Редактирование: TREX2

Three prime repair exonuclease 2 (EC 3.1.11.2) (3'-5' exonuclease TREX2)

==Publications==

{{medline-entry
|title=Increased Susceptibility to Skin Carcinogenesis in [[TREX2]] Knockout Mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19654293
|abstract=[[TREX2]] is a proofreading 3'-5' exonuclease that can be involved in genome maintenance; however, its biological role remains undefined. To better understand the function and physiologic relevance of [[TREX2]], we generated mice deficient in [[TREX2]] by targeted disruption of its unique coding exon. The knockout mice are viable and do not show relevant differences in growth, survival, lymphocyte development, or spontaneous tumor incidence compared with their wild-type counterparts over a period of up to 2 years. Also, we did not observe chromosomal instability or defects in cell proliferation and cell cycle upon loss of [[TREX2]]. We have observed that [[TREX2]] expression is not ubiquitous, being expressed preferentially in tissues with stratified squamous epithelia, such as the skin or esophagus, and specifically in keratinocytes. Interestingly, [[TREX2]]-null mice are more susceptible to skin carcinogenesis induced by 7,12-dimethylbenz(a)anthracene (DMBA) compared with wild-type mice. This phenotype correlates with a reduction of DMBA-induced apoptosis in both the epidermis and keratinocytes of [[TREX2]]-null mice. Altogether, our results suggest a tumor suppressor role for [[TREX2]] in skin carcinogenesis through which it contributes to keratinocyte apoptosis under conditions of genotoxic stress.
|mesh-terms=* 9,10-Dimethyl-1,2-benzanthracene
* Aging
* Animals
* Apoptosis
* Carcinogens
* Carcinoma
* Cells, Cultured
* Embryo, Mammalian
* Exodeoxyribonucleases
* Female
* Genetic Predisposition to Disease
* Keratinocytes
* Male
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Organ Specificity
* Skin Neoplasms
* Tissue Distribution

|full-text-url=https://sci-hub.do/10.1158/0008-5472.CAN-09-1208
}}