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MLLT4 encodes a multi-domain protein involved in signaling and organization of cell junctions during embryogenesis.
Showing 10 out of 38 products:
Human Monoclonal MLLT4 Primary Antibody for IF, IP - ABIN968143
Buchert, Schneider, Meskenaite, Adams, Canaani, Baechi, Moelling, Hovens: The junction-associated protein AF-6 interacts and clusters with specific Eph receptor tyrosine kinases at specialized sites of cell-cell contact in the brain. in The Journal of cell biology 1999
Show all 5 references for ABIN968143
Dog (Canine) Monoclonal MLLT4 Primary Antibody for EIA, IP - ABIN1108256
Sakisaka, Nakanishi, Takahashi, Mandai, Miyahara, Satoh, Takaishi, Takai: Different behavior of l-afadin and neurabin-II during the formation and destruction of cell-cell adherens junction. in Oncogene 1999
Show all 2 references for ABIN1108256
In pancreatic cancer cells, AF6 is expressed at reduced levels, causing Dvl2 (show DVL2 Antibodies) to be upregulated and available to bind and enhance FOXE1 (show FOXE1 Antibodies)-induced trans-activation of Snail (show SNAI1 Antibodies), 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 (show F11R Antibodies) regulates epithelial permeability via association with ZO-2 (show TJP2 Antibodies), afadin, and PDZ-GEF1 (show RAPGEF2 Antibodies) to activate Rap2c (show RAP2C Antibodies) and control contraction of the apical cytoskeleton.
MLL (show MLL Antibodies)-AF6 oncoprotein potentiates the activity of the RAS pathway through retention of AF6 within the nucleus.
The expression levels of CFTR (show CFTR Antibodies) and AF-6/afadin are significantly downregulated in human colon cancer tissues.
AF-6 is a positive modulator of the PINK1 (show PINK1 Antibodies)/parkin (show PARK2 Antibodies) pathway and is deficient in Parkinson's disease.
The interaction between the PDZ domain (show INADL Antibodies) of afadin (AF6_PDZ) and a series of polypeptides comprising the PDZ (show INADL Antibodies)-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 (show CTNND1 Antibodies)-ZO-1 (show TJP1 Antibodies) interactions.
the Necl-5 (show PVR Antibodies)-nectin (show PVRL1 Antibodies), nectin-nectin (show PVRL1 Antibodies), and nectin (show PVRL1 Antibodies)-afadin interactions cooperatively increase the clustering of the nectin (show PVRL1 Antibodies)-afadin complex at the cell-cell contact sites, promoting the formation of the nectin (show PVRL1 Antibodies)-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 (show PVRL3 Antibodies) 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 (show PVRL3 Antibodies) 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 (show CDH2 Antibodies) 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 (show PLEKHA7 Antibodies) plays a cooperative role with nectin (show PVRL1 Antibodies) and afadin in the proper formation of Adherens junction (AJ) in epithelial cell.
Afadin acts upstream of the Par (show AFG3L2 Antibodies) 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