Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
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 pour 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. dans The Journal of cell biology 1999
Show all 5 references for ABIN968143
Dog (Canine) Monoclonal MLLT4 Primary Antibody pour 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. dans Oncogene 1999
Show all 2 references for ABIN1108256
In pancreatic cancer cells, AF6 is expressed at reduced levels, causing Dvl2 (Montrer DVL2 Anticorps) to be upregulated and available to bind and enhance FOXE1 (Montrer FOXE1 Anticorps)-induced trans-activation of Snail (Montrer SNAI1 Anticorps), 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 Anticorps) regulates epithelial permeability via association with ZO-2 (Montrer TJP2 Anticorps), afadin, and PDZ-GEF1 (Montrer RAPGEF2 Anticorps) to activate Rap2c (Montrer RAP2C Anticorps) and control contraction of the apical cytoskeleton.
MLL (Montrer MLL Anticorps)-AF6 oncoprotein potentiates the activity of the RAS pathway through retention of AF6 within the nucleus.
The expression levels of CFTR (Montrer CFTR Anticorps) and AF-6/afadin are significantly downregulated in human colon cancer tissues.
AF-6 is a positive modulator of the PINK1 (Montrer PINK1 Anticorps)/parkin (Montrer PARK2 Anticorps) pathway and is deficient in Parkinson's disease.
The interaction between the PDZ domain (Montrer INADL Anticorps) of afadin (AF6_PDZ) and a series of polypeptides comprising the PDZ (Montrer INADL Anticorps)-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 Anticorps)-ZO-1 (Montrer TJP1 Anticorps) interactions.
the Necl-5 (Montrer PVR Anticorps)-nectin (Montrer PVRL1 Anticorps), nectin-nectin (Montrer PVRL1 Anticorps), and nectin (Montrer PVRL1 Anticorps)-afadin interactions cooperatively increase the clustering of the nectin (Montrer PVRL1 Anticorps)-afadin complex at the cell-cell contact sites, promoting the formation of the nectin (Montrer PVRL1 Anticorps)-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 (Montrer PVRL3 Anticorps) 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 Anticorps) 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 Anticorps) 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 (Montrer PLEKHA7 Anticorps) plays a cooperative role with nectin (Montrer PVRL1 Anticorps) and afadin in the proper formation of Adherens junction (AJ) in epithelial cell.
Afadin acts upstream of the Par (Montrer AFG3L2 Anticorps) 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