| DNA polymerase iota promotes EMT and metastasis of esophageal squamous cell carcinoma by interacting with USP7 to stabilize HIF-1alpha. | DNA polymerase iota promotes EMT and metastasis of esophageal squamous cell carcinoma by interacting with USP7 to stabilize HIF-1α.
Gao A, Zhang M, Zhu SQ, Zou S, Chen H, Li X, He C, Zhou L, Mei Y, Ding W, Zhou J, Zhou Y, Cao Y., Free PMC Article | 02/26/2024 |
| Pol iota occasionally accesses the replication fork to generate a first mutation, and Pol zeta extends the mismatch with a second mutation. | DNA polymerase ι functions in the generation of tandem mutations during somatic hypermutation of antibody genes.
Maul RW, MacCarthy T, Frank EG, Donigan KA, McLenigan MP, Yang W, Saribasak H, Huston DE, Lange SS, Woodgate R, Gearhart PJ., Free PMC Article | 08/12/2017 |
| 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. | Alternative splicing at exon 2 results in the loss of the catalytic activity of mouse DNA polymerase iota in vitro.
Kazachenko KY, Miropolskaya NA, Gening LV, Tarantul VZ, Makarova AV. | 08/12/2017 |
| Mouse DNA polymerase iota lacking exon 2 (42 amino acids) is catalytically inactive in vitro. | Mouse DNA polymerase ι lacking the forty-two amino acids encoded by exon-2 is catalytically inactive in vitro.
Frank EG, McDonald JP, Yang W, Woodgate R., Free PMC Article | 08/12/2017 |
| 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. | UV-induced mutations in epidermal cells of mice defective in DNA polymerase η and/or ι.
Kanao R, Yokoi M, Ohkumo T, Sakurai Y, Dotsu K, Kura S, Nakatsu Y, Tsuzuki T, Masutani C, Hanaoka F. | 02/13/2016 |
| Poliota causes the Par2 effect and inhibits tumorigenesis and mutagenesis | The error-prone DNA polymerase ι provides quantitative resistance to lung tumorigenesis and mutagenesis in mice.
Iguchi M, Osanai M, Hayashi Y, Koentgen F, Lee GH. | 09/6/2014 |
| in mammalian cells, both polymerases kappa and iota are necessary for the error-free bypass of N(2)-CEdG and N(2)-CMdG. | The roles of DNA polymerases κ and ι in the error-free bypass of N2-carboxyalkyl-2'-deoxyguanosine lesions in mammalian cells.
Yuan B, You C, Andersen N, Jiang Y, Moriya M, O'Connor TR, Wang Y., Free PMC Article | 07/30/2011 |
| 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 | Structural analysis of the conserved ubiquitin-binding motifs (UBMs) of the translesion polymerase iota in complex with ubiquitin.
Burschowsky D, Rudolf F, Rabut G, Herrmann T, Peter M, Wider G., Free PMC Article | 03/5/2011 |
| 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. | Effect of human cell malignancy on activity of DNA polymerase iota.
Kazakov AA, Grishina EE, Tarantul VZ, Gening LV. | 11/6/2010 |
| Pol iota gene may participate in error-free repair of damaged DNA and prevention of lung tumor development | Genetic linkage between Pol iota deficiency and increased susceptibility to lung tumors in mice.
Lee GH, Matsushita H., Free PMC Article | 01/21/2010 |
| 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. | 129-derived strains of mice are deficient in DNA polymerase iota and have normal immunoglobulin hypermutation.
McDonald JP, Frank EG, Plosky BS, Rogozin IB, Masutani C, Hanaoka F, Woodgate R, Gearhart PJ., Free PMC Article | 01/21/2010 |
| 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 | Ubiquitin-binding domains in Y-family polymerases regulate translesion synthesis.
Bienko M, Green CM, Crosetto N, Rudolf F, Zapart G, Coull B, Kannouche P, Wider G, Peter M, Lehmann AR, Hofmann K, Dikic I. | 01/21/2010 |
| suggest the involvement of the Pol eta and Pol iota proteins in UV-induced skin carcinogenesis | UV-B radiation induces epithelial tumors in mice lacking DNA polymerase eta and mesenchymal tumors in mice deficient for DNA polymerase iota.
Ohkumo T, Kondo Y, Yokoi M, Tsukamoto T, Yamada A, Sugimoto T, Kanao R, Higashi Y, Kondoh H, Tatematsu M, Masutani C, Hanaoka F., Free PMC Article | 01/21/2010 |
| Pol kappa and Pol iota double-deficient mice had the normal somatic hypermutation frequency | Normal immunoglobulin gene somatic hypermutation in Pol kappa-Pol iota double-deficient mice.
Shimizu T, Azuma T, Ishiguro M, Kanjo N, Yamada S, Ohmori H. | 01/21/2010 |
| 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 | Participation of mouse DNA polymerase iota in strand-biased mutagenic bypass of UV photoproducts and suppression of skin cancer.
Dumstorf CA, Clark AB, Lin Q, Kissling GE, Yuan T, Kucherlapati R, McGregor WG, Kunkel TA., Free PMC Article | 01/21/2010 |
| Nucleotide polymorphisms in DNA polymerase iota is associated with lung tumorigenesis in mouse and humans | Pol iota is a candidate for the mouse pulmonary adenoma resistance 2 locus, a major modifier of chemically induced lung neoplasia.
Wang M, Devereux TR, Vikis HG, McCulloch SD, Holliday W, Anna C, Wang Y, Bebenek K, Kunkel TA, Guan K, You M. | 01/21/2010 |