MALT1
- Known as:
- MALT1
- Catalog number:
- 000442A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- MALT1
Related genes to: MALT1
- Gene:
- MALT1 NIH gene
- Name:
- MALT1 paracaspase
- Previous symbol:
- MLT
- Synonyms:
- PCASP1
- Chromosome:
- 18q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-02
- Date modifiied:
- 2019-04-23
Related products to: MALT1
Related articles to: MALT1
- Neutrophils are key first responders in the host response to infection (CDI). Although a high number of tissue and blood neutrophils clearly correlates with adverse outcomes in CDI patients, their functional role remains poorly defined. Using murine (CMT-93) and human (Caco-2) intestinal epithelial cell (IEC) lines co-cultured with neutrophils and a pre-clinical mouse model of CDI, we show that activated neutrophils exacerbate -induced IEC injury. To identify neutrophil subtypes and biological pathways that contribute to CDI-associated IEC damage, we utilized single-cell RNAseq (scRNAseq) to generate the first transcriptomic atlas of murine bone marrow, blood, and colonic neutrophils in acute CDI. Our analyses identified a novel neutrophil population in the colonic lamina propria, "cNeu3," which exhibited high expression of genes associated with neutrophil activation and degranulation. Informed by cNeu3 signature genes from the scRNAseq dataset, we validated the presence of these neutrophils in mouse colon using flow cytometry (CD11bCD63IL-1βMIP-1αMALT1 cells). We found that their abundance correlated with increased epithelial damage. Tumor Necrosis Factor (TNF) was sufficient to polarize mouse bone marrow neutrophils to a cNeu3 phenotype . Finally, TNF-primed human neutrophils worsened toxin-induced IEC damage, which was improved when neutrophil degranulation was blocked. Collectively, our data provide novel insights into neutrophil-mediated pathology during CDI. - Source: PubMed
Publication date: 2026/04/23
Huber AlexanderMathew AnnKhondokar FaizaSharma DivyaMukherjee AninditaKhona Dolly KGabriel JucyJose ShinsmonMadan Rajat - Provided herein are novel compounds as MALT1 inhibitors, pharmaceutical compositions, use of such compounds in treating cancer, and processes for preparing such compounds. - Source: PubMed
Publication date: 2026/03/04
Sabnis Ram W - Tanshinone IIA (Tan IIA), a bioactive compound from , protects cardiomyocytes against ischemia-reperfusion (I/R) injury. This study aims to elucidate its underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/04/14
Yu HuiminLi YiliYang YuehongQian YanjinYang MinYang YixunSheng HongpingZhang XiaoyuPu YapingQian Yan - Dysregulation of the CARD11-BCL10-MALT1 (CBM) complex is associated with a group of inborn errors of immunity termed “CBM-opathies,” which encompass a spectrum of clinical manifestations including combined immunodeficiency, autoimmune inflammation, atopic disorders, and lymphoproliferation. In this study, we identified novel compound heterozygous variants in the CBM complex in a patient with a family history of immune dysfunction. The patient inherited the variants CARD11 p.K215N and MALT1 p.K543R/p.M732T from asymptomatic carrier parents. Phenotypically, the patient exhibited a developmental arrest of B lymphocytes at the transitional/naïve B cell stage, accompanied by activation of virus-response pathways. Impaired development of T follicular helper cells was linked to defective germinal center formation and agammaglobulinemia. Furthermore, the patient showed expansion of T peripheral helper cells and a deficiency in regulatory T cells, both associated with autoimmunity and colitis. In vitro studies confirmed an imbalance in Tph/Tfh cell differentiation. Single-cell RNA sequencing further revealed a deficiency in B cell development and an enriched population of pro-inflammatory CD3CD4CD8CD247 T cells, functionally enriched in the MAPK signaling pathway. Mechanistically, the MALT1 K543R and M732T variants attenuated MALT1’s enzymatic activity and compromised its protein stability, while the CARD11 variant disrupted CARD11-mediated promotion of BCL10 filament formation. We demonstrated that these three variants act synergistically to impair NF-κB activation. Specifically, CARD11 cooperates with the co-pathogenic MALT1 and the modifier variant MALT1 to destabilize the functional integrity of the CBM complex, thereby driving the patient’s phenotype. In summary, our study provides new insights into the pathogenesis of autoimmune inflammatory disorders within the spectrum of CBM-opathies and reveals a potential role for the CBM complex in regulating the balance between T peripheral helper and T follicular helper cells. - Source: PubMed
Publication date: 2026/03/26
Li RuiSun XiaochenBao WeiYu HaolanDan YuQingWu ChunmeiMa YanYin HanlinLin WanyiLu LiangjingFu QiongYang Chenghua - Asthma is a significant allergic condition affecting the respiratory system. Numerous compounds extracted from traditional Chinese herbal medicine show potential benefits for treating airway inflammation associated with bronchial asthma. Astragalus polysaccharide (APS), a class of major extracts from Astragalus membranaceus, exhibit many anti-inflammatory effects. Nonetheless, the underlying mechanisms of APS in asthma remain to be clarified. This study aims to assess the effect and the mechanism by which APS against asthma. The ovalbumin (OVA)-induced asthma mice were employed to assess the roles of APS . Lung tissues were used for H&E, PAS, and Masson staining. Inflammatory cells in bronchoalveolar lavage fluid (BALF) and chemokines in both BALF and serum samples were determined by hemocytometer and ELISA. The expression of the Hedgehog/NLRP3/GSDMD pathway in lung tissues was measured by quantitative real-time PCR and Western blotting. APS displayed lung-protective effects through decreasing airway inflammation and airway remodeling in OVA-induced asthma mice, which was demonstrated by decreasing the number of inflammatory cells and the cytokine levels in BALF and serum, and histopathological changes in lung tissues. Besides, APS treatment could decrease the expression of SHH, SMO, Gli1, Ptch1, NLRP3, GSDMD-N, ASC, Cleaved caspase-1, IL-18, IL-1β, CARMA3, BCL10, and MALT1 in lung tissues. APS improves clinical symptoms of OVA-induced bronchial asthma. The anti-asthmatic effects of APS may be related to the regulatory influences of the Hedgehog/NLRP3/GSDMD pathway. - Source: PubMed
Publication date: 2026/03/16
Yu LiliLiu ZibinZhang RuiLai Jian