DNA polymerase subunit gamma-1, ELISA Kit

FLJ27114; MDP1; PEO; POLG1; POLGA; SANDO; SCAE; DNA polymerase subunit gamma-1|DNA-directed DNA polymerase gamma|PolG; catalytic subunit|PolG-alpha|mitochondrial DNA polymerase catalytic subunit

For Research Use Only. Not for use in diagnostic procedures.

This assay has high sensitivity and excellent specificity for detection of Rat POLG. No significant cross-reactivity or interference between Rat POLG and analogues was observed.

Store at 2-8 degree C.

Select online data sheet information is drawn from bioinformatics databases, occasionally resulting in ambiguous or non-relevant product information. It is the responsibility of the customer to review, verify, and evaluate the information to make sure it matches their requirements before purchasing the kit. Our ELISA Kit assays are dynamic research tools and sometimes they may be updated and improved. If the format of this assay is important to you then please request the current manual or contact our technical support team with a presales inquiry before placing an order. We will confirm the current details of the assay. We cannot guarantee the sample manual posted online is the most current manual.

Small volumes of POLG elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS285434 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the DNA polymerase subunit gamma-1 (POLG) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing POLG. The ELISA analytical biochemical technique of the MBS285434 kit is based on POLG antibody-POLG antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect POLG antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, POLG. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

Principle of the Assay: This assay employs a two-site sandwich ELISA to quantitate POLG in samples. An antibody specific for POLG has been pre-coated onto a microplate. Standards and samples are pipetted into the wells and anyPOLG present is bound by the immobilized antibody. After removing any unbound substances, a biotin-conjugated antibody specific for POLG is added to the wells. After washing, Streptavidin conjugated Horseradish Peroxidase (HRP) is added to the wells. Following a wash to remove any unbound avidin-enzyme reagent, a substrate solution is added to the wells and color develops in proportion to the amount of POLG bound in the initial step. The color development is stopped and the intensity of the color is measured.

136,856 Da

DNA polymerase gamma, catalytic subunit

DNA polymerase subunit gamma-1

DNA polymerase subunit gamma-1

Mip1; Polg1  [Similar Products]

exhibits DNA polymerase activity; may mediate the final step of mitochondrial DNA repair [RGD, Feb 2006]

POLG: Involved in the replication of mitochondrial DNA. Associates with mitochondrial DNA. Defects in POLG are the cause of progressive external ophthalmoplegia with mitochondrial DNA deletions autosomal dominant type 1 (PEOA1). 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). 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). SANDO is a systemic disorder resulting from mitochondrial dysfunction associated with mitochondrial depletion in skeletal muscle and peripheral nerve tissue. The clinical triad of symptoms consists of sensory ataxic neuropathy, dysarthria, and ophthalmoparesis. However, the phenotype varies widely, even within the same family, and can also include myopathy, seizures, and hearing loss. An atypical form of the disease is characterized by headaches and/or seizures manifesting in childhood or adolescence, followed by development of cerebellar and sensory ataxia, dysarthria, progressive external ophthalmoplegia, and myoclonus in early *****hood. Defects in POLG are the cause of mitochondrial DNA depletion syndrome type 4A (MTDPS4A); also called Alpers diffuse degeneration of cerebral gray matter with hepatic cirrhosis. An autosomal recessive hepatocerebral syndrome. The typical course of the disease 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 are neuronal loss, spongiform degeneration, and astrocytosis of the visual cortex. Liver biopsy results show steatosis, often progressing to cirrhosis. Defects in POLG are the cause of mitochondrial DNA depletion syndrome type 4B (MTDPS4B); also known as mitochondrial DNA depletion syndrome 4B MNGIE type or mitochondrial neurogastrointestinal encephalopathy syndrome POLG- related. An autosomal recessive progressive multisystem disorder clinically characterized by chronic gastrointestinal dysmotility and pseudo-obstruction, cachexia, progressive external ophthalmoplegia, axonal sensory ataxic neuropathy, and muscle weakness. Defects in POLG are a cause of Leigh syndrome (LS). LS is a severe neurological disorder characterized by bilaterally symmetrical necrotic lesions in subcortical brain regions. Belongs to the DNA polymerase type-A family.

Protein type: DNA repair, damage; DNA replication; EC 2.7.7.7; Mitochondrial; Transferase

Chromosomal Location of Human Ortholog: 1q31

Cellular Component: gamma DNA polymerase complex; mitochondrial inner membrane; mitochondrion; protein complex; terminal bouton

Molecular Function: 3'-5' exonuclease activity; chromatin binding; DNA binding; DNA-directed DNA polymerase activity; exonuclease activity; protease binding

Biological Process: aging; base-excision repair, gap-filling; mitochondrial DNA replication; response to gamma radiation; response to hyperoxia; response to light stimulus

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