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Afadin (AFDN), a cytoskeletal and junction-associated protein, was present in 2D and 3D keratinocyte cultures, and validated as a so-far-unknown EphA2 (Montrer EPHA2 Kits ELISA)-interacting protein.
In pancreatic cancer cells, AF6 is expressed at reduced levels, causing Dvl2 (Montrer DVL2 Kits ELISA) to be upregulated and available to bind and enhance FOXE1 (Montrer FOXE1 Kits ELISA)-induced trans-activation of Snail (Montrer SNAI1 Kits ELISA), 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 (Montrer F11R Kits ELISA) regulates epithelial permeability via association with ZO-2 (Montrer TJP2 Kits ELISA), afadin, and PDZ-GEF1 (Montrer RAPGEF2 Kits ELISA) to activate Rap2c (Montrer RAP2C Kits ELISA) and control contraction of the apical cytoskeleton.
MLL (Montrer MLL Kits ELISA)-AF6 oncoprotein potentiates the activity of the RAS pathway through retention of AF6 within the nucleus.
The expression levels of CFTR (Montrer CFTR Kits ELISA) and AF-6/afadin are significantly downregulated in human colon cancer tissues.
AF-6 is a positive modulator of the PINK1/parkin (Montrer PARK2 Kits ELISA) pathway and is deficient in Parkinson's disease.
The interaction between the PDZ domain (Montrer INADL Kits ELISA) of afadin (AF6_PDZ) and a series of polypeptides comprising the PDZ (Montrer INADL Kits ELISA)-binding motif, was studied.
Results demonstrate a role for afadin in the regulation of vascular barrier function via coordination of adherens junction-tight junction and p120-catenin (Montrer CTNND1 Kits ELISA)-ZO-1 (Montrer TJP1 Kits ELISA) interactions.
the Necl-5 (Montrer PVR Kits ELISA)-nectin (Montrer PVRL1 Kits ELISA), nectin-nectin (Montrer PVRL1 Kits ELISA), and nectin (Montrer PVRL1 Kits ELISA)-afadin interactions cooperatively increase the clustering of the nectin (Montrer PVRL1 Kits ELISA)-afadin complex at the cell-cell contact sites, promoting the formation of the nectin (Montrer PVRL1 Kits ELISA)-based cell-cell adhesion.
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 (Montrer PVRL3 Kits ELISA) 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 (Montrer PVRL3 Kits ELISA) and raise the possibility that there are proteins other than nectins that more preferentially bind s-afadin than l-afadin.
A remarkable function of afadin was revealed, it was able to enhance cytokine expression through Rap1 activation in keratinocytes during inflammation.
Afadin regulates puncta adherentia junction formation and presynaptic differentiation in hippocampal neurons.
This study showed that the adherens junction proteins afadin and CDH2 (Montrer CDH2 Kits ELISA) are critical for the control of cell proliferation in the dorsal telencephalon and for the formation of its normal laminar structure. Inactivation.
Genetic deletion of afadin causes hydrocephalus by destruction of adherens junctions in radial glial and ependymal cells in the midbrain.
Results indicate that PLEKHA7 plays a cooperative role with nectin (Montrer PVRL1 Kits ELISA) and afadin in the proper formation of Adherens junction (AJ) in epithelial cell.
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