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Human Monoclonal MLLT4 Primary Antibody für 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 Pubmed References
Human Monoclonal MLLT4 Primary Antibody für IF, IP - ABIN968144
Prasad, Gu, Alder, Nakamura, Canaani, Saito, Huebner, Gale, Nowell, Kuriyama: Cloning of the ALL-1 fusion partner, the AF-6 gene, involved in acute myeloid leukemias with the t(6;11) chromosome translocation. in Cancer research 1994
Show all 5 Pubmed References
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.
The interaction between the PDZ domain (zeige INADL Antikörper) of afadin (AF6_PDZ) and a series of polypeptides comprising the PDZ (zeige INADL Antikörper)-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 Antikörper)-ZO-1 (zeige TJP1 Antikörper) interactions.
the Necl-5 (zeige PVR Antikörper)-nectin (zeige PVRL1 Antikörper), nectin-nectin (zeige PVRL1 Antikörper), and nectin (zeige PVRL1 Antikörper)-afadin interactions cooperatively increase the clustering of the nectin (zeige PVRL1 Antikörper)-afadin complex at the cell-cell contact sites, promoting the formation of the nectin (zeige PVRL1 Antikörper)-based cell-cell adhesion.
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.
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 Antikörper) 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 (zeige PLEKHA7 Antikörper) plays a cooperative role with nectin (zeige PVRL1 Antikörper) and afadin in the proper formation of Adherens junction (AJ) in epithelial cell.
Afadin acts upstream of the Par (zeige AFG3L2 Antikörper) 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