MALT EXTRACT
- Known as:
- MALT EXTRACT
- Catalog number:
- 1708
- Product Quantity:
- 500 grams
- Category:
- -
- Supplier:
- Condalab
- Gene target:
- MALT EXTRACT
Related genes to: MALT EXTRACT
- Gene:
- BIRC3 NIH gene
- Name:
- baculoviral IAP repeat containing 3
- Previous symbol:
- API2
- Synonyms:
- cIAP2, hiap-1, MIHC, RNF49, MALT2, c-IAP2
- Chromosome:
- 11q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2016-10-05
Related products to: MALT EXTRACT
Related articles to: MALT EXTRACT
- NK cells are promising candidates for adoptive cell therapy; however, their proliferative capacity and functional persistence may be limited. Genetic modification with hTERT enhances their proliferative potential, while co-expression of the iCASP9 suicide gene provides a safety mechanism based on late-stage apoptosis induction by chemical dimerizer (CID). Whether hTERT overexpression interferes with iCasp9-mediated cell death remains unclear, and the non-canonical functions of telomerase in this context are poorly understood. This study served a dual purpose: to assess the efficacy of the iCasp9 "suicide switch" in NK cells, and to investigate a non-canonical role of telomerase in NK cell-mediated evasion from cell death. Here, we demonstrate that hTERT-modified NK cells exhibit significant resistance to CID-induced apoptosis, an effect independent of telomerase catalytic activity, as confirmed using a dominant-negative hTERT (DN-hTERT) mutant. Transcriptomic profiling revealed that both CID-resistant iCasp9-NK cells and hTERT-iCasp9-NK cells share common gene expression signatures: upregulation of cell cycle-associated genes and downregulation of splicing-related factors, including HNRNPH1 and SNRPD3, accompanied by shared patterns of alternative splicing. Among apoptosis-related transcripts, BIRC3, which encodes c-IAP-2, a direct inhibitor of caspase 9, was consistently elevated in both "resistant" and "survived" NK cells. However, shRNA-mediated knockdown of BIRC3 failed to restore sensitivity to CID, indicating that BIRC3 upregulation is not the unique determinant of resistance and suggesting involvement of additional compensatory pathways. Overall, our findings define specific transcriptional signatures associated with evasion of NK cells from iCasp9-mediated apoptosis, implying the contribution of cell cycle progression, enhanced anti-apoptotic signaling, and alterations in splicing regulation, and highlighting the complex role of non-canonical hTERT functions in these adaptations. In the rational design of next-generation gene-modified NK cell therapies with improved safety and persistence, the uncovered insights should be considered. - Source: PubMed
Publication date: 2026/06/12
Palamarchuk Anastasia IUstiuzhanina Maria OVelichinskii Rodion AVavilova Julia DGrechikhina Maria VKovalenko Elena IStreltsova Maria A - Richter transformation of Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) into classic Hodgkin lymphoma (CHL-RT) is rare and remains incompletely understood. Two histologic subtypes are recognized: type 1 (CLL/SLL with scattered Hodgkin/Reed-Sternberg (HRS) cells) and type 2 (HRS cells within a polymorphous inflammatory background). In this multi-institutional study of 77 patients with CHL-RT (27 type 1 and 50 type 2), we characterized immune evasion markers, / copy number alterations, tumor microenvironment, and performed targeted next-generation sequencing on 37 CLL/SLL samples. HRS cells in CHL-RT displayed immune-evasion phenotypes similar to de novo CHL, though PD-L1 expression was lower in type 1 cases. gain/polysomy were frequent (83.3%). CLL/SLL with CHL-RT harbored increased mutations in , , , , and versus reference CLL/SLL. Similar mutational profiles, demographics, and survival outcomes support a biological continuum between type 1 and type 2 CHL-RT, with distinct genetic features in CLL/SLL predisposing to CHL transformation. - Source: PubMed
Publication date: 2026/05/20
Yan MingfeiParikh Sameer ASampaio De Melo Michelly KHampel Paul JAleynick NathanielChan AlexanderEren Ozgur CanLopez KatherineCohen AlexaRoshal MikhailLim Megan SBoiocchi LeonardoDogan AhmetZhang YanmingSinha SutapaRabe Kari GKay Neil EJaffe Elaine SKing Rebecca LXiao Wenbin - Cutaneous leishmaniasis is a common neglected parasitic disease in developing countries that primarily causes skin lesions but may also be associated with systemic manifestations. In this study, bioinformatics approaches were used to analyze gene expression data from blood samples of patients with cutaneous leishmaniasis in order to identify key molecular markers and mechanisms involved in the development of systemic manifestation. - Source: PubMed
Publication date: 2026/06/01
Dehghan ZeinabZarei-Behjani ZeinabRezaei MasoudArabi HamidrezaTaherimoghadam MonirHatam Gholamreza - Acute pancreatitis (AP) is a frequent exocrine inflammation of the pancreas that causes severe abdominal pain and multiorgan dysfunction that may lead to pancreatic necrosis and persistent organ failure. Previous studies have indicated that the pathogenesis of AP is based on the Cerulein-triggered experimental model, which simulates human AP in vivo. As reported, pancreatic acinar cells and peritoneal macrophages partake in pancreatic inflammation and injury. Nevertheless, the association between them is poorly understood. NLRC4 was highly expressed, and BIRC3 was reduced in AP patients and Cerulein-treated AR42J cells. Exosomes derived from Cerulein-treated AR42J cells induced rat peritoneal macrophage M1 polarization and pyroptosis, which were partly abolished by NLRC4 silencing. Moreover, BIRC3 triggered the ubiquitination of NLRC4 and promoted its degradation. Besides, exosomal BIRC3 repressed sodium taurocholate-induced pancreatic lesions in vivo. Exosomes derived from Cerulein-stimulated pancreatic acinar cells promote peritoneal macrophage M1 polarization and pyroptosis by a BIRC3/NLRC4 axis in AP, providing a promising strategy to protect against AP. - Source: PubMed
Publication date: 2026/05/01
Zhang ShengFu JunjingZhang HaiyunZhou BingZhou BinjieJiao Yang - Disease of the lung alveoli is frequently associated with acute or chronic inflammation. At present, there are no effective therapies to support regeneration of the alveolar epithelium, and ongoing inflammation adds an additional layer of complexity to many lung diseases. Here, we describe a primary adult human organoid model for investigating how inflammation shapes alveolar regeneration. Unlike previous models, this system supports long-term expansion of newly identified human-specific alveolar progenitor cells and serum-free differentiation into alveolar type 1 (AT1)-like cells. Using this platform, we find that interferon-gamma (IFN-γ) exerts cytotoxic effects on mature AT1-like cells while promoting survival of alveolar progenitor cells mediated by BIRC3. This unexpected selective positive effect of IFN-γ on alveolar progenitors underscores the need for nuanced and context-dependent evaluation of the influence of pro-inflammatory cytokines on alveolar regeneration. Our organoid model provides a reductionist platform for mechanistic studies and discovery of strategies to enhance alveolar regeneration. - Source: PubMed
Publication date: 2026/04/16
Dost Antonella F MBalážová KatarínaPou Casellas Carlavan Rooijen Lisanne MEpskamp Wissevan Son Gijs J Fvan de Wetering Willine JLopez-Iglesias CarmenBegthel HarryPeters Peter JSmakman Nielsvan Es Johan HClevers Hans