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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

NOT3 Not3p

NOT3, Not3p, CNOT3, LENG2, CCR4-NOT transcription complex subunit 3
Top mentioned proteins: CDC36, NotI, TBP, V1a, CAN
Papers on NOT3
CNOT3 contributes to early B cell development by controlling Igh rearrangement and p53 mRNA stability.
Kurosaki et al., Suita, Japan. In J Exp Med, Sep 2015
Here we show that mice lacking the CNOT3 subunit of this complex, specifically in B cells, have a developmental block at the pro- to pre-B cell transition.
MicroRNA biogenesis pathway from the salmon louse (Caligus rogercresseyi): emerging role in delousing drug response.
Gallardo-Escárate et al., Concepción, Chile. In Gene, Feb 2015
RNA-Seq analysis revealed that CCR4-Not complex subunit 3 (CNOT3) was upregulated at earlier developmental stages (nauplius I-II and copepodid), and also after the exposure to Azamethiphos, but not to Deltamethrin.
CNOT3 suppression promotes necroptosis by stabilizing mRNAs for cell death-inducing proteins.
Yamamoto et al., Okinawa, Japan. In Sci Rep, 2014
We show here that CNOT3-depleted mouse embryonic fibroblasts (MEFs) undergo cell death.
Identification of Ccr4-not complex components as regulators of transition from partial to genuine induced pluripotent stem cells.
Okuda et al., Saitama, Japan. In Stem Cells Dev, 2014
Subsequent analyses revealed that other core components, Cnot1 and Cnot3, also contributed to the conversion.
Stability of mRNA influences osteoporotic bone mass via CNOT3.
Noda et al., Tokyo, Japan. In Proc Natl Acad Sci U S A, 2014
CNOT3 is a component of the CCR4 family that regulates mRNA stability, but its function in bone is not known.
Dominant PRPF31 mutations are hypostatic to a recessive CNOT3 polymorphism in retinitis pigmentosa: a novel phenomenon of "linked trans-acting epistasis".
Bhattacharya et al., London, United Kingdom. In Ann Hum Genet, 2014
Variable expression of CNOT3 is one determinant of PRPF31 expression.
Structure and assembly of the NOT module of the human CCR4-NOT complex.
Izaurralde et al., Tübingen, Germany. In Nat Struct Mol Biol, 2013
We report the crystal structure of the human NOT module formed by the CNOT1, CNOT2 and CNOT3 C-terminal (-C) regions.
Exome sequencing identifies mutation in CNOT3 and ribosomal genes RPL5 and RPL10 in T-cell acute lymphoblastic leukemia.
Cools et al., Leuven, Belgium. In Nat Genet, 2013
We identify CNOT3 as a tumor suppressor mutated in 7 of 89 (7.9%) adult T-ALLs, and its knockdown causes tumors in a sensitized Drosophila melanogaster model.
NOT10 and C2orf29/NOT11 form a conserved module of the CCR4-NOT complex that docks onto the NOT1 N-terminal domain.
Izaurralde et al., Tübingen, Germany. In Rna Biol, 2013
The conserved core of the complex is assembled by the interaction of at least two modules: the NOT module, which minimally consists of NOT1, NOT2 and NOT3, and a catalytic module comprising two deadenylases, CCR4 and POP2/CAF1.
Genome-wide and species-wide in silico screening for intragenic MicroRNAs in human, mouse and chicken.
Kunej et al., Slovenia. In Plos One, 2012
Particularly interesting are miRNA genes located within genes encoding for miRNA silencing machinery (DGCR8, DICER1, and SND1 in human and Cnot3, Gdcr8, Eif4e, Tnrc6b, and Xpo5 in mouse).
The structural basis for the interaction between the CAF1 nuclease and the NOT1 scaffold of the human CCR4-NOT deadenylase complex.
Weichenrieder et al., Tübingen, Germany. In Nucleic Acids Res, 2012
The conserved core of the complex consists of a catalytic module comprising two deadenylases (CAF1/POP2 and CCR4a/b) and the NOT module, which contains at least NOT1, NOT2 and NOT3.
A high density SNP genotyping approach within the 19q13 chromosome region identifies an association of a CNOT3 polymorphism with ankylosing spondylitis.
López-Larrea et al., Oviedo, Spain. In Ann Rheum Dis, 2012
A high density SNP genotyping approach within the 19q13 chromosome region identifies an association of a CNOT3 polymorphism with ankylosing spondylitis.
Cnot1, Cnot2, and Cnot3 maintain mouse and human ESC identity and inhibit extraembryonic differentiation.
Hu et al., United States. In Stem Cells, 2012
Cnot1, Cnot2, and Cnot3 represent a novel component of the core self-renewal and pluripotency circuitry conserved in mouse and human ESCs.
Involvement of CNOT3 in mitotic progression through inhibition of MAD1 expression.
Yamamoto et al., Tokyo, Japan. In Biochem Biophys Res Commun, 2012
CNOT3 depletion stabilizes the MAD1 mRNA, and MAD1 knockdown attenuates the CNOT3 depletion-induced increase of the mitotic index.
The anti-proliferative activity of BTG/TOB proteins is mediated via the Caf1a (CNOT7) and Caf1b (CNOT8) deadenylase subunits of the Ccr4-not complex.
Winkler et al., Nottingham, United Kingdom. In Plos One, 2011
Furthermore, we show that the activity of BTG/TOB proteins in the regulation of mRNA abundance and translation is dependent on Caf1a/Caf1b, and does not appear to require other Ccr4-Not components, including the Ccr4a (CNOT6)/Ccr4b (CNOT6L) deadenylases, or the non-catalytic subunits CNOT1 or CNOT3.
CNOT3 is a modifier of PRPF31 mutations in retinitis pigmentosa with incomplete penetrance.
Rivolta et al., Lausanne, Switzerland. In Plos Genet, 2011
This gene was CNOT3, encoding a subunit of the Ccr4-not transcription complex.
Obesity resistance and increased hepatic expression of catabolism-related mRNAs in Cnot3+/- mice.
Yamamoto et al., Tokyo, Japan. In Embo J, 2011
CNOT3 responds to feeding conditions to regulate deadenylation-specific mRNAs and energy metabolism
Implication of Ccr4-Not complex function in mRNA quality control in Saccharomyces cerevisiae.
Jensen et al., Århus, Denmark. In Rna, 2011
report that four subunits of the Ccr4-Not complex-Ccr4p, Pop2p, Not2p, and Not4p-severely impact HSP104 RNA transcription site-associated retention induced by MFT1 gene deletion
A global in vivo Drosophila RNAi screen identifies NOT3 as a conserved regulator of heart function.
Penninger et al., Vienna, Austria. In Cell, 2010
Heterozygous not3 knockout mice showed spontaneous impairment of cardiac contractility and increased susceptibility to heart failure.
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