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Its overexpression represents a negative prognostic marker that has been linked to tumor grade, proliferating potential and angiogenesis and mediates intracellular transport of anticancer agents.
The AML1/ETO target gene LAT2 interferes with differentiation of normal hematopoietic precursor cells.
LAT2 is an early mediator of the anti-leukemic activity of alkylphospholipids and arsenic trioxide. Thus, LAT2 may be used as a target for the design of drugs for cancer therapy.
NTAL acts as a tumor suppressor that enhances the proximal signaling of leukemic blasts. The key downstream molecule responsible for the biological effect of TCR signaling is ERK.
LAB has the ability to modulate signaling in virtually every type of leukocyte.
LAT2 protein (NTAL) participates in the activation of the c-Met-Grb2-ERK-cPLA2 signalling cascade at early stages of H. pylori infection.
data show that NTAL (non-T cell activation linker) appears to be a structural and possibly also functional homologue of LAT (linker for activation of T cells)in non-T cells [non-T cell activation linker]
LAB links BCR engagement to downstream signaling pathways.
LAB was primarily phosphorylated on three membrane-distal tyrosines, Tyr(136), Tyr(193), and Tyr(233). Mutation of these three tyrosines abolished Grb2 binding and LAB function
LAB resembled a LAT molecule unable to bind phospholipase C-gamma1.
The NTAL/LAB is expressed in a variety of immune cells.
NTAL acts as a negative regulator of TNF-alpha and IL-8 production after stimulation via TREM-1
observations reported herein support the conclusion that NTAL may be differentially utilized by specific receptors for relaying alternative signals and this suggests a flexibility in the function of TRAPs not previously appreciated.
These data show that natural killer cell immunoreceptor tyrosine-based activation motifs preferentially use a signaling cassette regulated by interplay between LAT and LAB.
expression separates T lineage leukemias into two subgroups with good and poor prognostic outcome to prednisone therapy in acute lymphoblastic leukemia in children
NTAL is a negative regulator of FcepsilonRI activation events in murine bone marrow-derived mast cells, independently of possible compensatory developmental alterations.
Cerebral cortex hyperthyroidism of newborn mct8-deficient mice transiently suppressed by lat2 inactivation.
Our data define a novel link between LAB and beta-catenin nuclear accumulation in dendritic cells that facilitates IFN-gamma responses during anti-fungal immunity
chemotaxis toward antigen is controlled in mast cells by a cross-talk among FcepsilonRI, tetraspanin CD9, transmembrane adaptor proteins NTAL and LAT, and cytoskeleton-regulatory proteins of the ERM family
Dihydrotestosterone treatment increased the expression of LAT2.
Our study suggested a novel mechanism by which LAB functions in the regulation of innate immunity
The expression of Mct8 and L-type amino acid transporters Lat2 and Lat1 are determined in brain neurons during development.
a crucial role of NTAL in signaling, via RhoA, to mast cell cytoskeleton.
While SLP-76 and LAT1 depend on each other for many of their functions, LAT2/SLP-76 interactions and SLP-76-independent LAT1 functions also mediate a positive signaling pathway downstream of FcepsilonRI in mast cells.
LAB is a critical, LAT-independent regulator of TREM-2 signaling and macrophage development capable of controlling subsequent inflammatory responses
NTAL negatively regulates Fc-epsilon receptor I-mediated signaling events in bone marrow-derived mast cells.
LAB shares a redundant function with LAT to play a positive role in FcepsilonRI-mediated signaling.
LAB-deficient mice had increased levels of natural antibodies and slightly increased humoral response to a T-dependent antigen.
LAB mediates immunoglobulin E-induced sustained Erk activation critical for mast cell survival.
Our results show that system L isoform LAT2 is critical for alanine uptake into astrocytes. However, alanine does not provide any significant carbon for energy or neurotransmitter metabolism under the conditions studied.
NTAL negatively regulates mast cell activation by decreasing the recruitment, by T cell activation linker (LAT), of molecules involved in Fc epsilon RI-dependent positive signaling.
Phosphorylated LAB recruits a complex of Grb2-dynamin and the guanine nucleotide exchange factor Vav. Vav is required for activation of the small GTPases Rac1 and Rac2.
LAT2 and LAT1 form separate membrane microdomains in bone marrow-derived mast cells.
This gene is one of the contiguous genes at 7q11.23 commonly deleted in Williams syndrome, a multisystem developmental disorder. This gene consists of at least 14 exons, and its alternative splicing generates 3 transcript variants, all encoding the same protein.
Williams-Beuren syndrome chromosomal region 15 protein
, Williams-Beuren syndrome chromosomal region 5 protein
, linker for activation of B-cells
, linker for activation of T cells, transmembrane adaptor 2
, linker for activation of T-cells family member 2
, membrane-associated adapter molecule
, non-T-cell activation linker
, Williams-Beuren syndrome chromosome region 5 homolog
, non-T cell activation linker
, linker for activation of T cells family, member 2
, Williams-Beuren syndrome chromosome region 5-like protein
, Williams-Beuren syndrome chromosome region 15 homolog
, williams-Beuren syndrome chromosomal region 15 protein homolog