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our data suggest the involvement of hNOT-1/ALG3-1 in various molecular contexts determining essential processes associated with distinct cellular machineries and related to various pathologies, such as cancer, viral infections, neuronal and immunological disorders and Congenital Disorders of Glycosylation.
These results together with the authors' previous study, have identified that CNOT1 provides a platform for the recruitment of TTP and CNOT7, and is involved in TTPmediated ICAM1 and IL8 mRNA decay.
YTHDF2 recruits the CCR4-NOT complex through a direct interaction between the YTHDF2 N-terminal region and the SH domain of the CNOT1 subunit, and that this recruitment is essential for the deadenylation of m6A-containing RNAs by CAF1 and CCR4.
the CNOT1-LMNA-Hedgehog signaling pathway axis exerts an oncogenic role in osteosarcoma progression, which could be a potential target for gene therapy.
we demonstrate that joint deletion of two short conserved motifs that bind UNR and DDX6 relieves repression of 4E-T-bound mRNA, in part reliant on the 4E-T-DDX6-CNOT1 axis.
miRNAs, AGOs, GW182, the CCR4-NOT complex, and DDX6/Me31B repress and degrade polyadenylated mRNA targets that are translated via scanning-independent mechanisms in both human and Drosophila melanogaster cells
Single nucleotide polymorphism in CNOT1 gene is associated with osteosarcoma susceptibility.
CNOT1 facilitates recruitment of DDX6 to miRNA-targeted mRNAs, placing DDX6 as a downstream effector in the miRNA silencing pathway.
SNP rs7188697 A/G significantly associated with response to dendritic cells therapeutic HIV vaccine
Crystal structures of the DDX6, CNOT1 and CNOT9 complexes.
Crystal structure of the DDX6, CNOT9 and CNOT1 complex.
The CNOT2-CNOT3 heterodimer is stabilized and tightly anchored to the surface of CNOT1 through an unexpected intertwined arrangement of peptide regions lacking defined secondary structure.
Authors identify an evolutionarily conserved C-terminal motif in human TTP that directly binds a central domain of CNOT1, a core subunit of the CCR4-NOT complex.
The NOT1 MIF4G domain binds CAF1 through a pre-formed interface and leaves the CAF1 catalytic site fully accessible to RNA substrates.
Cnot1, Cnot2, and Cnot3 represent a novel component of the core self-renewal and pluripotency circuitry conserved in mouse and human ESCs.
Depletion of CNOT1 induces cell death in a caspase-dependent manner.
purification and characterization of 1.0 MDa yeast CCR4-NOT complex identifies two novel components, CAF40 and CAF130: yeast CAF40 binds human NOT1
CNOT1 interacts in a ligand-dependent manner with RXR and represses transcription mediated by several RXR heterodimers.
Data show that Ccr4-Not function in RNA splicing and nuclear export, and that CNOT1 binds CNOT4 in yeast two-hybrid assays.
Collectively, our data support a model of CNOT7, TOB1, CNOT1, and RNA-binding proteins collectively exerting post-transcriptional control on a metastasis suppressive transcriptional program to drive tumor cell metastasis
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.
Belongs to the CCR4-NOT complex that functions as general transcription regulation complex. Acts as a transcriptional repressor. Represses the ligand-dependent transcriptional activation by nuclear receptors (By similarity).
CCR4-NOT transcription complex subunit 1
, CCR4-associated factor 1
, NOT1 (negative regulator of transcription 1, yeast) homolog
, adrenal gland protein AD-005
, negative regulator of transcription subunit 1 homolog
, CCR4-NOT transcription complex, subunit 1
, CCR4-NOT transcription complex subunit 1-like
, LOW QUALITY PROTEIN: CCR4-NOT transcription complex subunit 1