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The crystal structure of the NED central region of Nanos bound to the NOT module reveals an unanticipated bipartite binding interface that contacts NOT1 (show CNOT1 ELISA Kits) and NOT3 and is distinct from the NOT1 (show CNOT1 ELISA Kits) interacting motif of vertebrate Nanos.
our findings implicate CNOT3 in the coordination of colonic epithelial cell self-renewal, suggesting this factor as a new biomarker for molecular and prognostic classification of early-stage colorectal cancer
A mutation in PRPF31 (show PRPF31 ELISA Kits) is hypostatic to a trait acting on CNOT3, with the RP11 (show PRPF31 ELISA Kits) phenotype only being observed when there is homozygous (recessive) inheritance of the higher expressivity CNOT3 ("symptomatic" or risk) allele.
The CNOT2 (show CNOT2 ELISA Kits)-CNOT3 heterodimer is stabilized and tightly anchored to the surface of CNOT1 (show CNOT1 ELISA Kits) through an unexpected intertwined arrangement of peptide regions lacking defined secondary structure.
In asymptomatic carriers CNOT3 is expressed at low levels, allowing higher amounts of wild-type PRPF31 (show PRPF31 ELISA Kits) transcripts to be produced and preventing manifestation of retinal degeneration.
CNOT3 is a tumor suppressor mutated in 7 of 89 (7.9%) adult T-cell acute lymphoblastic leukemias, and its knockdown causes tumors in a sensitized Drosophila melanogaster model.
Cnot1 (show CNOT1 ELISA Kits), Cnot2 (show CNOT2 ELISA Kits), and Cnot3 represent a novel component of the core self-renewal and pluripotency circuitry conserved in mouse and human ESCs (show NR2E3 ELISA Kits).
A high density SNP genotyping approach within the 19q13 chromosome region identifies an association of a CNOT3 polymorphism with ankylosing spondylitis.
CNOT3 depletion stabilizes the MAD1 (show MXD1 ELISA Kits) mRNA, and MAD1 (show MXD1 ELISA Kits) knockdown attenuates the CNOT3 depletion-induced increase of the mitotic index.
TBP-interacting protein 120B (show CAND2 ELISA Kits) binds to NOT3
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(ad-/-) mice exhibit lipodystrophy.
increases the number of ALP-positive colonies after iPSC induction and decreases expression levels of Eomes (show EOMES ELISA Kits) and p21 mRNAs. Based on these observations, we propose that the CCR4 (show CCR4 ELISA Kits)-NOT deadenylase activity contributes to iPSC induction.
CNOT3 suppression promotes necroptosis by stabilizing mRNAs for cell death-inducing proteins, Ripk1 (show RIPK1 ELISA Kits) and Ripk3 (show RIPK3 ELISA Kits).
data suggest that the CCR4 (show CCR4 ELISA Kits)-NOT complex regulates B cell differentiation by controlling Igh rearrangement and destabilizing p53 (show TP53 ELISA Kits) mRNA.
These data have uncovered a novel role of core components of the Ccr4 (show CCR4 ELISA Kits)-Not complex as regulators of transition from partial to genuine induced pluripotent stem cells.
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.
CNOT3 responds to feeding conditions to regulate deadenylation-specific mRNAs and energy metabolism
The CCR4-NOT complex functions as general transcription regulation complex.
CCR4-NOT transcription complex, subunit 3
, CCR4-NOT transcription complex subunit 3-like
, CCR4-NOT transcription complex subunit 3
, CCR4-associated factor 3
, NOT3 (negative regulator of transcription 3, yeast) homolog
, leukocyte receptor cluster member 2