FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2117577778> ?p ?o ?g. }

• W2117577778 abstract "MTA1 (a metastasis-associated gene) is a newly discovere d human gene (residing on chromsome 14q32.3) that belongs to a family of cancer progression-related genes ( MTA ). The mRNA product of MTA1 along with its protein product MTA1 have been reported to be over-expressed in a wide variety of animal and human tumors. For example, the expression of MTA1 and its encoded protein MTA1 correlates with the malignant properties of many human cancers, including cancers of the breast, colon, stomach, li ver, prostate and others. The MTA proteins have bee n shown to be ubiquitinated transcriptional co-repressors that fu nction in histone deacetylation and are part of the NuRD complex, a nucleosome remodeling and histone deacetylating complex whose stability appears to be regulated by ubi quitinated MTA1 binding to E3 ubiquitin ligase constitutive ph otomorphogenesis protein-1 (COP1). The MTA1 protein plays an essential role in c-MYC-mediated cell transformatio n, and its expression correlates with mammary gland tumor formation. In the latter, MTA1 helps convert mammary cells to more aggressive phenotypes by repression of the estrogen receptor (ER) via trans-activation through deacetylation of chromatin in the ER-responsive el ement of ERresponsive genes. Another member of the MTA family, MTA3, is induced by estrogen and represses the exp ression of the transcriptional repressor Snail, a master regul ator of epithelial to mesenchymal transformation, r esulting in the expression of the cell adhesion molecule E-cadherin and maintenance of a differentiated, normal epithel ial phenotype in mammary cells. An important activity mediated by both MTA1 and MTA2 is deacylation and inactivation of tumor suppressor p53protein, in part by controlling its s tability by inhibiting ubiquitination, leading to i nhibition of growth arrest and apoptosis. Another factor deacetylated a nd stabilized by MTA1 NuRD complex is hypoxia-inducible factor1α (HIF-1α), which is involved in angiogenesis. Therefore, th e MTA proteins represent a possible set of master c oregulatory molecules involved in the carcinogenesis and progression of various malignant tumors. As su ch, they could be important new tools for cancer diagnosis and tre atment." @default.
• W2117577778 created "2016-06-24" @default.
• W2117577778 creator A5032721795 @default.
• W2117577778 creator A5048191306 @default.
• W2117577778 date "2011-11-01" @default.
• W2117577778 modified "2023-10-18" @default.
• W2117577778 title "MTA1 of the MTA (metastasis-associated) gene family and its encoded proteins: molecular and regulatory functions and role in human cancer progression" @default.
• W2117577778 cites W1493846190 @default.
• W2117577778 cites W1512414376 @default.
• W2117577778 cites W1525573602 @default.
• W2117577778 cites W1559118563 @default.
• W2117577778 cites W1567517848 @default.
• W2117577778 cites W1627110251 @default.
• W2117577778 cites W1966261319 @default.
• W2117577778 cites W1969735755 @default.
• W2117577778 cites W1969966017 @default.
• W2117577778 cites W1974434304 @default.
• W2117577778 cites W1974989557 @default.
• W2117577778 cites W1977703157 @default.
• W2117577778 cites W1977931536 @default.
• W2117577778 cites W1978974174 @default.
• W2117577778 cites W1980527124 @default.
• W2117577778 cites W1982808760 @default.
• W2117577778 cites W1988863549 @default.
• W2117577778 cites W1995466174 @default.
• W2117577778 cites W2001932191 @default.
• W2117577778 cites W2006670766 @default.
• W2117577778 cites W2014817033 @default.
• W2117577778 cites W2020051788 @default.
• W2117577778 cites W2020346907 @default.
• W2117577778 cites W2021046438 @default.
• W2117577778 cites W2021541148 @default.
• W2117577778 cites W2022100512 @default.
• W2117577778 cites W2024076463 @default.
• W2117577778 cites W2024318677 @default.
• W2117577778 cites W2027873852 @default.
• W2117577778 cites W2030432716 @default.
• W2117577778 cites W2032456988 @default.
• W2117577778 cites W2033031091 @default.
• W2117577778 cites W2034549547 @default.
• W2117577778 cites W2034758024 @default.
• W2117577778 cites W2037136180 @default.
• W2117577778 cites W2043860921 @default.
• W2117577778 cites W2047553717 @default.
• W2117577778 cites W2048468827 @default.
• W2117577778 cites W2049621013 @default.
• W2117577778 cites W2051682149 @default.
• W2117577778 cites W2052549908 @default.
• W2117577778 cites W2052678194 @default.
• W2117577778 cites W2056401500 @default.
• W2117577778 cites W2057808719 @default.
• W2117577778 cites W2058039607 @default.
• W2117577778 cites W2060399166 @default.
• W2117577778 cites W2060597630 @default.
• W2117577778 cites W2064860664 @default.
• W2117577778 cites W2069928663 @default.
• W2117577778 cites W2073732266 @default.
• W2117577778 cites W2074034654 @default.
• W2117577778 cites W2074380974 @default.
• W2117577778 cites W2081635401 @default.
• W2117577778 cites W2100404512 @default.
• W2117577778 cites W2101446038 @default.
• W2117577778 cites W2104104416 @default.
• W2117577778 cites W2105436320 @default.
• W2117577778 cites W2107387177 @default.
• W2117577778 cites W2111611782 @default.
• W2117577778 cites W2115422485 @default.
• W2117577778 cites W2123095951 @default.
• W2117577778 cites W2126336008 @default.
• W2117577778 cites W2130556236 @default.
• W2117577778 cites W2148655885 @default.
• W2117577778 cites W2151581451 @default.
• W2117577778 cites W2152163156 @default.
• W2117577778 cites W2156058796 @default.
• W2117577778 cites W2158626602 @default.
• W2117577778 cites W2161093040 @default.
• W2117577778 cites W2161903432 @default.
• W2117577778 cites W2162802160 @default.
• W2117577778 cites W2164407724 @default.
• W2117577778 cites W2164463729 @default.
• W2117577778 cites W2168490864 @default.
• W2117577778 cites W2341759155 @default.
• W2117577778 cites W2396314216 @default.
• W2117577778 cites W2397558607 @default.
• W2117577778 cites W2406723952 @default.
• W2117577778 cites W2110463280 @default.
• W2117577778 doi "https://doi.org/10.4267/2042/44992" @default.
• W2117577778 hasPublicationYear "2011" @default.
• W2117577778 type Work @default.
• W2117577778 sameAs 2117577778 @default.
• W2117577778 citedByCount "0" @default.
• W2117577778 crossrefType "journal-article" @default.
• W2117577778 hasAuthorship W2117577778A5032721795 @default.
• W2117577778 hasAuthorship W2117577778A5048191306 @default.
• W2117577778 hasBestOaLocation W21175777781 @default.
• W2117577778 hasConcept C104317684 @default.
• W2117577778 hasConcept C121608353 @default.
• W2117577778 hasConcept C141231307 @default.
• W2117577778 hasConcept C2779013556 @default.
• W2117577778 hasConcept C502942594 @default.

• next