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In pancreatic cancer cells, AF6 is expressed at reduced levels, causing Dvl2 (zeige DVL2 ELISA Kits) to be upregulated and available to bind and enhance FOXE1 (zeige FOXE1 ELISA Kits)-induced trans-activation of Snail (zeige SNAI1 ELISA Kits), 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 ELISA Kits) regulates epithelial permeability via association with ZO-2 (zeige TJP2 ELISA Kits), afadin, and PDZ-GEF1 (zeige RAPGEF2 ELISA Kits) to activate Rap2c (zeige RAP2C ELISA Kits) and control contraction of the apical cytoskeleton.
MLL (zeige MLL ELISA Kits)-AF6 oncoprotein potentiates the activity of the RAS pathway through retention of AF6 within the nucleus.
The expression levels of CFTR (zeige CFTR ELISA Kits) and AF-6/afadin are significantly downregulated in human colon cancer tissues.
AF-6 is a positive modulator of the PINK1/parkin (zeige PARK2 ELISA Kits) pathway and is deficient in Parkinson's disease.
The interaction between the PDZ domain (zeige INADL ELISA Kits) of afadin (AF6_PDZ) and a series of polypeptides comprising the PDZ (zeige INADL ELISA Kits)-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 (zeige CTNND1 ELISA Kits)-ZO-1 (zeige TJP1 ELISA Kits) interactions.
the Necl-5 (zeige PVR ELISA Kits)-nectin (zeige PVRL1 ELISA Kits), nectin-nectin (zeige PVRL1 ELISA Kits), and nectin (zeige PVRL1 ELISA Kits)-afadin interactions cooperatively increase the clustering of the nectin (zeige PVRL1 ELISA Kits)-afadin complex at the cell-cell contact sites, promoting the formation of the nectin (zeige PVRL1 ELISA Kits)-based cell-cell adhesion.
AF6/afadin is a marker of poor outcome in breast cancer, and its loss induces cell migration, invasiveness and tumor growth
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 ELISA Kits) 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 ELISA Kits) 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 (zeige CDH2 ELISA Kits) 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 (zeige PVRL1 ELISA Kits) and afadin in the proper formation of Adherens junction (AJ) in epithelial cell.
Afadin acts upstream of the Par (zeige AFG3L2 ELISA Kits) complex to regulate the integration and/or coalescence of membrane microdomains, establishing apical-basal polarity and lumen formation/elongation during kidney tubulogenesis.
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