Anti-DNA Polymerase gamma antibody (ab97661)
- Product nameAnti-DNA Polymerase gamma antibodySee all DNA Polymerase gamma primary antibodies ...
- DescriptionRabbit polyclonal to DNA Polymerase gamma
- Tested applicationsWB more details
- Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
Synthetic peptide, corresponding to a sequence within amino acids 779-1201 of Human DNA Polymerase gamma (NP_002684).
- Positive control293T, HeLa, HepG2, MCF7 and MOLT4 cell lysates.
- Storage instructionsStore at -20°C or lower. Aliquot to avoid repeated freezing and thawing.
- Storage bufferPreservative: 0.01% Thimerosal (merthiolate)
Constituents: 20% Glycerol, 1% BSA, 1X PBS, pH 7.0
- Concentration information loading...
- PurityImmunogen affinity purified
- Clonality Polyclonal
- Research Areas
Our Abpromise guarantee covers the use of ab97661 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||WB: 1/1000. Predicted molecular weight: 140 kDa.|
- FunctionInvolved in the replication of mitochondrial DNA.
- Involvement in diseaseDefects in POLG are the cause of progressive external ophthalmoplegia with mitochondrial DNA deletions autosomal dominant type 1 (PEOA1) [MIM:157640]. Progressive external ophthalmoplegia is characterized by progressive weakness of ocular muscles and levator muscle of the upper eyelid. In a minority of cases, it is associated with skeletal myopathy, which predominantly involves axial or proximal muscles and which causes abnormal fatigability and even permanent muscle weakness. Ragged-red fibers and atrophy are found on muscle biopsy. A large proportion of chronic ophthalmoplegias are associated with other symptoms, leading to a multisystemic pattern of this disease. Additional symptoms are variable, and may include cataracts, hearing loss, sensory axonal neuropathy, ataxia, depression, hypogonadism, and parkinsonism.
Defects in POLG are a cause of progressive external ophthalmoplegia with mitochondrial DNA deletions autosomal recessive (PEOB) [MIM:258450]. PEOB is a severe form of progressive external ophthalmoplegia. It is clinically more heterogeneous than the autosomal dominant forms. Can be more severe.
Defects in POLG are a cause of sensory ataxic neuropathy dysarthria and ophthalmoparesis (SANDO) [MIM:607459]. SANDO is a clinically heterogeneous systemic disorder with variable features resulting from mitochondrial dysfunction. It shares phenotypic characteristics with autosomal recessive progressive external ophthalmoplegia and mitochondrial neurogastrointestinal encephalopathy syndrome. The clinical triad of symptoms consists of sensory ataxic, neuropathy, dysarthria, and ophthalmoparesis.
Defects in POLG are a cause of Alpers-Huttenlocher syndrome (AHS) [MIM:203700]; also called Alpers diffuse degeneration of cerebral gray matter with hepatic cirrhosis. AHS is an autosomal recessive hepatocerebral syndrome. The typical course of AHS includes severe developmental delay, intractable seizures, liver failure, and death in childhood. Refractory seizures, cortical blindness, progressive liver dysfunction, and acute liver failure after exposure to valproic acid are considered diagnostic features. The neuropathological hallmarks of AHS are neuronal loss, spongiform degeneration, and astrocytosis of the visual cortex. Liver biopsy results show steatosis, often progressing to cirrhosis.
Defects in POLG are a cause of mitochondrial neurogastrointestinal encephalopathy syndrome (MNGIE) [MIM:603041]; also known as myoneurogastrointestinal encephalomyopathy. MNGIE is an autosomal recessive disease associated with multiple deletions of skeletal muscle mitochondrial DNA (MtDNA). It is clinically characterized by onset between the second and fifth decades of life, ptosis, progressive external ophthalmoplegia, gastrointestinal dysmotility (often pseudoobstruction), diffuse leukoencephalopathy, thin body habitus, peripheral neuropathy, and myopathy.
Defects in POLG are a cause of Leigh syndrome (LS) [MIM:256000]. LS is a severe neurological disorder characterized by bilaterally symmetrical necrotic lesions in subcortical brain regions.
- Sequence similaritiesBelongs to the DNA polymerase type-A family.
- Cellular localizationMitochondrion.
- DNA directed DNA polymerase gamma antibodyDNA polymerase subunit gamma 1 antibodyDNA polymerase subunit gamma-1 antibody
- DPOG1_HUMAN antibodyMDP 1 antibodyMDP1 antibodyMitochondrial DNA polymerase catalytic subunit antibodyMitochondrial DNA polymerase gamma antibodyPEO antibodyPOLG 1 antibodyPOLG A antibodyPolG alpha antibodyPOLG antibodyPolG-alpha antibodyPOLG1 antibodyPOLGA antibodyPolymerase (DNA directed) gamma antibodySANDO antibodySCAE antibody
Anti-DNA Polymerase gamma antibody images
Anti-DNA Polymerase gamma antibody (ab97661) at 1/1000 dilution + MCF7 whole cell lysate at 30 µg
Predicted band size : 140 kDa
References for Anti-DNA Polymerase gamma antibody (ab97661)
ab97661 has not yet been referenced specifically in any publications.