| De novo variants in CNOT9 cause a neurodevelopmental disorder with or without epilepsy. | De novo variants in CNOT9 cause a neurodevelopmental disorder with or without epilepsy.
von Wintzingerode L, Ben-Zeev B, Cesario C, Chan KM, Depienne C, Elpeleg O, Iascone M, Kelley WV, Nassogne MC, Niceta M, Pezzani L, Rahner N, Revencu N, Bekheirnia MR, Santiago-Sim T, Tartaglia M, Thompson ML, Trivisano M, Hentschel J, Sticht H, Abou Jamra R, Oppermann H. | 07/24/2023 |
| overexpression of miR-361-5p might act as a suppressor in triple-negative breast cancer by targeting RQCD1 to inhibit the EGFR/PI3K/Akt signaling pathway | Overexpression of miR-361-5p in triple-negative breast cancer (TNBC) inhibits migration and invasion by targeting RQCD1 and inhibiting the EGFR/PI3K/Akt pathway.
Han J, Yu J, Dai Y, Li J, Guo M, Song J, Zhou X., Free PMC Article | 06/15/2019 |
| Data suggest that the CCR4-NOT transcription complex subunit 1 (CNOT1)-CCR4-NOT transcription complex subunit 9 (CNOT9) components stimulate deadenylation by the nuclease module. | The central region of CNOT1 and CNOT9 stimulates deadenylation by the Ccr4-Not nuclease module.
Pavanello L, Hall B, Airhihen B, Winkler GS. | 06/8/2019 |
| Authors show that a novel interaction between TTP and the CCR4-NOT subunit, CNOT9, is required for recruitment of the deadenylase complex. In addition to CNOT1, CNOT9 is now included in the identified CCR4-NOT subunits shown to interact with TTP. | Tryptophan-Mediated Interactions between Tristetraprolin and the CNOT9 Subunit Are Required for CCR4-NOT Deadenylase Complex Recruitment.
Bulbrook D, Brazier H, Mahajan P, Kliszczak M, Fedorov O, Marchese FP, Aubareda A, Chalk R, Picaud S, Strain-Damerell C, Filippakopoulos P, Gileadi O, Clark AR, Yue WW, Burgess-Brown NA, Dean JLE. | 03/30/2019 |
| Data indicate a recurrent somatic C > T change causing a P131L mutation in the RQCD1 (Required for Cell Differentiation1 Homolog) gene identified through whole exome sequencing of 20 metastatic melanomas. | Whole exome sequencing identifies a recurrent RQCD1 P131L mutation in cutaneous melanoma.
Wong SQ, Behren A, Mar VJ, Woods K, Li J, Martin C, Sheppard KE, Wolfe R, Kelly J, Cebon J, Dobrovic A, McArthur GA., Free PMC Article | 11/28/2015 |
| Crystal structure of the DDX6, CNOT9 and CNOT1 complex. | A DDX6-CNOT1 complex and W-binding pockets in CNOT9 reveal direct links between miRNA target recognition and silencing.
Chen Y, Boland A, Kuzuoğlu-Öztürk D, Bawankar P, Loh B, Chang CT, Weichenrieder O, Izaurralde E. | 08/9/2014 |
| Crystal structures of the DDX6, CNOT1 and CNOT9 complexes. | Structural and biochemical insights to the role of the CCR4-NOT complex and DDX6 ATPase in microRNA repression.
Mathys H, Basquin J, Ozgur S, Czarnocki-Cieciura M, Bonneau F, Aartse A, Dziembowski A, Nowotny M, Conti E, Filipowicz W. | 08/9/2014 |
| Our findings in this study imply the functional mechanism of RQCD1 in the Akt activity regulation as a mediator in the EGFR-signaling pathway | Critical involvement of RQCD1 in the EGFR-Akt pathway in mammary carcinogenesis.
Ajiro M, Nishidate T, Katagiri T, Nakamura Y. | 01/29/2011 |
| Report involvement of RQCD1 overexpression, a novel cancer-testis antigen, in the Akt pathway in breast cancer cells. | Involvement of RQCD1 overexpression, a novel cancer-testis antigen, in the Akt pathway in breast cancer cells.
Ajiro M, Katagiri T, Ueda K, Nakagawa H, Fukukawa C, Lin ML, Park JH, Nishidate T, Daigo Y, Nakamura Y. | 01/21/2010 |
| CCR4 plays a role in the regulation of certain endogenous RARalpha target genes and RCD1 and CCR4 might mediate their function through their interaction with NIF-1 | Components of the CCR4-NOT complex function as nuclear hormone receptor coactivators via association with the NRC-interacting Factor NIF-1.
Garapaty S, Mahajan MA, Samuels HH. | 01/21/2010 |
| mammalian protein is a novel transcriptional cofactor that mediates retinoic acid-induced cell differentiation | Mammalian Rcd1 is a novel transcriptional cofactor that mediates retinoic acid-induced cell differentiation.
Hiroi N, Ito T, Yamamoto H, Ochiya T, Jinno S, Okayama H., Free PMC Article | 01/21/2010 |