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CLDN6 (zeige CLDN6 Antikörper) enhances the chemoresistance to ADM (zeige ADM Antikörper) via activating the AF-6/ERK (zeige EPHB2 Antikörper) signaling pathway and up-regulating cancer stem cell characters in MDAMB231 cells.
AF6 employs a non-canonical, evolutionarily conserved alpha-helix to bind RAS, unique to AF6 and the classical RASSF effectors.
miR (zeige MLXIP Antikörper)-188-3p is a novel independent prognostic factor in colorectal cancer patients, which can be partly explained by its effect on MLLT4 expression and migration of cancer cells.
Afadin (AFDN), a cytoskeletal and junction-associated protein, was present in 2D and 3D keratinocyte cultures, and validated as a so-far-unknown EphA2 (zeige EPHA2 Antikörper)-interacting protein.
In pancreatic cancer cells, AF6 is expressed at reduced levels, causing Dvl2 (zeige DVL2 Antikörper) to be upregulated and available to bind and enhance FOXE1 (zeige FOXE1 Antikörper)-induced trans-activation of Snail (zeige SNAI1 Antikörper), which promotes proliferation and metastasis.
AF-6/afadin could be a useful selection marker for fertility-sparing therapy for patients with atypical hyperplasia or grade 1 endometrioid adenocarcinoma with no myometrial invasion.
JAM-A (zeige F11R Antikörper) regulates epithelial permeability via association with ZO-2 (zeige TJP2 Antikörper), afadin, and PDZ-GEF1 (zeige RAPGEF2 Antikörper) to activate Rap2c (zeige RAP2C Antikörper) and control contraction of the apical cytoskeleton.
MLL (zeige MLL Antikörper)-AF6 oncoprotein potentiates the activity of the RAS pathway through retention of AF6 within the nucleus.
The expression levels of CFTR (zeige CFTR Antikörper) and AF-6/afadin are significantly downregulated in human colon cancer tissues.
AF-6 is a positive modulator of the PINK1 (zeige PINK1 Antikörper)/parkin (zeige PARK2 Antikörper) pathway and is deficient in Parkinson's disease.
These results indicate that afadin plays multiple roles in the complex ultrastructural morphogenesis of hippocampal mossy fiber synapses.
Findings indicate that afadin plays an essential role in regulating apical-basal polarity and adherens junction integrity of radial glial cells.
Codepletion of the actomyosin regulator RhoA (zeige RHOA Antikörper) and Afadin results in defects in the central lumens and arrests lumen remodeling
Glutamate (zeige GRIN1 Antikörper) release and the postsynaptic responsiveness to glutamate (zeige GRIN1 Antikörper) were markedly reduced, but not completely lost, in the afadin-deficient mossy fiber synapse, whereas neither long-term potentiation nor long-term depression was affected.
Afadin regulates the differentiation of the CA3 (zeige CA3 Antikörper) pyramidal cells, elongation of the mossy fiber trajectory and the density of mossy fiber synapses.
afadin determines lumen placement by directing apical-basal spindle orientation, resulting in a continuous lumen and normal tubule morphogenesis.
Results indicate that afadin is required for the maintenance of the radial glial scaffold for neuronal migration and that the genetic ablation of afadin leads to the formation of double cortex
Here, the first crystal structure of the AFPDZ in complex with the nectin-3 (zeige PVRL3 Antikörper) C-terminal peptide containing the class II motif is reported.
Afadin plays a role in the restricted localization of Paneth cells at the base of the crypt by maintaining their adhesion to adjacent crypt cells and inhibiting their movement toward the top of villi.
S-afadin-specific C-terminal inserts may be involved in its preference of binding to nectin-3 (zeige PVRL3 Antikörper) and raise the possibility that there are proteins other than nectins that more preferentially bind s-afadin than l-afadin.
This gene encodes a multi-domain protein involved in signaling and organization of cell junctions during embryogenesis. It has also been identified as the fusion partner of acute lymphoblastic leukemia (ALL-1) gene, involved in acute myeloid leukemias with t(6\;11)(q27\;q23) translocation. Alternatively spliced transcript variants encoding different isoforms have been described for this gene, however, not all have been fully characterized.
myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila); translocated to, 4
, ALL1-fused gene from chromosome 6 protein
, protein AF-6
, myeloid/lymphoid or mixed lineage-leukemia translocation to 4 homolog
, protein Af-6
, myeloid/lymphoid or mixed-lineage leukemia 4