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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.
20                                 Paracaspase (MALT1), a member of an evolutionarily conserved superfam
21 lective, as shown by the fact that it spared Malt1, a direct Bcl10 binding partner.
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
24                               We developed a MALT1 activity assay and identified chemically diverse M
25                             The CARMA1-Bcl10-Malt1 adaptor complex regulates NFkappaB activation by a
26 tivation-associated aggregation of Bcl10 and Malt1 also demonstrate both digital behavior and high co
27       However, it remains unclear which role MALT1, an essential component of the CARD11-BCL10-MALT1
28 D1 and IgH, BCL2 and IgH, c-myc and IgH, and MALT1 and API2 were detected using probes with a dual-fu
29  lack of caspase-8 results in the absence of MALT1 and Bcl-10 in the active caspase complex.
30 ization analyses with commercially available MALT1 and IgH break-apart and centromere 3, 7, 12, and 1
31                    Expression of recombinant mALT1 and mALT2 proteins in Escherichia coli (E. coli) p
32 LT1 translocations having high expression of MALT1 and RARA, samples with plasmacytic differentiation
33 d compound, MI-2, featured direct binding to MALT1 and suppression of its protease function.
34 ow provide evidence that the death domain of MALT1 and the CARD of Bcl10 also contribute to Bcl10-MAL
35         The deduced peptides of murine ALT1 (mALT1) and ALT2 (mALT2) share 87% and 93% identity, resp
36 oid tissue lymphoma translocation protein 1 (MALT1), and caspase recruitment domain-containing (CARD)
37 phocyte defects, are associated with CARD11, MALT1, and BCL10 deficiencies.
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
41 eral, immune defects were more pronounced in Malt1(-/-) animals.
42                         While both BCL10 and MALT1 are critically involved in antigen receptor-mediat
43 he CARD domain protein BCL10 and paracaspase MALT1 are essential for the activation of IkappaB kinase
44                                    Bcl10 and MALT1 are essential mediators of NF-kappaB activation in
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
51                                   Therefore, MALT1, Bcl10, and CARMA1 form a trimolecular complex.
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
55                            Studies of c-IAP2/MALT1 BIR1 mutant (E47A/R48A) that fails to activate NF-
56                 Knocking down both HMGA1 and MALT1 by RNAi had a silencing effect on NF-kappaB-respon
57 ly, only these oligomeric forms of BCL10 and MALT1 can activate IKK in vitro.
58 eover, individuals with inherited defects of MALT1, CARD9, and CARD11 present with immunological and
59  oligomerization-dependent activation of the MALT1 caspase-like domain.
60 es the oligomerization and activation of the MALT1 caspase-like domain.
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
63 ein complex that contains CARMA1, BCL10, and MALT1 (CBM complex).
64 hat requires the triad of CARMA3, Bcl10, and MALT1 (CBM signalosome).
65 P9X interacts with Bcl10 of the Carma1-Bcl10-Malt1 (CBM) complex and removes the TCR-induced ubiquiti
66      The mechanism by which the Carma1-Bcl10-MALT1 (CBM) complex couples T cell antigen receptor (TCR
67                    However, the Card11-Bcl10-Malt1 (CBM) complex that is essential for TCR activation
68                             The CARMA1/Bcl10/Malt1 (CBM) complex, comprised of adaptors that link the
69                           These 3 CARD-BCL10-MALT1 (CBM) complexes activate nuclear factor kappaB in
70 nical NF-kappaB pathway via the CARD11/BCL10/MALT1 (CBM) signalosome involving key, yet ill-defined r
71                             The CARMA1/Bcl10/MALT1 (CBM) signalosome mediates antigen receptor-induce
72 theta-dependent assembly of the CARMA1-BCL10-MALT1 (CBM) signalosome, which coordinates downstream ac
73 mphoid tissue lymphoma translocation gene 1 (MALT1 [CBM]) signalosome complex.
74 (Bcl10)-mucosa-associated lymphatic tissue 1(MALT1) (CBM) complex, which appears to be independent of
75                                              MALT1 cleavage activity is linked to the pathogenesis of
76                              The paracaspase MALT1 cleaves and removes negative checkpoint proteins,
77 hich requires signals from the CARD11-BCL-10-MALT1 (CMB) complex.
78      Genetic deficiencies of either BCL10 or MALT1 completely rescued the phenotype, and pharmacologi
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
81 ing stimuli that require correct CARMA-BCL10-MALT1 complex formation and functioning.
82        A recent study reveals that the Bcl10-Malt1 complex promotes mast-cell interleukin-6 and tumor
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
86 NF-kappaB signaling through the CARD11-BCL10-MALT1 complex.
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
90                             Mechanistically, MALT1 deficiency abolished both NF-kappaB and STAT3 acti
91                                 In contrast, Malt1 deficiency did not affect Th1 cells.
92                               In comparison, MALT1 deficiency does not affect tumor progression in a
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
95                             Using Bcl10- and MALT1-deficient cells, we show that CARD11 can recruit s
96 ficient T cells, suggesting the inability of MALT1-deficient effector T cells to induce demyelinating
97                                              MALT1-deficient mice show significantly less lung tumor
98 tor-kappaB activation and IL-2 production in MALT1-deficient mouse T cells.
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
101             The unique enzymatic activity of MALT1 degrades one of its binding partners, BCL-10, as w
102                              Expression of a MALT1 deletion mutant containing only the N-terminal dea
103 iquitination as a critical component of API2-MALT1-dependent lymphomagenesis.
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
106 RAF2 binding both contribute to maximal API2-MALT1-dependent NF-kappaB stimulation.
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
109                                              MALT1 diminishes the activation of apoptotic effector ca
110 sequent spleen tyrosine kinase 2-CARD9/BCL10/MALT1-driven signaling cascade, impairing nuclear factor
111                             Here, we induced MALT1 expression in mouse Sca1(+)Lin(-) hematopoietic st
112 ymphomas can be modeled in mice by targeting MALT1 expression to hematopoietic stem/progenitor cells,
113  lung cancer was developed in the absence of MALT1 expression.
114 ARD11), mucosa-associated lymphoid tissue 1 (MALT1) for combined immunodeficiencies, and tetratricope
115                  We show here that Bcl10 and MALT1 form a strong and specific complex within the cell
116                            Bimp1, Bcl10, and MALT1 form a ternary complex, with Bcl10 bridging the Bi
117                 We demonstrate that the API2-MALT1 fusion oncoprotein created by the recurrent t(11;1
118                                     The API2-MALT1 fusion oncoprotein is created by the recurrent t(1
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
123                        Furthermore, the API2-MALT1 fusion protein also strongly activates NF-kappaB a
124                                   The c-IAP2.MALT1 fusion protein associates with TRAF1 and TRAF2 usi
125                                   The c-IAP2.MALT1 fusion protein constitutively activates the NF-kap
126 tional evidence for the contribution of API2/MALT1 fusion proteins to transformation of cells in cult
127 nscripts encoding structurally distinct API2/MALT1 fusion proteins.
128         To investigate the incidence of API2-MALT1 fusion transcripts among marginal zone lymphomas a
129                                         API2-MALT1 fusion transcripts were detected in 12 of 57 extra
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
133                          The function of the MALT1 gene is subverted by oncogenic chimeric fusions ar
134 e strongest signal is in the promoter of the MALT1 gene, involved in insulin and glycaemic pathways,
135 d CARD11 and the 2 core components BCL10 and MALT1, have recently been reported.
136 tive WT Th cells successfully induced EAE in Malt1-/- hosts.
137 r cells, demonstrating the oncogenic role of MALT1 in lymphomagenesis.
138 ed Bcl10 and its binding partners Carma1 and MALT1 in mediating the ability of the BCR to activate NF
139 tes a unique signaling cascade via Bcl10 and Malt1 in NK cells.
140 icantly to the association between Bcl10 and MALT1 in T cells in vivo.
141                       We studied the role of MALT1 in the development of experimental autoimmune ence
142  to caspases, suggesting a possible role for MALT1 in the regulation of apoptosis.
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
145                    The paracaspase domain of MALT1, in a protease-independent manner, induces caspase
146                                 Treatment of MALT1-induced lymphomas with a specific inhibitor of MAL
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
149  we investigated the role of TRAF2 in c-IAP2/MALT1-induced NF-kappaB activation.
150                       Here we show that API2-MALT1 induces paracaspase-mediated cleavage of the tumou
151          Gene expression profiling following MALT1 inhibition demonstrated that MALT1 controls an MYC
152                                Functionally, MALT1 inhibition shows significant defects in EGFR-assoc
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
155 ABC-DLBCL, and provides mouse models to test MALT1 inhibitors.
156 vity assay and identified chemically diverse MALT1 inhibitors.
157                          Moreover, the Bcl10-MALT1 interaction is the second reported example of inte
158 rnary complex, with Bcl10 bridging the Bimp1/MALT1 interaction.
159 d the CARD of Bcl10 also contribute to Bcl10-MALT1 interactions.
160 ding of the Bcl10 CARD strongly impair Bcl10-MALT1 interactions.
161                                      Loss of Malt1 interfered with expression of the Th17 effector cy
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
164                    Our results indicate that MALT1 is a central, cell-intrinsic factor that determine
165        Together, these results indicate that MALT1 is a crucial signaling component in the TCR signal
166 contain caspase recruitment domains (CARDs), MALT1 is a paracaspase with structural similarity to cas
167                        LIMA1 binding by API2-MALT1 is API2 dependent and proteolytic cleavage is depe
168         By regulating linear ubiquitination, MALT1 is both a positive and negative pleiotropic regula
169                          This recruitment of MALT1 is dependent on CARMA1 because CD3/CD28 costimulat
170             Recently, it has been shown that MALT1 is involved in mediating TCR signal transduction,
171                  In this study, we show that MALT1 is recruited into the lipid rafts of the immunolog
172 h its heterozygous controls, suggesting that MALT1 is required for the progression of EGFR-induced lu
173                                              MALT1 is the only known paracaspase and is a critical me
174                                              MALT1 is thought to function as a scaffold and protease
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
178 )) and compared their phenotype with that of MALT1 knockout animals (Malt1(-/-)).
179 hat CD4(+) T cells from PKCtheta, Bcl10, and Malt1 knockout mice show severe impairment of proliferat
180                                              MALT1-knockout mice did not develop any clinical symptom
181 iltration into the spinal cord was absent in MALT1-knockout mice, as were demyelination and proinflam
182                                        cIAP2-MALT1 lacks E3 activity, and concomitantly, the BCL10 pr
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
185 )(q21;q21), fuses the IAP-2 gene to the MLT1/MALT1 locus, which encodes the human paracaspase.
186                                              MALT1 mainly functions as a scaffold protein by recruiti
187 , mice deficient for the NF-kappaB regulator MALT1 (Malt1-/- mice) exhibit strong lymphocytic infiltr
188             Together, our data indicate that MALT1 may be an interesting therapeutic target in the tr
189 hat TRAF2 interaction is critical for c-IAP2/MALT1-mediated increases in the NF-kappaB activity, incr
190                           Intriguingly, API2-MALT1-mediated proteolysis generates a LIM domain-only (
191                                              MALT1 mediates Ag-induced signaling to the transcription
192 sue lymphoma-translocation gene 1-deficient (Malt1(-/-)) mice.
193 deficient for the NF-kappaB regulator MALT1 (Malt1-/- mice) exhibit strong lymphocytic infiltration i
194 g the concerted actions of both the API2 and MALT1 moieties of the fusion.
195 PI2 moiety of one monomer interacts with the MALT1 moiety of another monomer.
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
202 te the therapeutic efficacy of targeting the MALT1-MYC axis in MCL patients.
203 0 CARD is essential for interaction with the MALT1 N terminus.
204              In addition, we also found that MALT1 not only binds to Bcl10 directly, but also associa
205                                          The MALT1 oligomers bind to TRAF6, induce TRAF6 oligomerizat
206 ene on chromosome 11 and a novel gene termed MALT1 on chromosome 18.
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.
209                           Trisomy 3, but not MALT1 or IgH translocation, is a common genetic abnormal
210  lead to the upregulation of either BCL10 or MALT1 or the generation of a fusion protein, cIAP2-MALT1
211 ent and proteolytic cleavage is dependent on MALT1 paracaspase activity.
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/
214                                              MALT1/paracaspase is a caspase-like protein that contain
215 re propose that the pathology characterizing Malt1(PD/PD) animals arises from an immune imbalance fea
216                                Surprisingly, Malt1(PD/PD) animals developed a multiorgan inflammatory
217                                              Malt1(PD/PD) mice displayed defects in multiple cell typ
218                                Consequently, Malt1(PD/PD) mice were protected in a Th17-dependent exp
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
221                              The paracaspase MALT1 plays an important role in immune receptor-driven
222                                         API2-MALT1-positive MALT lymphomas manifest antibiotic resist
223 n TCR signaling through PKCtheta, Bcl10, and Malt1 predominantly impair NF-kappaB activation and down
224                                    Bcl10 and MALT1, products of distinct chromosomal translocations i
225                                         API2-MALT1 promotes cell survival and proliferation via activ
226                                              MALT1 promotes signaling by acting as a scaffold, recrui
227                                         API2-MALT1 promotes ubiquitination of RIP1 at lysine (K) 377,
228  10 PLCG1 and 3 of 3 CARD11 variants induced MALT1 protease activity and increased transcription from
229                    In vitro, inactivation of MALT1 protease activity caused reduced stimulation-induc
230 r a previously unappreciated key function of MALT1 protease activity in immune homeostasis and underl
231                New data shows that targeting MALT1 protease activity may be a promising therapeutic s
232 overall immune cell regulation, we generated MALT1 protease-deficient mice (Malt1(PD/PD)) and compare
233 ptosis protein 2) fused with portions of the MALT1 protein.
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
236   We find that a small fraction of BCL10 and MALT1 proteins form high molecular weight oligomers.
237  uncover a function of the CARMA, Bcl10, and MALT1 proteins in cells outside the immune system.
238                       The CARMA1, Bcl10, and MALT1 proteins together constitute a signaling complex (
239                           To investigate how MALT1 proteolytic activity contributes to overall immune
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
243 RNA inhibited NF-kappaB activation by c-IAP2/MALT1 showing that TRAF2 is indispensable.
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
253 o TRAF1 and TRAF2 is not required for c-IAP2.MALT1-stimulated NF-kappaB activation.
254 the importance of TRAF1 and TRAF2 for c-IAP2.MALT1-stimulated NF-kappaB activation.
255 ion of TRAF1 and TRAF2 did not affect c-IAP2.MALT1-stimulated signaling.
256  ubiquitin chain assembly complex as a novel MALT1 substrate.
257                                 Finally, the MALT1 substrates A20 and CYLD were completely processed
258                        To identify new human MALT1 substrates, we compare B cells from the only known
259 cells and irreversibly inhibited cleavage of MALT1 substrates.
260                 Furthermore, BCL10 and cIAP2-MALT1 synergistically activate NF-kappaB.
261                   RNAi-mediated silencing of MALT1, TAK1, TRAF6, and TRAF2 suppressed TCR-dependent I
262                                              Malt1-/- Th cells failed to cleave RelB, a suppressor of
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-
265                                   Mutants of MALT1 that fail to activate caspase-8 and permit c-FLIP(
266 atients of a homozygous missense mutation in MALT1 that resulted in loss of protein expression.
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
269               In contrast to wild-type human MALT1, the patients' MALT1 mutant failed to correct defe
270 d RIP1 interact with the API2 moiety of API2-MALT1, this moiety alone is insufficient to induce RIP1
271 ion and protein kinase C activation to Bcl10/MALT1, thus leading to NF-kappaB induction.
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
276 s followed by assembling of the CARMA1/BCL10/MALT1/TRAF6 complex to SMO.
277 ologic characteristics, such as samples with MALT1 translocations having high expression of MALT1 and
278                 One subset, characterized by MALT1 translocations, showed overexpression of nuclear f
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
281 aB regulators PKC theta, CARMA1, Bcl-10, and MALT1, which connect to the TCR.
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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