| CNOT3 interacts with the Aurora B and MAPK/ERK kinases to promote survival of differentiating mesendodermal progenitor cells. | CNOT3 interacts with the Aurora B and MAPK/ERK kinases to promote survival of differentiating mesendodermal progenitor cells.
Sarkar M, Martufi M, Roman-Trufero M, Wang YF, Whilding C, Dormann D, Sabbattini P, Dillon N., Free PMC Article | 03/26/2022 |
| Loss of beta-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation. | Loss of β-cell identity and diabetic phenotype in mice caused by disruption of CNOT3-dependent mRNA deadenylation.
Mostafa D, Yanagiya A, Georgiadou E, Wu Y, Stylianides T, Rutter GA, Suzuki T, Yamamoto T., Free PMC Article | 06/19/2021 |
| Cnot3 plays a crucial role in liver functional maturation | Postnatal liver functional maturation requires Cnot complex-mediated decay of mRNAs encoding cell cycle and immature liver genes.
Suzuki T, Kikuguchi C, Nishijima S, Nagashima T, Takahashi A, Okada M, Yamamoto T., Free PMC Article | 01/4/2020 |
| Data indicate that autophagy-related protein 7 (Atg7) promotes cardiac dysfunction of CCR4-NOT complex component Cnot3 knockout (Cnot3 mKO) mice independently of the canonical autophagy pathway. | The CCR4-NOT deadenylase complex controls Atg7-dependent cell death and heart function.
Yamaguchi T, Suzuki T, Sato T, Takahashi A, Watanabe H, Kadowaki A, Natsui M, Inagaki H, Arakawa S, Nakaoka S, Koizumi Y, Seki S, Adachi S, Fukao A, Fujiwara T, Natsume T, Kimura A, Komatsu M, Shimizu S, Ito H, Suzuki Y, Penninger JM, Yamamoto T, Imai Y, Kuba K. | 09/21/2019 |
| we propose that CNOT3 maintains the pluripotent state by promoting differentiation gene mRNA deadenylation and degradation, and we identify poly(A) tail-length regulation as a post-transcriptional mechanism that controls pluripotency. | CNOT3-Dependent mRNA Deadenylation Safeguards the Pluripotent State.
Zheng X, Yang P, Lackford B, Bennett BD, Wang L, Li H, Wang Y, Miao Y, Foley JF, Fargo DC, Jin Y, Williams CJ, Jothi R, Hu G., Free PMC Article | 11/26/2017 |
| Cnot3(ad-/-) mice exhibit lipodystrophy. | Adipocyte-specific disruption of mouse Cnot3 causes lipodystrophy.
Li X, Morita M, Kikuguchi C, Takahashi A, Suzuki T, Yamamoto T. | 05/13/2017 |
| increases the number of ALP-positive colonies after iPSC induction and decreases expression levels of Eomes and p21 mRNAs. Based on these observations, we propose that the CCR4-NOT deadenylase activity contributes to iPSC induction. | The CCR4-NOT deadenylase activity contributes to generation of induced pluripotent stem cells.
Zukeran A, Takahashi A, Takaoka S, Mohamed HMA, Suzuki T, Ikematsu S, Yamamoto T. | 05/13/2017 |
| CNOT3 suppression promotes necroptosis by stabilizing mRNAs for cell death-inducing proteins, Ripk1 and Ripk3. | CNOT3 suppression promotes necroptosis by stabilizing mRNAs for cell death-inducing proteins.
Suzuki T, Kikuguchi C, Sharma S, Sasaki T, Tokumasu M, Adachi S, Natsume T, Kanegae Y, Yamamoto T., Free PMC Article | 08/13/2016 |
| data suggest that the CCR4-NOT complex regulates B cell differentiation by controlling Igh rearrangement and destabilizing p53 mRNA. | CNOT3 contributes to early B cell development by controlling Igh rearrangement and p53 mRNA stability.
Inoue T, Morita M, Hijikata A, Fukuda-Yuzawa Y, Adachi S, Isono K, Ikawa T, Kawamoto H, Koseki H, Natsume T, Fukao T, Ohara O, Yamamoto T, Kurosaki T., Free PMC Article | 11/7/2015 |
| These data have uncovered a novel role of core components of the Ccr4-Not complex as regulators of transition from partial to genuine induced pluripotent stem cells. | Identification of Ccr4-not complex components as regulators of transition from partial to genuine induced pluripotent stem cells.
Kamon M, Katano M, Hiraki-Kamon K, Hishida T, Nakachi Y, Mizuno Y, Okazaki Y, Suzuki A, Hirasaki M, Ueda A, Nishimoto M, Kato H, Okuda A., Free PMC Article | 05/16/2015 |
| CNOT3 is a critical regulator of bone mass acting on bone resorption through posttranscriptional down-regulation of RANK mRNA stability, at least in part, even in aging-induced osteoporosis. | Stability of mRNA influences osteoporotic bone mass via CNOT3.
Watanabe C, Morita M, Hayata T, Nakamoto T, Kikuguchi C, Li X, Kobayashi Y, Takahashi N, Notomi T, Moriyama K, Yamamoto T, Ezura Y, Noda M., Free PMC Article | 04/19/2014 |
| Cnot1, Cnot2, and Cnot3 represent a novel component of the core self-renewal and pluripotency circuitry conserved in mouse and human ESCs. | Cnot1, Cnot2, and Cnot3 maintain mouse and human ESC identity and inhibit extraembryonic differentiation.
Zheng X, Dumitru R, Lackford BL, Freudenberg JM, Singh AP, Archer TK, Jothi R, Hu G., Free PMC Article | 08/4/2012 |
| CNOT3 responds to feeding conditions to regulate deadenylation-specific mRNAs and energy metabolism | Obesity resistance and increased hepatic expression of catabolism-related mRNAs in Cnot3+/- mice.
Morita M, Oike Y, Nagashima T, Kadomatsu T, Tabata M, Suzuki T, Nakamura T, Yoshida N, Okada M, Yamamoto T., Free PMC Article | 01/21/2012 |