DOI 10.1016/j.gene.2017.05.019
MTUS1, a gene encoding angiotensin-II type 2 (AT2) receptor-interacting proteins, in health and disease, with special emphasis on its role in carcinogenesis.
Аннотация
Loss of tumor suppressor activity is a frequent event in the formation and progression of tumors and has been listed as an important hallmark of cancers. Microtubule-Associated Scaffold Protein 1 (MTUS1) is a candidate tumor suppressor gene which is reported to be frequently down-regulated in a variety of human cancers including pancreas, colon, bladder, head-and-neck, ovarian, breast cancers, gastric, lung cancers. It is also reported to be implicated in several types of pathologies such as cardiac hypertrophy, atherosclerosis, and SLE-like lymphoproliferative diseases. Moreover, MTUS1-encoded proteins are shown to be involved in the regulation of vital cellular processes such as proliferation, differentiation, DNA repair, inflammation, vascular remodeling and senescence. However, the current knowledge is very limited about the role of this gene in human cancers as well as other type diseases. Besides, there is no literature report which summarizes and criticizes the importance of MTUS1 in the cellular processes, especially in the processes of carcinogenesis. Accordingly, in this comprehensive review, we tried to shed light on the role of tumor suppressor MTUS1/ATIP in health and disease, putting special emphasis on its role in the development and progression of human cancers as well as associated molecular mechanisms and the reasons behind MTUS1/ATIP deficiency, which have been not well documented previously.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.