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MALT1 Antibody
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Application 
| WB, IF, E, IHC-P |
|---|---|
| Primary Accession | Q9UDY8 |
| Other Accession | NP_006776, 5803078 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 92272 Da |
| Concentration (mg/ml) | 1 mg/mL |
| Conjugate | Unconjugated |
| Application Notes | MALT1 antibody can be used for detection of MALT1 by Western blot at 1 - 2 µg/mL. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL. |
| Gene ID | 10892 |
|---|---|
| Other Names | Mucosa-associated lymphoid tissue lymphoma translocation protein 1, 3.4.22.-, MALT lymphoma-associated translocation, Paracaspase, MALT1, MLT |
| Target/Specificity | MALT1; MALT1 antibody is human, mouse and rat reactive. At least two isoforms of MALT1 are known to exist; this antibody will detect both isoforms. |
| Reconstitution & Storage | MALT1 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. |
| Precautions | MALT1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | MALT1 {ECO:0000303|PubMed:10523859, ECO:0000312|HGNC:HGNC:6819} |
|---|---|
| Function | Protease that enhances BCL10-induced activation: acts via formation of CBM complexes that channel adaptive and innate immune signaling downstream of CARD domain-containing proteins (CARD9, CARD11 and CARD14) to activate NF-kappa-B and MAP kinase p38 pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines (PubMed:11262391, PubMed:18264101, PubMed:24074955). Mediates BCL10 cleavage: MALT1-dependent BCL10 cleavage plays an important role in T-cell antigen receptor-induced integrin adhesion (PubMed:11262391, PubMed:18264101). Involved in the induction of T helper 17 cells (Th17) differentiation (PubMed:11262391, PubMed:18264101). Cleaves RC3H1 and ZC3H12A in response to T-cell receptor (TCR) stimulation which releases their cooperatively repressed targets to promote Th17 cell differentiation (By similarity). Also mediates cleavage of N4BP1 in T-cells following TCR-mediated activation, leading to N4BP1 inactivation (PubMed:31133753). May also have ubiquitin ligase activity: binds to TRAF6, inducing TRAF6 oligomerization and activation of its ligase activity (PubMed:14695475). |
| Cellular Location | Cytoplasm, perinuclear region. Nucleus Note=Shuttles between the nucleus and cytoplasm. Found in perinuclear structures together with BCL10. |
| Tissue Location | Highly expressed in peripheral blood mononuclear cells. Detected at lower levels in bone marrow, thymus and lymph node, and at very low levels in colon and lung |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
MALT1 was initially identified as a novel gene that was recurrently rearranged in t(11;18)(q21;q21) mucosa-associated lymphoid tissue lymphomas along with the apoptosis inhibitor protein c-IAP2 (1). MALT1, along with the proteins CARMA1 and Bcl10 form an NF-kappaB-activating complex, termed the CBM signalsome, that acts downstream of lymphocyte antigen receptors as well as many other non-lymphoid cell-surface receptors that play a role in multiple cellular functions (2,3). MALT1 has proteolytic activity, and this activity is critical for full NF-kappaB response in T cell activation (4).
REFERENCES
Dielamm J, Baens M, Wlodarska I, et al. The apoptosis inhibitor gene API2 and a novel 18q gene, MLT, are recurrently rearranged in the t(11;18)(q21;q21) associated with mucosa-associated lymphoid tissue lymphomas. Blood 1999; 93:3601-9.
Lin X and Wang D. The roles of CARMA1, Bcl10, and MALT1 in antigen receptor signaling. Semin. Immunol. 2004; 16:429-35.
Rosebeck S, Rehman AO, Lucas PC, et al. From MALT lymphoma to the CBM signalsome: three decades of discovery. Cell Cycle 2011; 10:2485-96.
Staal J, Bekaert T, and Beyaert R. Regulation of NF-kB signaling by caspases and MALT1 paracaspase. Cell Res. 21:40-54.
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