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Human Polyclonal POLI Primary Antibody for ICC, IF - ABIN151275
Choi, Besaratinia, Lee, Lee, Pfeifer: The role of DNA polymerase iota in UV mutational spectra. in Mutation research 2006
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Human Monoclonal POLI Primary Antibody for ELISA, WB - ABIN564869
Wang, Woodgate, McManus, Mead, McCormick, Maher: Evidence that in xeroderma pigmentosum variant cells, which lack DNA polymerase eta, DNA polymerase iota causes the very high frequency and unique spectrum of UV-induced mutations. in Cancer research 2007
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Human Polyclonal POLI Primary Antibody for WB - ABIN540334
Frank, Tissier, McDonald, Rapi?-Otrin, Zeng, Gearhart, Woodgate: Altered nucleotide misinsertion fidelity associated with poliota-dependent replication at the end of a DNA template. in The EMBO journal 2001
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Human Polyclonal POLI Primary Antibody for IP, WB - ABIN253139
Ziv, Zeisel, Mirlas-Neisberg, Swain, Nevo, Ben-Chetrit, Martelli, Rossi, Schiesser, Canman, Carell, Geacintov, Falini, Domany, Livneh: Identification of novel DNA-damage tolerance genes reveals regulation of translesion DNA synthesis by nucleophosmin. in Nature communications 2014
Human Polyclonal POLI Primary Antibody for IHC, WB - ABIN5663975
Xiang, Laurent, Hsu, Nachtergaele, Lu, Sheng, Xu, Chen, Ouyang, Wang, Ling, Hsu, Zou, Jambhekar, He, Shi: RNA m6A methylation regulates the ultraviolet-induced DNA damage response. in Nature 2017
Findings indicate that DNA polymerase iota (poli) plays a positive role in lung cancer progression via promoting the migration and invasion of lung cancer cells.
Data suggest that translesion DNA synthesis mediated by (1) POLI-dependent pathway (2) REV1- and POLN-dependent pathway, or (3) POLtheta-dependent pathway occur in predominantly error-free manner in human cells. (POLI = DNA polymerase iota; REV1 = DNA repair protein-REV1; POLN = DNA polymerase nu; POLtheta = DNA polymerase theta)
Findings indicate the function of tumor suppressor protein p53 (p53) and DNA polymerase iota (POLiota) in the DNA damage response to endogenous or exogenous replication stress.
DNA polymerase iota increased the expression of MMP-2/9 to promote invasion and metastasis of esophageal squamous cell carcinoma.
Data suggest that error-free DNA replication through 3-deaza-3-methyladenine adduct is mediated via three different pathways dependent upon POL-iota/POL-kappa, POL-theta, and POL-zeta.
The predominant isoform of DNA poliota in human cells is the shorter 715 amino acid protein and that if, or when, expressed, the longer 740 amino acid isoform has identical properties to the considerably more abundant shorter isoform.
Kinetic and Structural Impact of Metal Ions and Genetic Variations on Human DNA Polymerase iota.
Mass spectrometry analysis of monoubiquitinated poliota revealed that it is ubiquitinated at over 27 unique sites. Many of these sites are localized in different functional domains of the protein.
Germline genetic variations in human POLI gene may either hinder or promote the translesion synthesis (TLS) capability of pol iota with various DNA lesions in vitro, emphasizing the potential translational importance of these pol iota genetic variations, e.g., individual differences in TLS, mutation, and cancer susceptibility to genotoxic carcinogens.
a single residue in pol iota is able to discriminate between NTPs and dNTPs during DNA synthesis.
Dysregulation of pol iota by JNK/c-Jun is involved in carcinogenesis and offer a novel understanding of the role of pol iota or c-Jun in mutagenesis.
Human Pol iota and yeast Pol zeta complex could function efficiently in the insertion and extension steps, respectively, of ranslesion synthesis and human Pol kappa and Pol eta could also extend past these lesions, albeit much less efficiently.
POLI and MC4R nearby single nucleotide polymorphisms in human chromosome 18 are associated with a moderate risk of type 2 diabetes.
Results show that the physical and functional interaction between pols eta and iota occurs between ubiquitinated forms of either polymerase via their respective ubiquitin-binding domains.
this review briefly discusses the main structural features and possible functional mechanisms of the active center of Pol iota. [review]
in mammalian cells, both polymerases kappa and iota are necessary for the error-free bypass of N(2)-CEdG and N(2)-CMdG.
structural mechanism of high-fidelity 8-oxo-G replication by a human DNA polymerase
Structural basis for proficient incorporation of dTTP opposite O6-methylguanine by human DNA polymerase iota.
In the presence of Mn2+, the Pol iota activity in carcinoma was 2.5-fold higher than the control cells.
The solution structures of the C-terminal UBM of human pol iota and its complex with ubiquitin are reported.
Pol iota occasionally accesses the replication fork to generate a first mutation, and Pol zeta extends the mismatch with a second mutation.
Mouse DNA polymerase iota lacking exon 2 (42 amino acids) is catalytically inactive in vitro.
Exon 2 deletion abrogates both the DNA polymerase and dRP lyase activities of Pol iota in the presence of either Mg(2+) or Mn(2+) ions. Thus, 129-derived strains of mice express catalytically inactive alternatively spliced Pol iota variant.
PolH contributes to accurate translesion synthesis (TLS) past both T- & C-containing dimers. PolI is involved in error-prone TLS past cytosine-containing dimers when Poleta is inactivated.
Poliota causes the Par2 effect and inhibits tumorigenesis and mutagenesis
Upon DNA damage, the UBDs (UBM domains) of polymerase iota (Pol iota) interact with ubiquitinated proliferating cell nuclear antigen to regulate the interchange between processive DNA polymerases and translesional synthesis
In the presence of Mg2+, the enzyme was active only in testicles and brain, whereas in the presence of Mn2+ the activity was found in all organs.
Data suggest that either DNA polymerase iota does not participate in hypermutation, or its role is nonessential and can be readily assumed by another low-fidelity polymerase.
Nucleotide polymorphisms in DNA polymerase iota is associated with lung tumorigenesis in mouse and humans
Pol kappa and Pol iota double-deficient mice had the normal somatic hypermutation frequency
Pol iota gene may participate in error-free repair of damaged DNA and prevention of lung tumor development
identification of two previously unknown ubiquitin-binding domains in the Y-family translesion synthesis polymerases that enable them to interact with monoubiquitinated targets and undergo monoubiquitination in vivo
suggest the involvement of the Pol eta and Pol iota proteins in UV-induced skin carcinogenesis
Although pol iota deficiency alone had no effect, UV-induced skin tumors in pol eta-deficient mice developed 4 weeks earlier in mice concomitantly deficient in pol iota
Error-prone DNA polymerase specifically involved in DNA repair. Plays an important role in translesion synthesis, where the normal high-fidelity DNA polymerases cannot proceed and DNA synthesis stalls. Favors Hoogsteen base-pairing in the active site. Inserts the correct base with high-fidelity opposite an adenosine template. Exhibits low fidelity and efficiency opposite a thymidine template, where it will preferentially insert guanosine. May play a role in hypermutation of immunogobulin genes. Forms a Schiff base with 5'-deoxyribose phosphate at abasic sites, but may not have lyase activity (By similarity).
DNA polymerase iota
, polymerase (DNA directed) iota
, DNA polymerase iota-like
, RAD30 homolog B
, polymerase (DNA-directed), iota