Ask about this productRelated genes to: TAB2 antibody
- Gene:
- TAB2 NIH gene
- Name:
- TGF-beta activated kinase 1 (MAP3K7) binding protein 2
- Previous symbol:
- MAP3K7IP2
- Synonyms:
- KIAA0733
- Chromosome:
- 6q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-22
- Date modifiied:
- 2018-02-12
Related products to: TAB2 antibody
Related articles to: TAB2 antibody
- Macrophage antimicrobial programs are regulated not only by transcriptional networks but also by RNA processing mechanisms affecting signal transduction and effector responses. One such mechanism, alternative polyadenylation (APA), determines mRNA fate by changing the length of the 3' UTR. However, our understanding of the impact of APA on antibacterial functions and how we can manipulate it to influence infection outcomes remains limited. In this study, we identify the APA regulator CFIm25 (NUDT21) as a promoter of macrophage defense against serovar Typhimurium (STM). STM infection is known to drive macrophages toward an M2-like immunosuppressive state conducive to bacterial survival. Concurrent with this transition, the CFIm25 level is reduced, and the 3' UTRs of CFIm25 targets encoding key immune proteins, such as TAB2 and TBL1XR1, are lengthened, suggesting a role for APA changes in the response to STM. Overexpression of CFIm25 in infected macrophages blocks these -induced 3' UTR changes, leading to greater mRNA and protein expression. Significantly, the increase in CFIm25 suppresses infection, thereby creating a more antimicrobial intracellular environment, improving macrophage survival, and reducing M2 properties that support bacterial replication. Specifically, CFIm25 enhances production of the antibacterial peptide LL-37, increases reactive oxygen species and nitric oxide levels, suppresses arginase activity and lactate production, and stimulates release of pro-inflammatory cytokines while inhibiting anti-inflammatory cytokines. Depletion studies show TAB2 mediates CFIm25's antibacterial effects by activating both MAPK and NF-kB pathways. Our findings highlight APA regulation as a potential target for boosting immune defenses and developing treatments for chronic bacterial infections. - Source: PubMed
Publication date: 2026/02/28
Barua AtishMukherjee SrimoyeeBourgeois JeffMoore Claire L - Nuclear factor kappa B (NF-κB) signaling plays a central role in inflammation, immunity, cell survival, and cancer progression. Its constitutive activation is frequently observed in breast cancer, contributing to tumor growth, treatment resistance, and metastasis. MicroRNAs (miRNAs) are key post-transcriptional regulators of gene expression and may modulate NF-κB signaling in a subtype-specific or -independent manner. The aim of the study was to identify miRNAs that may potentially regulate the activity of genes associated with NF-κB signaling across five molecular subtypes of breast cancer in Polish women. Tumor and matched normal tissue samples were collected from 405 patients with five breast cancer subtypes: luminal A ( = 130), HER2-negative luminal B ( = 100), HER2-positive luminal B ( = 96), non-luminal HER2-positive ( = 36), and triple-negative breast cancer (TNBC, = 43). Expression profile of selected NF-κB-related genes were evaluated using mRNA microarrays and RT-qPCR. Protein levels were assessed by ELISA. Candidate regulatory miRNAs were identified via miRNA microarrays and validated using the miRDB database. A consistent upregulation of , , , , , , , and was observed across all subtypes, suggesting activation of canonical NF-κB signaling. Downregulation of specific miRNAs, miR-1297 and miR-30a (targeting ), miR-134 (), miR-125b (), and miR-4329 (), may contribute to this deregulation. For , , , and , no regulatory miRNAs meeting our criteria were identified. Our study reveals a subtype-independent activation of the canonical NF-κB signaling pathway in breast cancer, underpinned by consistent upregulation of key components (at both the transcript and protein levels. Dysregulation of specific miRNAs likely contributes to this altered gene expression. These findings suggest the presence of a common NF-κB-driven oncogenic program across molecular subtypes, with potential implications for developing miRNA-based therapeutic strategies targeting inflammation, survival signaling, and treatment resistance in breast cancer. - Source: PubMed
Publication date: 2026/04/30
Mitka-Krysiak ElżbietaKról-Jatręga KatarzynaOssowski PiotrZmarzły NikolaBereza KrzysztofOrdon PawełSirek TomaszSirek AgataBoroń KacperBoroń DariuszWyrobiec GrzegorzSzczepanik TomaszSkorek MartaGrabarek Beniamin Oskar - Nuclear magnetic resonance (NMR) measurements of the hyperfine parameters (quadrupolar, shifts) at the metal and boron sites are reported from an isomorphous set of eleven stable AlB structure-type space group 191 metal diborides, the main group metal diborides MgB and AlB, and transition metal diborides ScB, TiB, VB, CrB, YB, ZrB, NbB, HfB, TaB. Nuclear quadrupole resonance (NQR) studies were performed to locate resonances from Hf and Ta in the respective diborides. The electric field gradients, V, nuclear quadrupole coupling constants, C, and Knight shift values, K, at the both the metal and boron sites, are reported and are discussed in terms of current state-of-the-art quantum chemical first-principles calculations, as well as being correlated with electronic and cohesive properties of these materials. New experimental results and calculations are presented in addition to re-analysis of existing literature data to test hypotheses of how structure and composition can be tailored to achieve desired physical properties. This comprehensive set of experimental NMR data provides a direct link between measurable hyperfine parameters, calculated bonding parameters, and important physical properties including catalytic activity and asymptotic bulk hardness. The use of magnetic resonance for detection of critical metal diborides via their hyperfine interactions and linking these interactions to physical characteristics opens improved pathways for materials design with novel properties, as well as a method to fingerprint material signatures useful in the circular economy for resource identification, verification, recovery, and reuse. - Source: PubMed
Publication date: 2026/04/21
Bastow Timothy JHill Anita JSeeber AaronNairn Katherine MHolmes Sean TSchurko Robert WTrinchi AdrianMulder Roger JSmith Mark E - Polyvalvular dysplasia, characterized by abnormalities involving more than two cardiac valves, may be associated with chromosomal and genetic abnormalities. A genetic diagnosis is often not pursued as it is perceived that it does not alter clinical management. Microdeletions of the long arm of chromosome 6, which include the TAB2 gene, as well as truncating variants in the TAB2 gene, result in a syndromic form of polyvalvular dysplasia and dysmorphism. A subset of children and adults with this disease may develop dilated cardiomyopathy and would hence need careful follow-up. We report two Indian children with TAB2-related polyvalvular dysplasia and normal ventricular function. - Source: PubMed
Publication date: 2025/10/07
Krishna Mani RamSennaiyan Usha Nandhini - This study investigates the protective effect of GB against cerebral I/R injury and explores its underlying mechanism involving the TRIM45- TAB2-TAK1-TAB1 axis. - Source: PubMed
Publication date: 2026/03/30
Lv ZhiyangJi ZhipingChen JingLong TianningNiu HongyunFu PeinanLu MengHao XiaobeiYang Yuwei