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Transcription factor A, mitochondrial

TFAM, mitochondrial transcription factor A, mtTFA
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, Jul 2008] (from NCBI)
Top mentioned proteins: PGC, Nuclear Respiratory Factor 1, NRF, CAN, PGC-1alpha
Papers using TFAM antibodies
Effect of adipocyte beta3-adrenergic receptor activation on the type 2 diabetic MKR mice
Luque Raul M., In PLoS ONE, 2005
... rabbit polyclonal CD36 (H-300), rabbit polyclonal β- tubulin antibody (Santa Cruz Biotechnology, Santa Cruz, CA); TFAM MaxPab rabbit polyclonal antibody D01 (Abnova, Taipei, Taiwan); mouse monoclonal ...
Papers on TFAM
FNDC5 relates to skeletal muscle IGF-I and mitochondrial function and gene expression in obese men with reduced growth hormone.
Makimura et al., Boston, United States. In Growth Horm Igf Res, Feb 2016
P=0.04) and TFAM (ρ=0.79,
Chronic Arsenic Exposure-Induced Oxidative Stress is Mediated by Decreased Mitochondrial Biogenesis in Rat Liver.
Kumar et al., Rohtak, India. In Biol Trace Elem Res, Feb 2016
The entire phenomenon was associated with decrease in mitochondrial biogenesis as evident by decreased protein and mRNA expression of nuclear respiratory factor 1 (NRF-1), nuclear respiratory factor 2 (NRF-2), peroxisome proliferator activator receptor gamma-coactivator 1α (PGC-1α), and mitochondrial transcription factor A (Tfam) in arsenic-treated rat liver.
HO-1/CO system and embryonic stem cell differentiation and maturation into cardiomyocytes.
Piantadosi et al., Durham, United States. In Antioxid Redox Signal, Feb 2016
These effects are prevented by silencing HO-1 and by mitochondrial ROS scavenging while disruption of mitochondrial biogenesis and mtDNA depletion by loss of mitochondrial transcription factor-A (Tfam) compromises infrastructure.
FOXO1 and GSK-3β Are Main Targets of Insulin-Mediated Myogenesis in C2C12 Muscle Cells.
Orzechowski et al., Warsaw, Poland. In Plos One, Dec 2015
Insulin-dependent myogenesis was accompanied by the rise of mtTFA, MtSSB, Mfn2, and mitochondrially encoded Cox-1 gene expressions and elevated levels of proteins which control functions of mitochondria (kinase-PKB/AKT, mitofusin 2 protein-Mfn-2).
Mitochondrial Respiration Controls Lysosomal Function during Inflammatory T Cell Responses.
Mittelbrunn et al., Madrid, Spain. In Cell Metab, Oct 2015
We have generated a mouse model with defective mitochondrial function in CD4(+) T lymphocytes by genetic deletion of the mitochondrial transcription factor A (Tfam).
Mitochondrial DNA stress primes the antiviral innate immune response.
Shadel et al., New Haven, United States. In Nature, May 2015
The abundant mtDNA-binding protein TFAM (transcription factor A, mitochondrial) regulates nucleoid architecture, abundance and segregation.
BMPR2 preserves mitochondrial function and DNA during reoxygenation to promote endothelial cell survival and reverse pulmonary hypertension.
Rabinovitch et al., Stanford, United States. In Cell Metab, May 2015
Mice with EC deletion of BMPR2 develop hypoxia-induced pulmonary hypertension that, in contrast to non-transgenic littermates, does not reverse upon reoxygenation and is associated with reduced PA microvessels and lung EC p53, PGC1α and TFAM, regulators of mitochondrial biogenesis, and mitochondrial DNA.
Age-related changes of mitochondrial transcription factor a expression in rotator cuff degeneration.
Matsumoto et al., Kanazawa, Japan. In Am J Transl Res, 2014
Using Rat rotator cuff we determined age-related changes in mitochondrial transcription factor A (TFAM) expression in rotator cuff degeneration to clarify the presence/absence of mitochondrial stress.
mTOR coordinates protein synthesis, mitochondrial activity and proliferation.
Topisirovic et al., Montréal, Canada. In Cell Cycle, 2014
In mammals, mTOR coordinates energy consumption by the mRNA translation machinery and mitochondrial energy production by stimulating synthesis of nucleus-encoded mitochondria-related proteins including TFAM, mitochondrial ribosomal proteins and components of complexes I and V.
Mitochondrial Transcription Factor A and Mitochondrial Genome as Molecular Targets for Cisplatin-Based Cancer Chemotherapy.
Matsumoto et al., Kitakyūshū, Japan. In Int J Mol Sci, 2014
In this review, we present novel aspects regarding the unique characteristics of the mitochondrial genome in relation to the use of platinum-based chemotherapy and describe our recent work demonstrating the importance of the mitochondrial transcription factor A (mtTFA) expression in cancer cells.
Quality matters: how does mitochondrial network dynamics and quality control impact on mtDNA integrity?
Spelbrink et al., Osnabrück, Germany. In Philos Trans R Soc Lond B Biol Sci, 2014
This is discussed in the light of new results presented here showing that mitochondrial transcription factor A/nucleoids are restricted in their intramitochondrial mobility and probably have a limited sphere of influence.
Mitochondrial adaptations evoked with exercise are associated with a reduction in age-induced testicular atrophy in Fischer-344 rats.
Adhihetty et al., Gainesville, United States. In Biogerontology, 2013
However, relative mitochondrial content was not reduced with age and this was consistent with the lack of change in the mitochondrial biogenesis regulator protein, peroxisome proliferator-activated receptor gamma coactivator 1-alpha and its downstream targets nuclear respiratory factor-1 and mitochondrial transcription factor A. No effect was observed in the pro- or anti-apoptotic proteins, Bax and Bcl-2, respectively, but age increased apoptosis inducing factor levels.
Mitochondrial biogenesis in health and disease. Molecular and therapeutic approaches.
Pallardó et al., Valencia, Spain. In Curr Pharm Des, 2013
PGC-1α and mtTFA), are candidates for therapeutic intervention in diverse diseases, like neurodegenerative disorders, metabolic syndrome, sarcopenia, cardiac pathophysiology and physiological processes like aging.
Adipose-specific deletion of TFAM increases mitochondrial oxidation and protects mice against obesity and insulin resistance.
Kahn et al., Boston, United States. In Cell Metab, 2013
To understand the impact of adipose tissue mitochondria on whole-body metabolism, we have generated a mouse model with disruption of the mitochondrial transcription factor A (TFAM) specifically in fat.
Mitochondrial transcription factor A serves as a danger signal by augmenting plasmacytoid dendritic cell responses to DNA.
Crouser et al., Columbus, United States. In J Immunol, 2012
Plasmacytoid dendritic cells (pDC) contribute to sterile immune responses by recognizing the mitochondrial component of necrotic cells (TFAM), with TFAM and mitochondrial DNA as likely mediators of pDC activation.
Mitochondrial transcription factor A is a proinflammatory mediator in hemorrhagic shock.
Wang et al., United States. In Int J Mol Med, 2012
TFAM can act as a damage-associated molecular pattern and may contribute to the initiation of inflammatory responses in hemorrhagic shock.
Effect of mitochondrial transcription factor a overexpression on motor neurons in amyotrophic lateral sclerosis model mice.
Abe et al., Okayama, Japan. In J Neurosci Res, 2012
The present study suggests that overexpression of TFAM has a potential to reduce oxidative stress in motor neuron and delay onset of the disease in amyotrophic lateral sclerosis model mice
Damage to mtDNA in liver injury of patients with extrahepatic cholestasis: the protective effects of mitochondrial transcription factor A.
Bie et al., Chongqing, China. In Free Radic Biol Med, 2012
study demonstrates that mtDNA damage is involved in liver damage in extrahepatic cholestatic patients. The mtDNA damage is attributable to the loss of TFAM
Clinical significance of mitochondrial transcription factor A expression in patients with colorectal cancer.
Yamaguchi et al., Kitakyūshū, Japan. In Oncol Rep, 2012
The survival of patients with positive mtTFA expression was significantly worse than that of patients with negative mtTFA expression.
Mitochondrial dynamics, biogenesis, and function are coordinated with the cell cycle by APC/C CDH1.
Moncada et al., London, United Kingdom. In Cell Metab, 2012
Changes in mitochondrial morphology and mass are due to accumulation of OPA1, MFN1, and TFAM, silencing any of which hinders cell proliferation.
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