Bcl10 Is a Positive Regulator of Antigen Receptor–Induced Activation of NF-κ B and Neural Tube Closure

Ruland, Jürgen; Duncan, Gordon S.; Elia, Andrew; Barrantes, Iván del Barco; Nguyen, Linh T.; Plyte, Sue; Millar, Douglas G.; Bouchard, Denis; Wakeham, Andrew; Ohashi, Pamela S.; Mak, Tak W.

doi:10.1016/s0092-8674(01)00189-1

Cited by 519 publications

(554 citation statements)

References 38 publications

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“…This notion is supported by data from the mice deficient in PKC-b, CARMA1, MALT and Bcl10, which indicate that these molecules are largely dispensable for overall B cell development and survival [17,[54][55][56]. However, all these knockout mice showed specific B cell defects such as complete absence of B1 B cell compartment and defected terminal differentiation of immature B cells into MZ B cells in the spleen [17,[54][55][56]. Strikingly, splenic B cells from all these mice are also defective in CD40-induced proliferation.…”

Section: Discussionmentioning

confidence: 78%

Potential role of CARMA1 in CD40‐induced splenic B cell proliferation and marginal zone B cell maturation

Pappu¹,

Lin²

2006

Eur J Immunol

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NF‐κB activation through B cell receptor (BCR) ligation is critical for B cell development, survival and antigen‐mediated activation of B cells. CARD domain and MAGUK‐domain containing protein‐1 (CARMA1), recently identified adaptor molecule, has been shown to play an essential role in BCR‐induced NF‐κB activation. CARMA1‐deficient B cells fail to proliferate upon BCR stimulation, leading to defective humoral responses. Surprisingly, CARMA1‐deficient B cells are also defective in CD40‐induced proliferation. The mechanisms responsible for CD40‐induced proliferation defect have not yet been characterized. In this study, we show that signaling cascades activated by CD40 stimulation are largely unaffected in CARMA1‐deficient B cells. Instead, we have found that the defective proliferation of CARMA1‐deficient B cells is due to two events. First, CARMA1‐deficient B cells show defective cell‐cycle progression. Secondly, the numbers of marginal zone (MZ) B cells, which are the main responders upon CD40 stimulation, are greatly diminished in CARMA1‐deficient mice. Since B cell maturation requires basal signaling through BCR and NF‐κB activation, we propose that impaired BCR signaling in CARMA1‐deficient mice leads to defective maturation of MZ B cell population, which in turn, contributes to impaired proliferation upon CD40 stimulation.

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Section: Discussionmentioning

confidence: 78%

Potential role of CARMA1 in CD40‐induced splenic B cell proliferation and marginal zone B cell maturation

Pappu¹,

Lin²

2006

Eur J Immunol

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“…The signaling pathway from the receptor to NF-kB requires PKCy (PKCb in B cells), CARMA1/CARD11, BCL10 and MALT1 (Sun et al, 2000;Ruland et al, 2001Ruland et al, , 2003Saijo et al, 2002;Hara et al, 2003;RuefliBrasse et al, 2003;). Although there has been some controversy, available data suggest that PKCy is largely essential for activation of NF-kB via T-cell stimulation (Sun et al, 2000;Pfeifhofer et al, 2003) and can mediate the activation of IKK .…”

Section: Role Of Nf-jb In the Adaptive Responsementioning

confidence: 99%

“…The MAGUK family protein CARMA1 is required for activation of NF-kB in T cells following TCR ligation, but its loss has no effect on the development of thymocyte (Gaide et al, 2002;Egawa et al, 2003;Hara et al, 2003). Similarly, BCL10 is critical for NF-kB activation via the BCR and TCR, yet normal numbers of peripheral T cells are seen in BCL10 knockouts, and no clear defects in B-cell development is observed (Ruland et al, 2001). BCL10 interacts with CARMA1 leading to BCL10 phosphorylation, although CARMA1 lacks kinase activity (Bertin et al, 2001;Gaide et al, 2001).…”

Section: Role Of Nf-jb In the Adaptive Responsementioning

confidence: 99%

NF-κB and the immune response

2006

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“…75 Activation upon TcR stimulation triggers recruitment of FADD and caspase-8 to the CARMA-Bcl10-MALT1 complex, which can in turn recruit the IKK complex, with consequent activation of NF-kB. 76 In addition to the CARMA-Bcl10-MALT1 complex, 77 TRAF2, TRAF6 and RIP2 were also shown to be essential for TcRinduced NF-kB activation. 51,78 Recruitment of caspase-8 to FADD is competed by FLIP L , which can also bind RIP1 and TRAF2.…”

Section: Role Of Rip1 In T-cell Development and Homeostasismentioning

confidence: 99%

RIP1, a kinase on the crossroads of a cell's decision to live or die

et al. 2007

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Binding of inflammatory cytokines to their receptors, stimulation of pathogen recognition receptors by pathogen-associated molecular patterns, and DNA damage induce specific signalling events. A cell that is exposed to these signals can respond by activation of NF-jB, mitogen-activated protein kinases and interferon regulatory factors, resulting in the upregulation of antiapoptotic proteins and of several cytokines. The consequent survival may or may not be accompanied by an inflammatory response. Alternatively, a cell can also activate death-signalling pathways, resulting in apoptosis or alternative cell death such as necrosis or autophagic cell death. Interplay between survival and death-promoting complexes continues as they compete with each other until one eventually dominates and determines the cell's fate. RIP1 is a crucial adaptor kinase on the crossroad of these stress-induced signalling pathways and a cell's decision to live or die. Following different upstream signals, particular RIP1-containing complexes are formed; these initiate only a limited number of cellular responses. In this review, we describe how RIP1 acts as a key integrator of signalling pathways initiated by stimulation of death receptors, bacterial or viral infection, genotoxic stress and T-cell homeostasis. Cell Death and Differentiation (2007) 14, 400-410. doi:10.1038/sj.cdd.4402085Receptor interacting protein (RIP) kinases constitute a family of seven members, all of which contain a kinase domain (KD) (Figure 1a). They are crucial regulators of cell survival and death 1 (Figure 2). Based on sequence similarities, mode of regulation and substrate specificities of their catalytic domain, RIP kinases are classified as serine/threonine kinases and are closely related to members of the interleukin-1-receptorassociated kinase (IRAK) family. RIP1 and RIP2 (CARDIAK/ RICK) also bear a C-terminal domain belonging to the death domain (DD) superfamily, namely, a DD and a caspase recruitment domain (CARD), respectively, allowing recruitment to large protein complexes initiating different signalling pathways. The unique C-terminus of RIP3 bears a RIP homotypic interaction motif (RHIM), which is also present in the intermediate domain (ID) of RIP1. This RHIM domain is sufficient for interaction of RIP1 with RIP3. 1 RIP4 (DIK/PKK) and RIP5 (SgK288) are characterized by the presence of ankyrin repeats in their C-terminal domains. 1 RIP6 (LRRK1) and RIP7 (LRRK2) are RIP members containing a leucine-rich repeat (LRR) motif 1 that may be involved in recognition of pathogen-, damage-or stress-associated molecular patterns (PAMP, DAMP, SAMP). In addition, they harbor Roc/COR domains (Ras of complex proteins/C-terminal of Roc). Binding of GTP to the GTPase-like Roc domain leads to the stimulation of LRRK1 kinase activity. 2 Mutation analysis indicated that the COR domain might be important for transmitting the stimulating signal to the KD. 2 The function of RIP6 and RIP7 is yet unknown; however, mutations in the human LRRK2 gene are associated with both fam...

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Bcl10 Is a Positive Regulator of Antigen Receptor–Induced Activation of NF-κ B and Neural Tube Closure

Cited by 519 publications

References 38 publications

Potential role of CARMA1 in CD40‐induced splenic B cell proliferation and marginal zone B cell maturation

Potential role of CARMA1 in CD40‐induced splenic B cell proliferation and marginal zone B cell maturation

NF-κB and the immune response

RIP1, a kinase on the crossroads of a cell's decision to live or die

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