ReviewFrontiers in immunology2018
CARMA3 Is a Critical Mediator of G Protein-Coupled Receptor and Receptor Tyrosine Kinase-Driven Solid Tumor Pathogenesis.
Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- MALT1 protease inhibition restrains glioblastoma progression by reversing tumor-associated macrophage-dependent immunosuppression in mice.Nature communications · 2026Article
- Unanchored K63-linked polyubiquitin chains: a novel second messenger involved in G protein-coupled receptors early signaling events.Cell communication and signaling : CCS · 2026Article
- The role of CARMA3 in regulating fibrosis to prevent hypertrophic cardiomyopathy.Cell death discovery · 2025Article
- Disrupting CARMA3 Signaling with Triptolide Reverses Sorafenib Resistance in Hepatocellular Carcinoma.International journal of medical sciences · 2025Article
- High-expression of BCL10 inhibits cell-mediated immunity within the tumor immune microenvironment.Frontiers in immunology · 2025Article
- CARMA3 Drives NF-κB Activation and Promotes Intervertebral Disc Degeneration: Involvement of CARMA3-BCL10-MALT1 Signalosome.Inflammation · 2024Article
- Bioinformatic analysis of molecular characteristics and oncogenic features of CARD14 in human cancer.Scientific reports · 2024Article
- MALT1 substrate cleavage: what is it good for?Frontiers in immunology · 2024Review
- Combining precision oncology and immunotherapy by targeting the MALT1 protease.Journal for immunotherapy of cancer · 2022Review
- Article
- MALT1 Is a Targetable Driver of Epithelial-to-Mesenchymal Transition in Claudin-Low, Triple-Negative Breast Cancer.Molecular cancer research : MCR · 2022Article
- CARMA3: A potential therapeutic target in non-cancer diseases.Frontiers in immunology · 2022Review
- A Claudin-Based Molecular Signature Identifies High-Risk, Chemoresistant Colorectal Cancer Patients.Cells · 2021Article
- CARD10 cleavage by MALT1 restricts lung carcinoma growth in vivo.Oncogenesis · 2021Article
- Targeting BCL10 by small peptides for the treatment of B cell lymphoma.Theranostics · 2020Article
- CARD10 promotes the progression of renal cell carcinoma by regulating the NF‑κB signaling pathway.Molecular medicine reports · 2020Article
- MALT1 is a critical mediator of PAR1-driven NF-κB activation and metastasis in multiple tumor types.Oncogene · 2019Article
- Caspase recruitment domain family member 10 regulates carbamoyl phosphate synthase 1 and promotes cancer growth in bladder cancer cells.Journal of cellular and molecular medicine · 2019Article
- CARMA3/NF-κB signaling contributes to tumorigenesis of hepatocellular carcinoma and is inhibited by sodium aescinate.World journal of gastroenterology · 2019Article
- CARMA3 Transcriptional Regulation of STMN1 by NF-κB Promotes Renal Cell Carcinoma Proliferation and Invasion.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The CARMA-Bcl10-MALT1 (CBM) signalosome is an intracellular protein complex composed of a CARMA scaffolding protein, the Bcl10 linker protein, and the MALT1 protease. This complex was first recognized because the genes encoding its components are targeted by mutation and chromosomal translocation in lymphoid malignancy. We now know that the CBM signalosome plays a critical role in normal lymphocyte function by mediating antigen receptor-dependent activation of the pro-inflammatory, pro-survival NF-κB transcription factor, and that deregulation of this signaling complex promotes B-cell lymphomagenesis. More recently, we and others have demonstrated that a CBM signalosome also operates in cells outside of the immune system, including in several solid tumors. While CARMA1 (also referred to as CARD11) is expressed primarily within lymphoid tissues, the related scaffolding protein, CARMA3 (CARD10), is more widely expressed and participates in a CARMA3-containing CBM complex in a variety of cell types. The CARMA3-containing CBM complex operates downstream of specific G protein-coupled receptors (GPCRs) and/or growth factor receptor tyrosine kinases (RTKs). Since inappropriate expression and activation of GPCRs and/or RTKs underlies the pathogenesis of several solid tumors, there is now great interest in elucidating the contribution of CARMA3-mediated cellular signaling in these malignancies. Here, we summarize the key discoveries leading to our current understanding of the role of CARMA3 in solid tumor biology and highlight the current gaps in our knowledge.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.