Sentences with phrase «b cell signaling pathways»

Epstein - Barr virus, the closest human relative of Kaposi's sarcoma - associated herpesvirus, mimics host B cell signaling pathways to direct B cell development toward a memory B cell phenotype.

The researchers found that in B cell tumors, mutated overactive versions of the Notch protein directly drive the expression of the Myc gene and many other genes that participate in B cell signaling pathways.

B cell signaling pathways are the current targets of several therapies used to treat B cell malignancies such as CLL.

Another surprising finding was the direct link between Notch and genes involved in other B cell signaling pathways.

Not exact matches

Use of exon - based transcriptome profiling to identify novel signaling pathways and survival - associated genes in diffuse large B - cell lymphoma.

Coligation of the B cell receptor with complement receptor type 2 (CR2 / CD21) using its natural ligand C3dg: activation without engagement of an inhibitory signaling pathway.

Previous work demonstrated that loss of either DGKζ or Cbl - b results in enhanced activation of both Erk and NF - κB pathways in T cells after stimulation of the TCR (29); however, the relative intensity of signaling changes downstream of the TCR in T cells after loss of each protein has not been directly compared.

With the recent development, by our group, of cell - permeant NAADP (NAADP - aceteoxymethyl ester) and a selective NAADP receptor antagonist (Ned - 19; 1 -(3 --LRB-(4 -(2 - fluorophenyl) piperazin -1-yl) methyl)-4-methoxyphenyl)-2,3,4,9-tetrahydro-1H-pyrido [3,4 - b] indole -3-carboxylic acid), the ability to investigate this signaling pathway has improved.

In CLL and other B - cell malignancies researchers have previously observed that deregulation of the NF kappa B (NF - kB) signalling pathway appears to be particularly important.

This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.

Amplification of the JAK2 locus has been described in Hodgkin disease and mediastinal B - cell lymphoma, 18,19 and biallelic inactivating mutations in suppressor of cytokine signaling - 1 (SOCS - 1), a negative regulator of JAK2, have been identified in mediastinal B - cell lymphoma.20 Genomic analysis of JAK2 and of other JAK - STAT pathway members may lead to the identification of mutations of the JAK - STAT pathway in lymphoid diseases and other malignancies.

We have shown that cyclic activation of the Wnt / b - catenin signalling pathway enhances cell - fusion - mediated reprogramming of a variety of somatic cells (Lluis et al., Cell Stem Cell 2008, Marucci et cell - fusion - mediated reprogramming of a variety of somatic cells (Lluis et al., Cell Stem Cell 2008, Marucci et Cell Stem Cell 2008, Marucci et Cell 2008, Marucci et al..

These include: a) Global Clusters that consist of a small, tight subset of genes that are co-expressed under the entire spectrum of experimental conditions; b) Time Series of gene expression profiles during successive days of standard ES cell differentiation; c) Specific Gene Classes based on hierarchical clustering of transcriptional factors and ESTs; d) Expression Waves of genes with characteristic expression profiles during ES cell differentiation, juxtaposed to waves of genes that behave in the exact opposite way; e) Pathway Animations that illustrate dynamic changes in the components of individual KEGG signaling and metabolic pathways viewed in time - related manner; and, f) Search Engines to display the expression pattern of any transcript, or groups of transcripts, during the course of ES cell differentiation, or to query the association of candidate genes with various FunGenES database clusters.

Oxidative stress in tissue cells may trigger an inflammatory response by the NF - kappa B nuclear signaling pathway.