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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 (显示 EPHA2 ELISA试剂盒)-interacting protein.
In pancreatic cancer cells, AF6 is expressed at reduced levels, causing Dvl2 (显示 DVL2 ELISA试剂盒) to be upregulated and available to bind and enhance FOXE1 (显示 FOXE1 ELISA试剂盒)-induced trans-activation of Snail (显示 SNAI1 ELISA试剂盒), 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 (显示 F11R ELISA试剂盒) regulates epithelial permeability via association with ZO-2 (显示 TJP2 ELISA试剂盒), afadin, and PDZ-GEF1 (显示 RAPGEF2 ELISA试剂盒) to activate Rap2c (显示 RAP2C ELISA试剂盒) and control contraction of the apical cytoskeleton.
MLL (显示 MLL ELISA试剂盒)-AF6 oncoprotein potentiates the activity of the RAS pathway through retention of AF6 within the nucleus.
The expression levels of CFTR (显示 CFTR ELISA试剂盒) and AF-6/afadin are significantly downregulated in human colon cancer tissues.
AF-6 is a positive modulator of the PINK1/parkin (显示 PARK2 ELISA试剂盒) pathway and is deficient in Parkinson's disease.
The interaction between the PDZ domain (显示 INADL ELISA试剂盒) of afadin (AF6_PDZ) and a series of polypeptides comprising the PDZ (显示 INADL ELISA试剂盒)-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 (显示 CTNND1 ELISA试剂盒)-ZO-1 (显示 TJP1 ELISA试剂盒) interactions.
the Necl-5 (显示 PVR ELISA试剂盒)-nectin (显示 PVRL1 ELISA试剂盒), nectin-nectin (显示 PVRL1 ELISA试剂盒), and nectin (显示 PVRL1 ELISA试剂盒)-afadin interactions cooperatively increase the clustering of the nectin (显示 PVRL1 ELISA试剂盒)-afadin complex at the cell-cell contact sites, promoting the formation of the nectin (显示 PVRL1 ELISA试剂盒)-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 (显示 PVRL3 ELISA试剂盒) 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 (显示 PVRL3 ELISA试剂盒) 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 (显示 CDH2 ELISA试剂盒) 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 (显示 PVRL1 ELISA试剂盒) 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