TFAM
Uniprot:	Q00059
Entrez:	7019

Family

Belongs to:
No superfamily

Alternative Names

mitochondrial transcription factor A; MtTF1; mtTFA; TCF-6; TCF6L1; TCF6L2Mitochondrial transcription factor 1; TCF6TCF6L3; Transcription factor 6; Transcription factor 6-like 2 (mitochondrial transcription factor); Transcription factor 6-like 2; transcription factor A, mitochondrial

Molecular Weight

Mass (kDA):
29.097 kDA

Genomic Context

Human
Location:	10q21.1
Sequence:	10; NC_000010.11 (58385143..58399230)

Subcellular Localizations

Mitochondrion. Mitochondrion matrix, mitochondrion nucleoid.

Diseases

• Diabetes Mellitus
• Mitochondrial Diseases
• Insulin Resistance
• Malignant Neoplasms
• Neoplasms
• Nerve Degeneration
• Inflammation
• Diabetes Mellitus, Non-insulin-dependent
• Obesity
• Heart Failure
• Hypertrophy
• Cardiomyopathies
• Parkinson Disease

• Myopathy
• Infarction
• Alzheimer's Disease
• Neurodegenerative Disorders
• Mitochondrial Dna Depletion
• Mitochondrial Myopathies
• Nervous System Disorder

Interacting Proteins

• AGTRAP
• ARL6IP1
• MGST3
• TFB1M

Pathways

• Oxidative Phosphorylation
• Aging
• Pathogenesis
• Transport
• Translation
• Electron Transport
• Dna Replication
• Cell Death
• Localization
• Electron Transport Chain
• Mitochondrial Dna Replication
• Embryo Development
• Cell Proliferation

• Rna Interference
• Methylation
• Secretion
• Dna Repair
• Energy Homeostasis
• Insulin Secretion
• Regeneration

PTMs

• Phosphorylation
• Oxidation
• Methylation

• Cleavage
• Nitration
• Glycosylation

• Acetylation

Research Areas

• Cell Cycle and Replication
• Transcription Factors and Regulators

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TFAM

Best Uses Of The TFAM Marker

TFAM is a mitochondrial transcription factor that regulates the copy number of mtDNA. Its degraded form is not a good marker of mitochondrial biogenesis. Let's take a look at the best uses of the TFAM marker. It regulates the copy number of mtDNA and is not degraded by Lon. It has been used successfully in many different research applications.

TFAM is a mitochondrial transcription factor

The human TFAM has a strong affinity for the light-strand promoters of the mitochondrial genome. TFAM binds to mtDNA to increase the transcription of mitochondrial genes. It also promotes the expression of mitochondrial transcription factors B1 and B2. This complex encoding system enables cellular metabolism and mitochondrial biogenesis. Its high affinity for the light-strand promoters is important for mitochondrial biogenesis.

When bound to mtDNA, TFAM shields lysine residues from spontaneous acetylation in the mitochondrial matrix. In its free state, however, TFAM is susceptible to acetylation in mitochondrial matrix and may occur during transit to the nucleus or through another mechanism that dissociates it from the mtDNA. Thus, TFAM is required for mitochondrial biogenesis.

Human TFAM expression is similar to that of its mouse counterpart. In skeletal muscle, multiple serine-threonine kinases regulate the expression of nuclear-encoded mitochondrial proteins. Increases in AMP/ATP ratio activate AMPK, which enhances transcription of PGC-1a, a key regulator of mitochondrial biogenesis. Similarly, constitutive expression of AMPK promotes the expression of mitochondrial proteins. In mice, AMPK increases Tfam mRNA by 50-100%.

In addition, TFAM can cooperatively bind to DNA. This has been demonstrated in three types of experiments. In the EMSA method, the DNA ligand mobility shifted more than expected when compared to the concentration of protein. In AFM, low protein occupancy DNA remains adjacent to highly protein-loaded molecules. This pattern of binding is not explained by protein clumping. Furthermore, individual TFAM seeding is evident in uncompressed DNA.

TFAM is a phosphorylation enzyme. It completes the coordinated compaction of DNA in vitro and in vivo. Takamatsu et al. have determined the phosphorylation activities of TFAM and also found that it can phosphorylate DNA without DNA. These experiments reveal that TFAM is an essential component of the mitochondrial bioenergetics.

It regulates mtDNA copy number

It is not clear why TFAM and mtDNA copy number are interrelated, and it remains a mystery. But it appears that TFAM is involved in regulating mtDNA copy number in mammals. There is genetic evidence to support this theory. It is possible that TFAM regulates mtDNA copy number in response to endogenous danger signals. Moreover, TFAM regulates mtDNA copy number in a manner that is independent of mtDNA expression and mitochondrial biogenesis.

Several genome-wide association studies have been conducted, with mtDNA-CN as the target gene. A number of GWAS have been published, including studies from Cai et al., Workalemahu et al., and Hagg et al. Using more than 300,000 participants from the UK Biobank, the authors identified a number of genes that influence mtDNA copy number.

A limited number of studies have examined the relationship between mtDNA copy number and TFAM levels in aging-related pathologies. However, the results suggest that altered levels of TFAM may contribute to neurodegenerative conditions. The results of these studies will provide useful information for those wishing to investigate the role of mtDNA in neurodegenerative disease. However, it is important to note that there is still more research needed to understand how TFAM and mtDNA work together in the development of neurodegenerative diseases.

The mtDNA copy number machinery is comprised of TFAM and several other proteins. This packaging consists of a structure called nucleoids, which is analogous to bacteria and containing replication proteins and other proteins involved in cellular processes. However, in yeast, nucleoid maintenance may be regulated by the mitochondrial translation machinery, which is absent in metazoan cells.

It is not a good marker of mitochondrial biogenesis

A recent study has concluded that TFAM expression in developing muscle cells has a weak correlation with mtDNA copy number, and a POLRMT knockout (KO) mouse model of skeletal muscle showed a significantly decreased rate of mitochondrial biogenesis. This finding suggests that TFAM expression is not a sufficient marker of mitochondrial biogenesis. Even though mtDNA copy number increased in POLRMT KO mice, TFAM levels remained unchanged.

Recent studies have uncovered an intriguing factor in mitochondrial biogenesis: a genetic mutation in the gene TFAM may lead to an increased risk for cancer. The rs1937 SNP encodes a nonsynonymous change in the mitochondrial targeting peptide, and increased TFAM expression was associated with cancer risk. TFAM expression also increases risk for Alzheimer's disease, coronary artery disease, and multiple sclerosis.

The gene TFB2M, a protein that cooperates with TFAM, was downregulated by TFAM depletion, but was not affected. The decrease in TFAM mRNA expression was significant in only ten of the ten genes studied. In contrast, six genes were upregulated and three were downregulated when TFAM was downregulated. This suggests that TFAM is not a good marker of mitochondrial biogenesis, and further studies are needed to confirm these findings.

In tumor cells, increased TFAM expression has a negative correlation with overall survival. Moreover, TFAM knockdown results in increased mtDNA depletion, enhanced calcium-mediated mitochondrial retrograde signaling, and increased ROS levels. In ovarian cells, TFAM knockdown has a significant impact on cell growth and proliferation, and increased expression of TFAM has a negative impact on tumor metastasis.

It is available from a number of suppliers

TFAM Marker is a gene that is involved in mitochondrial biogenesis. It is also involved in the prognosis of glioblastoma and has been associated with glioma progression. Various suppliers offer TFAM Marker for researchers. This gene is present in the human genome and is available from a number of suppliers. Here are the benefits of using this marker in your research.