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4 edition of Bcl10 is an essential regulator of antigen receptor induced NF-[kappa]B activation found in the catalog.

Bcl10 is an essential regulator of antigen receptor induced NF-[kappa]B activation

Gordon S. Duncan

Bcl10 is an essential regulator of antigen receptor induced NF-[kappa]B activation

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Published by National Library of Canada in Ottawa .
Written in English


Edition Notes

Thesis (M.Sc.) -- University of Toronto, 2002.

SeriesCanadian theses = -- Th`eses canadiennes
The Physical Object
FormatMicroform
Pagination2 microfiches : negative.
ID Numbers
Open LibraryOL21789796M
ISBN 100612687686
OCLC/WorldCa54414942


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Bcl10 is an essential regulator of antigen receptor induced NF-[kappa]B activation by Gordon S. Duncan Download PDF EPUB FB2

Bcl10 is a positive regulator of antigen receptor-induced activation of NF-kappaB and neural tube closure. Cell 33–42 ; Ruland J, Duncan GS, Wakeham A, Mak TW Differential requirement for Malt1 in T and B cell antigen receptor signaling. Immunity – ; Sagaert X, De Wolf-Peeters C, Noels H, Baens M Cited by: Bcl10 is a critical regulator of NF-kappa B activity in T and B cells, coupling antigen receptor signaling to NF-kappa B activation via protein kinase C (PKC).

Here we show that PKC or T-cell receptor (TCR)/CD28 signaling results in downregulation of Bcl10 protein levels, thereby attenuating NF-kappa B transcriptional by:   Early tyrosine phosphorylation, MAPK and AP-1 activation, and Ca 2+ signaling were normal in mutant lymphocytes, but antigen receptor–induced NF-κ B activation was absent.

Thus, Bcl10 functions as a positive regulator of lymphocyte proliferation that specifically connects antigen receptor signaling in B and T cells to NF-κ B by: Function.

Bcl10 was identified by its translocation in a case of mucosa-associated lymphoid tissue (MALT) protein encoded by this gene contains a caspase recruitment domain (CARD), and has been shown to induce apoptosis and to activate protein is reported to interact with other CARD and coiled coil domain containing proteins including CARD9,andwhich are Aliases: BCL10, CARMEN, CIPER, CLAP, c-E10.

Both BCL10 and MALT1 are cytosolic adaptor proteins involved in a ternary complex with the CARD11 protein, which together mediate antigen receptor-induced activation of the nuclear factor kappa B (NF-κB) signal transduction pathway in normal B cells. Ligation of antigen receptors (TCR, BCR) on T and B lymphocytes leads to the activation of new transcriptional programs and cell cycle progression.

Antigen receptor-mediated activation of NF-κB, required for proliferation of B and T cells, is disrupted in T cells lacking PKCθ and in B and T cells lacking Bcl10, a caspase recruitment domain (CARD)-containing adaptor protein [1, 2]. Gaide O, Favier B, Legler DF, Bonnet D, Brissoni B, Valitutti S, et al.

CARMA1 is a critical lipid raft-associated regulator of TCR-induced NF-kappa B activation. Nat Immunol () – doi/ni   Although the molecular mechanism by which antigen receptors activate NF-κB is not fully understood, recent studies have demonstrated that several adaptor proteins, including CARMA1,, Bcl10, and MALT1, are required for antigen receptor-induced NF-κB activation.

In this review, we will briefly discuss recent progresses in. Bcl10 is an essential positive mediator of IgE receptor Fc epsilon RI-dependent mast cell activation that selectively uncouples NF-kappa B-induced proinflammatory cytokine production from degranulation and leukotriene synthesis.

others have demonstrated that CARMA1 plays an essential role in mediating antigen receptor-induced NF-kB activation (25–27). Recent studies demonstrated that CARMA3, a scaf-fold protein, is required for GPCR- and PKC-induced NF-kB activation (28, 29) and its potential role in cancer progression (30).

Inaddition,several studiesindicatethat. NF‐ĸB activation induced by transient overexpression of wild‐type Bcl10 in cell lines is dependent on its amino‐terminal CARD. T lymphocytes from Bcl10–/– mice show no activation of NF‐ĸB in response to T cell costimulation (53), thereby revealing Bcl10 as an essential component of this signaling pathway.

The NF-kappaB family of transcription factors is activated in response to many stimuli, including pro-inflammatory cytokines, environmental stresses and, in the case of B and T lymphocytes, by antigenic stimulation.

Bcl10 is essential for NF-kappaB activation by T- and B-cell receptors. The B cell antigen receptor (BCR) and pathogen recognition receptors, such as Toll-like receptor 4 (TLR4), act in concert to control adaptive B cell responses.

However, little is known about the signaling pathways that integrate BCR activation with intrinsic TLR4 stimulation. Antigen receptors initialize activation of the inducible transcription factor nuclear factor-κB (NF-κB) via.

Results and Discussion. Antigen receptor stimulation in B and T lymphocytes results in rapid activation of membrane-proximal tyrosine kinases of the Src and Syk families, phosphorylation of adaptor proteins, and binding of various cytosolic proteins to the newly phosphorylated T cells, these events are required for recruitment of PKCθ to the immunological synapse (IS) and for.

Abstract. A20, a tumor suppressor in several types of lymphomas, has been suggested to be an nuclear factor kappa B (NF-κB) target gene; conversely, the deubiquitylation activity of A20 is required for inhibition of Bclmediated activation of NF-κB.

The paracaspase MALT1 is essential for the activation of NF-κB in response to T cell receptor (TCR) stimulation. Thome M. CARMA1 is a critical lipid raft-associated regulator of TCR-induced NF-kappa B activation. Nat Immunol. ; 3 Millar D.G., Bouchard D., Wakeham A., Ohashi P.S., et al. Bcl10 is a positive regulator of antigen.

Introduction. Nuclear Factor kappa B (NF-κB) is a family of transcription factors that regulates immunological and inflammatory responses, as well as cell survival ().They are often constitutively activated in cancers ().NF-κB controls the expression of prosurvival and antiapoptotic genes, proinflammatory cytokines, and cyclins ().Therefore, the constitutively activated NF-κB contributes to.

Bcldeficient mice exhibit defects in neural tube closure, humoral and cellular immune responses, antigen-induced proliferation and activation of NF-κB, but no impairment of activator protein 1 (AP-1) activation in T or B cells. TNF-α, IL-1 and lipopolysaccharide (LPS)-induced NF-κB activation.

Calcium signals resulting from antigen receptor activation are important in determining the responses of a T or B lymphocyte to an antigen. Calmodulin (CaM), a multi-functional sensor of intracellular calcium (Ca(2+)) signals in cells, is required in the pathway from the T cell receptor (TCR) to activation of the key transcription factor NF-kappaB.

Bcl10 is an essential adaptor mol-ecule connecting antigen receptor signaling cascades to NF- B activation in lymphocytes. However, the function of Bcl10 in nonlymphoid cells remains to be determined.

In this study, we induced NF- B activation in Bcl10 / MEF cells, this induction. Antigen receptor stimulation assembles an NF-kappaB activating platform containing the scaffold protein CARMA1 (also called CARD11), the adaptor BCL10 and the paracaspase MALT1 (the CBM complex), linked to the inhibitor of NF-kappaB kinase complex, but signal transduction is.

To further characterise the mechanism by which GSK3β augments BCLinduced NF-κB activation, a FLAG-tagged BCL10 protein was ectopically expressed in HEK cells either alone or.

The transcription factor NF-kappaB is required for lymphocyte activation and proliferation as well as the survival of certain lymphoma types. Antigen receptor stimulation assembles an NF-kappaB activating platform containing the scaffold protein CARMA1 (also called CARD11), the adaptor BCL10 and the paracaspase MALT1 (the CBM complex), linked to the inhibitor of NF-kappaB kinase complex, but.

The signaling pathway controlling antigen receptor-induced regulation of the transcription factor NF-κB plays a key role in lymphocyte activation and development and the generation of lymphomas. Work of the past decade has led to dramatic progress in the identification and.

Genetic studies using Bcldeficient mice have revealed that Bcl10 is an essential component in the T cell receptor (TCR)- and B cell receptor (BCR)-induced NF-κB activation. The study of signalling to NF-κB from T and B lymphocyte antigen receptors is a field of intense investigation, and much attention is focused on the complex of the molecular scaffolding proteins Carma1, Bcl10 and MALT1.

Together, these are crucial for the organisation of a structure beneath the activated receptor, termed the immunological synapse.

For instance, PKCβ and PKCθ mediate B- and T-cell antigen receptor-induced NF-κB activation CARMA1/3-BclMALT1 play an essential role in cooperate in a novel NF-kappa B. Scharschmidt, E. Wegener, V. Heissmeyer, A. Rao, and D. Krappmann, Degradation of Bcl10 induced by T-cell activation negatively regulates NF-kappa B.

Recent study from our lab indicates that CARMA3, similar to the function of CARMA1 in mediating antigen receptor-mediated NF-κB activation, plays an essential role in mediating EGFR-induced NF-κB activation.

However, the mechanism on how EGFR induces NF-κB activation is. deficient for Bcl10 [11], Malt1 [12,13] or Carma1 [14–17] display severely impaired T cell receptor (TCR) and B cell receptor (BCR) responses. Antigen triggering of T- and B-cells activates a. The signaling pathway controlling antigen receptor-induced regulation of the transcription factor NF-kB plays a key role in lymphocyte activation and development and the genera-tion of lymphomas.

Work of the past decade has led to dramatic progress in the identifi-cation and characterization of new players in the pathway.

Moreover, novel enzymatic. Activation of NF-κB transcription factors by receptors of the innate or adaptive immune system is essential for host defense.

However, after danger is eliminated, NF-κB signaling needs to be. The signaling pathway controlling antigen receptor-induced regulation of the transcription factor NF-kappaB plays a key role in lymphocyte activation and development and the generation of lymphomas.

Work of the past decade has led to dramatic progress in the identification and characterization of new players in the pathway. Ruland, J. et al. Bcl10 is a positive regulator of antigen receptor-induced activation of NF-κB and neural tube closure. Cell33–42 ().

CAS PubMed PubMed Central Google Scholar. These include both bcl10, an intracellular protein which is necessary for NF-κB activation following antigen receptor stimulation in B and T lymphocytes (19, 23), and NIP45, a nuclear protein which augments NFATp- and c-Maf-induced activation of the IL-4 promoter in activated T cells.

NF-kappa-B essential modulator (NEMO) also known as inhibitor of nuclear factor kappa-B kinase subunit gamma (IKK-γ) is a protein that in humans is encoded by the IKBKG is a subunit of the IκB kinase complex that activates NF-κB. The human gene for IKBKG is located on chromosome Xq Multiple transcript variants encoding different isoforms have been found for this gene.

completely abrogates activation of NF-κB mediated by BCL10, while it has no effect on activation of NF- κB induced by expression of the NF-B-inducing kinase NIK. Ruland J, Duncan GS, Elia A, del Barco Barrantes I, Nguyen L, Plyte S, Millar DG, Bouchard D, Wakeham A, Ohashi PS, Mak TW () Bcl10 is a positive regulator of antigen receptor-induced activation of NF-kappaB and neural tube closure.

Cell –42 Google Scholar. Bcl10 was first shown as an adaptor protein that mediates antigen receptor-induced NF-κB activation in lymphocytes. 27, 59, 60 However, in recent years the role of Bcl10 in mediating the proinflammatory signaling cascade leading to NF-κB activation has been reported in various nonimmune tissues.

35, 36, 43 In this study we have conclusively. The CARMA1-BCLMALT1 (CBM) complex bridges T cell receptor (TCR) signaling to the canonical IκB kinase (IKK)/NF-κB pathway. The CBM complex constitutes a signaling cluster of more than 1 Mio Dalton.

Little is known about factors that facilitate the rapid assembly and maintenance of this dynamic higher order complex. Here, we report the novel interaction of the aryl hydrocarbon receptor.

Activator protein (AP)-1 and nuclear factor (NF)-κB largely control T-cell activation, following binding of foreign antigens to the T-cell receptor leading to cytokine secretion.

Elevated levels of pro-inflammatory cytokines and chemokines such as TNF, IL-6 and CXCL8 are associated with several human diseases including cystic fibrosis, pulmonary fibrosis and AIDS.Inducible activation of transcription through the NF-κB family is essential for the regulation of many immune response genes, such as those of IL-2, the alpha chain of IL-2 receptor (CD25) and Bcl-X L.

Induction of these gene products in T cells is the main event in CDmediated co-stimulatory activities.

One putative STAT5 responsive region was identified within the first intron of the BCL10 gene, a known regulator of NFκB activity and an essential positive regulator of T and B cell development and activation.

The BCL10 gene is located on chromosome 1 and is composed of four exons and three introns. The STAT5 binding region was confined to.