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1 enotype with that of MALT1 knockout animals (Malt1(-/-)).
2 mphoid tissue lymphoma-translocation gene 1 (MALT1).
3 ilitates the association of Carma1 with Bcl0-Malt1.
4 D is associated with homozygous mutations in MALT1.
5 on after activation, 2 events that depend on MALT1.
6 and mechanism of paracaspases exemplified by MALT1.
7 f helix 5 of the Bcl10 CARD directly contact MALT1.
8 s activation is dependent on the paracaspase MALT1.
9 ting with the immunoglobulin-like domains of MALT1.
10 that is independent of PKCtheta, Bcl10, and Malt1.
11 -kappaB signalling related factors HMGA1 and MALT1.
12 and cIAP2) fused to C-terminal sequences of MALT1.
13 three principal proteins, CARMA3, Bcl10, and MALT1.
14 or the generation of a fusion protein, cIAP2-MALT1.
15 n kinase mediate IKK activation by BCL10 and MALT1.
16 he synthesis of a novel fusion protein, API2-MALT1.
17 ding sequence fusion point for both API2 and MALT1.
18 e-1 proteins were cleaved by the paracaspase MALT1.
19 adaptor molecule BCL10, and the paracaspase MALT1.
22 pment was restored by compound deficiency of MALT1, a key downstream component of TCR signaling in T
23 ed interfaces in Bcl10 filament assembly and MALT1 activation in vitro and NF-kappaB activation in ce
26 tivation-associated aggregation of Bcl10 and Malt1 also demonstrate both digital behavior and high co
28 D1 and IgH, BCL2 and IgH, c-myc and IgH, and MALT1 and API2 were detected using probes with a dual-fu
30 ization analyses with commercially available MALT1 and IgH break-apart and centromere 3, 7, 12, and 1
32 LT1 translocations having high expression of MALT1 and RARA, samples with plasmacytic differentiation
34 ow provide evidence that the death domain of MALT1 and the CARD of Bcl10 also contribute to Bcl10-MAL
36 oid tissue lymphoma translocation protein 1 (MALT1), and caspase recruitment domain-containing (CARD)
38 in that nucleates a complex including BCL10, MALT1, and other IkappaB kinase (IKK)-signalosome compon
39 quires Bcl10 lysines 17, 31, and 63, CARD11, MALT1, and the HOIP subunit of the linear ubiquitin chai
40 with B cell lymphoma 10 (BCL10), paracaspase MALT1, and the inhibitors of kappaB kinase (IKK) complex
43 he CARD domain protein BCL10 and paracaspase MALT1 are essential for the activation of IkappaB kinase
45 e paracaspase (protease related to caspases) MALT1 as critical intermediates linking the TCR to the I
46 API2 moiety mediates oligomerization of API2-MALT1 as well as interaction with tumor necrosis factor
47 we show that a subset of MCLs is addicted to MALT1, as its inhibition by either RNA or pharmacologic
48 nents of the CBM complex, Carma3, Bcl10, and Malt1, as key mediators of the CXCL8/IL8-induced NFkappa
49 interacting protein-1 (RIP1) as a novel API2-MALT1-associated protein, and demonstrate that RIP1 is r
50 ne and somatic gain-of-function mutations of MALT1, BCL10, and CARD11 have also been found in patient
52 IP, and IKKalpha/beta/gamma but also CARMA1, MALT1, BCL10, and PKC, molecules previously shown to reg
53 B cell lymphoma (DLBCL), engages the CARD11-MALT1-BCL10 (CBM) adapter complex to activate IkappaB ki
54 e (ie, IKK-alpha,-beta,-gamma/NEMO and CARMA/MALT1/Bcl10 complex) are present in anucleate platelets
58 eover, individuals with inherited defects of MALT1, CARD9, and CARD11 present with immunological and
61 ot required for assembly of the CARMA1/Bcl10/Malt1 (caspase-recruitment domain (CARD) membrane-associ
62 f a scaffold consisting of CARD9, BCL10, and MALT1 (CBM complex) is critical for effective signaling
65 P9X interacts with Bcl10 of the Carma1-Bcl10-Malt1 (CBM) complex and removes the TCR-induced ubiquiti
70 nical NF-kappaB pathway via the CARD11/BCL10/MALT1 (CBM) signalosome involving key, yet ill-defined r
72 theta-dependent assembly of the CARMA1-BCL10-MALT1 (CBM) signalosome, which coordinates downstream ac
74 (Bcl10)-mucosa-associated lymphatic tissue 1(MALT1) (CBM) complex, which appears to be independent of
79 With the identification of the CARMA1-BCL10-MALT1 complex and ongoing progress in understanding the
80 We propose a model whereby both the Bcl10.MALT1 complex and the API2-MALT1 fusion protein activate
83 , an essential component of the CARD11-BCL10-MALT1 complex that links BCR signaling to the NF-kappaB
84 TCR-stimulated assembly of the CARMA1-BCL-10-MALT1 complex was substantially impaired in the absence
85 as PDK1-associated CARD11 recruits the Bcl10-MALT1 complex, thereby allowing activation of the IKK co
87 ta strongly suggest that the death domain of MALT1 contributes significantly to the association betwe
88 following MALT1 inhibition demonstrated that MALT1 controls an MYC-driven gene expression network pre
89 Although a direct interaction between the MALT1 death domain and Bcl10 cannot be detected via immu
93 -kappaB activation in cancer cells, and that MALT1 deficiency impaired EGFR-induced NF-kappaB activat
94 Adoptive transfer experiments showed that MALT1 deficiency in splenocytes is sufficient for EAE re
96 ficient T cells, suggesting the inability of MALT1-deficient effector T cells to induce demyelinating
99 during EAE, which was partially impaired in MALT1-deficient T cells, suggesting a contribution of MA
100 e T cell activation was severely impaired in MALT1-deficient T cells, suggesting the inability of MAL
104 To further access a physiological role of MALT1-dependent NF-kappaB activation in EGFR-driven tumo
105 cellular and genetic evidence that suggests MALT1-dependent NF-kappaB activation is important in EGF
107 or activate NF-kappaB, indicating that API2-MALT1-dependent RIP1 ubiquitination represents a gain of
108 activation of the IKK complex through Bcl10-MALT1-dependent ubiquitination of the IKK complex subuni
110 sequent spleen tyrosine kinase 2-CARD9/BCL10/MALT1-driven signaling cascade, impairing nuclear factor
112 ymphomas can be modeled in mice by targeting MALT1 expression to hematopoietic stem/progenitor cells,
114 ARD11), mucosa-associated lymphoid tissue 1 (MALT1) for combined immunodeficiencies, and tetratricope
119 usly unknown functional diversity among API2/MALT1 fusion products and their function in NF-kappaB si
120 e reprogramming, expression of distinct API2/MALT1 fusion products inhibits DNA damage-induced, p53-m
121 by both the Bcl10.MALT1 complex and the API2-MALT1 fusion protein activate a common downstream signal
122 )(q21;q21) translocation creating the c-IAP2.MALT1 fusion protein activates NF-kappaB and contributes
126 tional evidence for the contribution of API2/MALT1 fusion proteins to transformation of cells in cult
130 , primary MALT lymphomas harbouring the API2-MALT1 fusion uniquely demonstrate LIMA1 cleavage fragmen
131 genes localize to separate chromosomes, with mALT1 gene (gpt1) on chromosome 15 and mALT2 gene (gpt2)
132 Chromosomal translocations involving the MALT1 gene are hallmarks of mucosa-associated lymphoid t
134 e strongest signal is in the promoter of the MALT1 gene, involved in insulin and glycaemic pathways,
138 ed Bcl10 and its binding partners Carma1 and MALT1 in mediating the ability of the BCR to activate NF
143 in a mouse model (LSL-K-ras(G12D); CCSP-Cre; Malt1(-/-)) in which lung cancer is induced by expressin
144 ic mouse model (tetO-EGFR(L858R); CCSP-rtTA; Malt1(-/-)), in which mutant EGFR-driven lung cancer was
147 However, the mechanisms underlying API2-MALT1-induced MALT lymphomagenesis are not fully underst
148 mouse splenocytes, we could demonstrate that MALT1-induced MYC regulation is not restricted to MCL, b
153 al rationale for the clinical development of MALT1 inhibitors in CLL, in particular for ibrutinib-res
154 olleagues and Fontan and colleagues describe MALT1 inhibitors suitable for clinical use that are sele
162 use CD3/CD28 costimulation failed to recruit MALT1 into lipid rafts in CARMA1-deficient T cells.
163 trate that the association between Bcl10 and MALT1 involves a complex interaction between multiple pr
166 contain caspase recruitment domains (CARDs), MALT1 is a paracaspase with structural similarity to cas
172 h its heterozygous controls, suggesting that MALT1 is required for the progression of EGFR-induced lu
175 oid tissue lymphoma translocation protein 1 (MALT1) is intact in our series, arguing against its invo
176 nd that mucosa-associated lymphoid tissue 1 (MALT1) is involved in EGFR-induced NF-kappaB activation
177 small molecule inhibitor of the para-caspase MALT1, is effective in preclinical models of another typ
179 hat CD4(+) T cells from PKCtheta, Bcl10, and Malt1 knockout mice show severe impairment of proliferat
181 iltration into the spinal cord was absent in MALT1-knockout mice, as were demyelination and proinflam
183 associated with low miR-26 and high HMGA1 or MALT1 levels and not with levels of any of them individu
184 ex of proteins containing CARMA3, Bcl10, and MALT1 links PAR-1 activation to stimulation of the Ikapp
187 , mice deficient for the NF-kappaB regulator MALT1 (Malt1-/- mice) exhibit strong lymphocytic infiltr
189 hat TRAF2 interaction is critical for c-IAP2/MALT1-mediated increases in the NF-kappaB activity, incr
193 deficient for the NF-kappaB regulator MALT1 (Malt1-/- mice) exhibit strong lymphocytic infiltration i
196 e (IKK) to associate with the upstream Bcl10-MALT1 (mucosa-associated lymphatic tissue) adapter compl
197 e BIR domains of c-IAP2 with the paracaspase/MALT1 (mucosa-associated lymphoid tissue) protein, a cri
198 e compare B cells from the only known living MALT1(mut/mut) patient with healthy MALT1(+/mut) family
199 n living MALT1(mut/mut) patient with healthy MALT1(+/mut) family members using 10-plex Tandem Mass Ta
200 rast to wild-type human MALT1, the patients' MALT1 mutant failed to correct defective nuclear factor-
201 /MALT1 oncoprotein and BIR1 E47A/R48A c-IAP2/MALT1 mutant that cannot bind TRAF2 in a lymphoid cell l
207 parisons of the bioactivity of intact c-IAP2/MALT1 oncoprotein and BIR1 E47A/R48A c-IAP2/MALT1 mutant
208 ix of 12 patients, with no rearrangements of MALT1 or IgH and no trisomies of 7, 12, or 18 detected.
210 lead to the upregulation of either BCL10 or MALT1 or the generation of a fusion protein, cIAP2-MALT1
212 e 1.75-A resolution crystal structure of the MALT1 paracaspase region, which contains the paracaspase
213 ed lymphoid tissue lymphoma translocation 1 (MALT1) paracaspase, a key component of the Carma1/Bcl10/
215 re propose that the pathology characterizing Malt1(PD/PD) animals arises from an immune imbalance fea
219 we generated MALT1 protease-deficient mice (Malt1(PD/PD)) and compared their phenotype with that of
220 protein kinase Ctheta (PKCtheta), Bcl10, and Malt1 play critical roles in TCR signaling to the transc
223 n TCR signaling through PKCtheta, Bcl10, and Malt1 predominantly impair NF-kappaB activation and down
228 10 PLCG1 and 3 of 3 CARD11 variants induced MALT1 protease activity and increased transcription from
230 r a previously unappreciated key function of MALT1 protease activity in immune homeostasis and underl
232 overall immune cell regulation, we generated MALT1 protease-deficient mice (Malt1(PD/PD)) and compare
234 demonstrate that different forms of the API2/MALT1 proteins activate both unique and overlapping gene
235 udies have shown that the CARMA1, Bcl10, and MALT1 proteins are critical for coupling the common elem
240 duced lymphomas with a specific inhibitor of MALT1 proteolytic activity decreased cell viability, ind
241 icient T cells, suggesting a contribution of MALT1 proteolytic activity in T cell activation and EAE
242 nt of CLL cells in vitro with MI-2 inhibited MALT1 proteolytic activity reduced BCR and NF-kappaB sig
244 Therefore, we conclude that the Carma1-Bcl10-Malt1 signaling axis is critical for cytokine and chemok
245 ate that enforced activation of CARD11/BCL10/MALT1 signaling is sufficient to drive transformed B-cel
246 d cell viability, indicating that endogenous Malt1 signaling was required for tumor cell survival.
247 non-immune cells to assemble a CARMA3-Bcl10-MALT1 signalosome and mediate G protein-coupled receptor
248 rotein CARD9, a component of the CARD9-Bcl10-MALT1 signalosome complex involved in NF-kappaB transloc
249 her, we find that although this CARMA3.Bcl10.MALT1 signalosome shares features with a CARMA1-containi
250 caspase, a key component of the Carma1/Bcl10/MALT1 signalosome, is critical for NF-kappaB signaling i
251 requires an intact endothelial CARMA3.Bcl10.MALT1 signalosome, underscoring the importance of the si
252 However, TRAF1/2-binding mutants of c-IAP2.MALT1 still oligomerize and activate NF-kappaB, suggesti
263 n line with their impaired GM-CSF secretion, Malt1-/- Th cells failed to recruit myeloid cells to the
264 reased secretion of Th17 effector cytokines, Malt1-/- Th17 cells showed normal expression of lineage-
267 BCR signaling, including CARD11, BCL10, and MALT1, that have complex 5'UTRs and encode proteins with
268 RD11), the adaptor BCL10 and the paracaspase MALT1 (the CBM complex), linked to the inhibitor of NF-k
270 d RIP1 interact with the API2 moiety of API2-MALT1, this moiety alone is insufficient to induce RIP1
272 r 2 (TRAF2) recruitment is required for API2-MALT1 to induce RIP1 ubiquitination, NF-kappaB activatio
273 d demonstrate that RIP1 is required for API2-MALT1 to stimulate canonical nuclear factor kappa B (NF-
274 mphoid tissue lymphoma translocation gene 1 (MALT1) to simultaneously activate the NF-kappaB and c-Ju
275 ctivation in vitro with purified proteins of MALT1, TRAF6, TAK1, and ubiquitination enzymes including
277 ologic characteristics, such as samples with MALT1 translocations having high expression of MALT1 and
279 itously expressed gene, which we refer to as MALT1, was identified within this sequence and was found
280 B kinase (IKK) complex via Carma1, Bcl10 and MALT1, whereas BAFF-R engagement promotes processing of
282 gative CARMA3 or silencing CARMA3, Bcl10 and MALT1 with specific siRNAs diminished these LPA-induced
283 nding, suggesting that interaction of c-IAP2/MALT1 with TRAF6 is insufficient for NF-kappaB induction
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