Target：POLH

Fields：Platinum drug resistance;Fanconi anemia pathway

Gene Name：POLH RAD30 RAD30A XPV

Protein Name：DNA polymerase eta (EC 2.7.7.7) (RAD30 homolog A) (Xeroderma pigmentosum variant type protein)

Human Gene Id：5429

Human Swiss Prot No：Q9Y253

Mouse Swiss Prot No：Q9JJN0

Immunogen：Synthesized peptide derived from part region of human protein

Specificity：POLH Polyclonal Antibody detects endogenous levels of protein.

Formulation：Liquid in PBS containing 50% glycerol, and 0.02% sodium azide.

Source：Polyclonal, Rabbit,IgG

Dilution：WB 1:500-2000 ELISA 1:5000-20000

Purification：The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

Concentration：1 mg/ml

Storage Stability：-15°C to -25°C/1 year(Do not lower than -25°C)

Observed Band(KD)：78kD

Background： This gene encodes a member of the Y family of specialized DNA polymerases. It copies undamaged DNA with a lower fidelity than other DNA-directed polymerases. However, it accurately replicates UV-damaged DNA; when thymine dimers are present, this polymerase inserts the complementary nucleotides in the newly synthesized DNA, thereby bypassing the lesion and suppressing the mutagenic effect of UV-induced DNA damage. This polymerase is thought to be involved in hypermutation during immunoglobulin class switch recombination. Mutations in this gene result in XPV, a variant type of xeroderma pigmentosum. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, May 2014],

Function：catalytic activity:Deoxynucleoside triphosphate + DNA(n) = diphosphate + DNA(n+1).,cofactor:Divalent metal cations. Prefers magnesium, but can also use manganese.,disease:Defects in POLH are the cause of xeroderma pigmentosum variant type (XPV) [MIM:278750]; also designated as XP-V. Xeroderma pigmentosum (XP) is an autosomal recessive disease due to deficient nucleotide excision repair. It is characterized by hypersensitivity of the skin to sunlight, followed by high incidence of skin cancer and frequent neurologic abnormalities. XPV shows normal nucleotide excision repair, but an exaggerated delay in recovery of replicative DNA synthesis. Most XPV patients do not develop clinical symptoms and skin neoplasias until a later age. Clinical manifestations are limited to photo-induced deterioration of the skin and eyes.,domain:The catalytic core consists of fingers, palm and thumb subdomains,

Subcellular Location：Nucleus . Binding to ubiquitinated PCNA mediates colocalization to replication foci during DNA replication and persists at sites of stalled replication forks following UV irradiation (PubMed:12606586, PubMed:16357261, PubMed:24553286). After UV irradiation, recruited to DNA damage sites within 1 hour, to a maximum of about 80%; this recruitment may not be not restricted to cells active in DNA replication (PubMed:22801543). Colocalizes with TRAIP to nuclear foci (PubMed:24553286). .

Expression： Cervix carcinoma,Epithelium,Skin,