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Mitochondrial DNA polymerase is heterotrimeric, consisting of a homodimer of accessory subunits plus a catalytic subunit. Additionally we are shipping POLG Proteins (12) and POLG Kits (4) and many more products for this protein.
Showing 10 out of 59 products:
Human Polyclonal POLG Primary Antibody for ICC, IF - ABIN4305533
Wu, Li, Zhang, Wu, Huang, Chen: Mitochondrial DNA base excision repair and mitochondrial DNA mutation in human hepatic HuH-7 cells exposed to stavudine. in Mutation research 2009
Show all 3 Pubmed References
Human Polyclonal POLG Primary Antibody for IF (p) - ABIN1696002
Prasad, Çağlayan, Dai, Nadalutti, Zhao, Gassman, Janoshazi, Stefanick, Horton, Krasich, Longley, Copeland, Griffith, Wilson: DNA polymerase β: A missing link of the base excision repair machinery in mammalian mitochondria. in DNA repair 2017
Human Polyclonal POLG Primary Antibody for IF (p), IHC (p) - ABIN1714946
Chen, Zhao, Cai, Sun, Hu, Huang, Kong, Kong: The role of sodium hydrosulfide in attenuating the aging process via PI3K/AKT and CaMKKβ/AMPK pathways. in Redox biology 2017
Cow (Bovine) Polyclonal POLG Primary Antibody for WB - ABIN2783430
Mancini, Roncaglia, Brussino, Stevanin, Lo Buono, Krmac, Maltecca, Gazzano, Bartoletti Stella, Calvaruso, Iommarini, Cagnoli, Forlani, Le Ber, Durr, Brice, Ghigo, Casari, Porcelli, Funaro, Gasparre et al.: Genome-wide expression profiling and functional characterization of SCA28 lymphoblastoid cell lines reveal impairment in cell growth and activation of apoptotic pathways. ... in BMC medical genomics 2013
The POLG1 CAG repeat (show CELF3 Antibodies) length variation and the GBA (show GBA Antibodies) p.L444P variant are associated with Parkinson's disease in the Finnish population
Two tag SNPs of TFAM and POLG were associated with multibacillary leprosy in Han Chinese from Southwest China.
POLG phenotypes and natural history of early-onset POLG-related disorders in a large multinational pediatric cohort
Together with mitochondrial dysfunction in bipolar disorder, the present results suggested deleterious POLG1 variants as a credible risk for the multifactorial disease.
This study suggests that, at variance with mouse and un/de-differentiated human cells, differentiated human cells control mtDNA levels irrespective of POLG methylation.
One patient presented with Leigh syndrome and had a homozygous deletion in the NDUFAF2 gene, while the second patient had a homozygous mutation in the POLG gene, [c.1399G>A; p.Ala467Thr].
The rs758130 in POLG gene was significantly associated with the prognosis of patients in a dose-dependent manner. Moreover, GG genotype in rs1061316 showed significantly high mtDNA content, an indicator of better prognosis.
Pol G composes the mtDNA replication machinery, this replication machinery and failure to repair these mtDNA errors results in mtDNA mutations and as a result mitochondrial dysfunction - a major driving force behind aging and age-related diseases.
POLG mutations are associated with progressive external ophthalmoplegia.
tudies on the impact of mitochondrial DNA variants present conflicting data but highlight POLG as a particularly interesting candidate gene for both male and female infertility.
Cardiac mitochondrial polymerase gamma dysfunction alters nuclear DNA methylation (show HELLS Antibodies).
Taken together, our findings may provide clues to further investigate the molecular mechanism underlying premature aging phenotype in Polg mutant mice.
POLG's 3'-5' exonuclease (show EXOSC10 Antibodies) proofreading activity is required for the creation of ligatable ends during mtDNA replication.
PolG mice display an enhanced reliance on glycolysis as compared to their wild-type counterparts.
mitochondrial respiratory chain proteins are specifically decreased in abundance in the brains of the polg mutator mice, including several nuclear encoded mitochondrial components.
in a mouse odel of diabetic retinopathy, POLG1 continued to be down-regulated, the D-loop region damaged, and the CpG islands at the regulatory region of POLG hyper-methylated even after three months of glycemic control
This method gives us insights into the pausing of two pol-gamma variants: the A467T substitution that causes PEO (show C10ORF2 Antibodies) and Alpers syndrome, and the exonuclease (show EXO1 Antibodies) deficient pol-gamma (exo (show XRN1 Antibodies)(-)) in premature aging mouse models.
reduced diabetic symptoms of aging Polg (D257A mutation in mitochondrial DNA polymerase gamma) Akita males results from appetite suppression triggered by decreased testosterone associated with damage to the Leydig cells of the testis
Control region multimers demonstrate that polymerase-gamma 3'-5' exonuclease (show EXOSC10 Antibodies) activity is required for preserving mtDNA integrity.
causative link between mtDNA mutations and ageing phenotypes, seen in Polg mutant knock-in mice
Mitochondrial DNA polymerase is heterotrimeric, consisting of a homodimer of accessory subunits plus a catalytic subunit. The protein encoded by this gene is the catalytic subunit of mitochondrial DNA polymerase. The encoded protein contains a polyglutamine tract near its N-terminus that may be polymorphic. Defects in this gene are a cause of progressive external ophthalmoplegia with mitochondrial DNA deletions 1 (PEOA1), sensory ataxic neuropathy dysarthria and ophthalmoparesis (SANDO), Alpers-Huttenlocher syndrome (AHS), and mitochondrial neurogastrointestinal encephalopathy syndrome (MNGIE). Two transcript variants encoding the same protein have been found for this gene.
DNA polymerase gamma
, DNA polymerase subunit gamma-1
, DNA-directed DNA polymerase gamma
, mitochondrial DNA polymerase catalytic subunit
, polymerase (DNA directed), gamma
, DNA polymerase subunit gamma-1-like
, DNA polymerase gamma subunit 1 (Mitochondrial DNA polymerase catalytic subunit) (PolG-alpha)
, Pol gamma
, mitochondrial DNA polymerase gamma
, mitochondrial DNA polymerase-gamma
, mitochondrial polymerase gamma
, polymerase, gamma