Browse our anti-MALT1 (MALT1) Antibodies

Human Mucosa Associated Lymphoid Tissue Lymphoma Translocation Gene 1 (MALT1) interaction partners

1. MALT1 activation by TRAF6 in lymphocytes needs neither BCL10 nor CARD11.

2. MALT1 C-terminal region covering the Ig2-paracaspase-Ig3 domain is flexibly attached to the BCL10-MALT N-terminal death domain core filaments

3. High MALT1 expression is associated with Breast Cancer.

4. Mutations in the translocated MALT1 allele is associated with IGH-MALT1-positive MALT lymphoma.

5. Cellular metabolism constrains innate immune responses in preterm infants due to perturbations in the expression of PPARgamma, MALT1, DDIT4, and most of the cytokines.

6. this first report show that MALT1 integrates several T-cell activation pathways and indirectly controls gamma-chain receptor dependent survival, to impact on T-cell expansion

7. These findings suggested that cleavage at R781 of MALT1 played a role in the survival of activated B-cell like diffuse large B-cell lymphoma cells.

8. MALT1 and TRAF6 cooperatively interact with CARMA1-BCL10 filaments and form CARMA1-BCL10-MALT1-TRAF6 signalosome.

9. The results suggest that the involvement of MALT1 in DNA damage-induced NF-kappaB is through the recruitment of TRAF6.

10. A missense mutation in mucosa-associated lymphoid tissue lymphoma translocation 1 gene (MALT1) was identified in a family with siblings with IPEX-Like Syndrome. MALT1 deficiency should now be considered as a possible cause of IPEX-like syndrome associated with immunodeficiency.

11. Thrombin-mediated MALT1 protease activation triggers acute disruption of endothelial barrier integrity via CYLD cleavage.

12. Authors utilized transcriptomic data and experimental evidences to prove that miR-181d was a novel regulator of NFkappaB signaling pathway by directly repressing MALT1, leading to induced PN markers and reduced MES genes.

13. Taken together, this present study indicates that miR-649 promotes herpes simplex virus type 1 replication through regulation of the MALT1-mediated antiviral signaling pathway and suggests a promising target for antiviral therapies.

14. These results demonstrate a key role for the proteolytic activity of MALT1 in PEL, and provide a rationale for the pharmacological targeting of MALT1 in PEL therapy.

15. MALT1 deficiency or pharmacological inhibition of MALT1 catalytic activity inhibits pathogenic mutant CARD14-induced cytokine and chemokine expression in human primary keratinocytes.

16. results unveil HOIL1 as a negative regulator of lymphocyte activation cleaved by MALT1.

17. CARD14/MALT1-mediated signaling in keratinocytes has a role in psoriasis [review]

18. Psoriasis mutations disrupt CARD14 autoinhibition promoting BCL10-MALT1-dependent NF-kappaB activation

19. Studies indicate that t(11;18)(q21;q21) translocation involves MALT1 (MALT lymphoma translocation protein 1) gene.

20. Targeting MALT1 proteolytic activity in autoimmune disease and B-cell lymphoma might not be a successful strategy. (Review)

Mouse (Murine) Mucosa Associated Lymphoid Tissue Lymphoma Translocation Gene 1 (MALT1) interaction partners

1. Malt1 protease activity plays an important role in the production of IL-17 in the blood and colon upon T cell receptor stimulation. In addition, Malt1 protease inactivation attenuates the development of experimental colitis with the regulation of the population of Th17 and Th1/17 cells.

2. These findings highlight the important regulatory role of MALT1 in the NF-kappaB-NFATc1-signalling axis during osteoclastogenesis and suggest that targeting MALT1 is a promising treatment option for rheumatoid arthritis.

3. CARD11-BCL10-MALT1 (CBM) signaling mediates TCR-induced NF-kappaB activation in Tregs and controls the conversion of resting Tregs to effector Tregs under homeostatic conditions. However, in inflammatory milieus, cytokines can bypass the CBM requirement for this differentiation step.

4. data presented here shows that Malt1 deficiency (Malt1-/-) exacerbates dextran sodium sulfate-induced inflammation

5. Malt1 self-cleavage is important in regulating expression of NF-kappaB target genes and subsequent T cell activation for anti-tumor immunity.

6. IKKbeta is involved in membrane fusion, and serves as a critical protein kinase required for initial formation and the regulation of the CARMA1/MALT1/Bcl10/CBM complex in platelets.

7. this study shows that Malt1 protease activity plays an important role in the activation of innate immune cells via FcgammaR, and the development of FcgammaR-mediated autoimmune diseases

8. the importance of MALT1-mediated inflammation and T cell activation to control ERA virus, providing new insights in the biology of MALT1 and rabies virus infection.

9. MALT1 as a key molecule that contributes to immune tolerance at steady-state while facilitating immune reactivity under stress conditions.

10. Data show that inhibition of the protease activity of MALT1 might be a strategy to treat inflammatory bowel disease and the NLRP3 inflammasome and NF-kappaB activation are critical components in MALT1 signaling cascades in this disease model.

11. Thrombin-mediated MALT1 protease activation triggers acute disruption of endothelial barrier integrity via CYLD cleavage.

12. MALT1 function is required in B cells for germinal center formation.

13. Studies indicate an important role for mucosa associated lymphoid tissue lymphoma translocation gene 1 protein (MALT1) in the development of experimental autoimmune encephalomyelitis (EAE)

14. Targeting MALT1 proteolytic activity in autoimmune disease and B-cell lymphoma might not be a successful strategy. (Review)

15. TCR-induced alternative splicing augments MALT1 scaffolding to enhance downstream signalling and to promote optimal T-cell activation.

16. MALT1-dependent NF-kappaB activation is crucial for the development of EGFR-associated solid-tumor progression

17. By regulating linear ubiquitination, MALT1 is both a positive and negative pleiotropic regulator of the canonical NF-kappaB pathway.

18. Results demonstrate that MALT1 protease activity plays key roles in both innate and adaptive immune responses, and in regulating immune homeostasis in vivo.

19. data demonstrate that MALT1 ubiquitination is critical for the engagement of CBM and IKK complexes, thereby directing platelet signals to the NF-kappaB pathway.

20. Malt1 protease inactivation efficiently dampens immune responses but causes spontaneous autoimmunity.