IGF2BP2
- Known as:
- IGF2BP2
- Catalog number:
- Y213885
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- IGF2BP2
Related genes to: IGF2BP2
- Gene:
- IGF2BP2 NIH gene
- Name:
- insulin like growth factor 2 mRNA binding protein 2
- Previous symbol:
- -
- Synonyms:
- IMP-2
- Chromosome:
- 3q27.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-09
- Date modifiied:
- 2015-11-23
Related products to: IGF2BP2
Related articles to: IGF2BP2
- Negative regulators are crucial for maintaining immune homeostasis, yet the complexities of their regulatory mechanisms are not fully elucidated. In this study, we reveal that IGF2BP2, an m6A reader protein, orchestrates the formation of phase-separated condensates dependent on G3BP1, acting as a pivotal negative regulator of bacterial-induced inflammation. The absence of IGF2BP2 amplifies the production of pro-inflammatory cytokines such as IL-6, TNF-α, and IL-1β, whereas its overexpression attenuates these inflammatory responses. Mechanistically, IGF2BP2 depletion enhances NF-κB signaling by diminishing DOK3 expression upon bacterial stimulation. Restoration of DOK3 expression in IGF2BP2-deficient cells markedly mitigates this hyper-inflammatory phenotype. Additionally, we identify m6A modifications at nucleotides 1056 and 1101 on DOK3 mRNA that facilitate its binding and stabilization by IGF2BP2. These insights provide a novel understanding of how IGF2BP2 modulates immune responses via m6A-dependent stabilization of DOK3 mRNA and highlight potential therapeutic avenues for treating inflammatory diseases. - Source: PubMed
Chen JianChen WeixinShan XiaojingLu PengSun ZhangyiChen SiyunLiu BoWu ChengleiLu Bing - While insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has been extensively studied in tumor cells, its role in immune cells within the tumor microenvironment, particularly in macrophages, remains largely unknown. Here, we reveal a critical function of IGF2BP2 in macrophages, demonstrating that myeloid-specific deletion of IGF2BP2 profoundly alters macrophage metabolism and polarization, and markedly impairs tumor progression. Bulk RNA sequencing of IGF2BP2 knockout (KO) macrophages revealed significant alterations in gene expression profiles, particularly impacting pathways associated with glycolysis, mitochondrial function, cell motility, and cell migration. Functional assays confirmed increased glycolytic activity and a concomitant reduction in maximal respiration and reserve respiratory capacity, indicating a metabolic shift towards glycolysis. Furthermore, IGF2BP2 deficiency impaired tumor-associated macrophage (TAM)-like polarization , as evidenced by decreased expression of TAM markers, such as , , and . Lipidomic profiling revealed distinct lipid signatures in IGF2BP2 KO TAM-like macrophages, including alterations in triglycerides and cardiolipins, crucial for mitochondrial integrity. , deletion of IGF2BP2 specifically in the myeloid lineage was sufficient to reduce tumor growth in a subcutaneous Lewis lung carcinoma model, accompanied by decreased TAM infiltration and a shift towards a pro-inflammatory macrophage phenotype. Additionally, IGF2BP2-deficient macrophages showed impaired migratory capacity both and . These findings underscore the critical role of IGF2BP2 in controlling macrophage metabolism, polarization, and tumor-supporting functions within the tumor microenvironment, and identify myeloid IGF2BP2 as a potential therapeutic target in cancer. - Source: PubMed
Publication date: 2026/02/18
Schymik Hanna SWrublewsky SelinaHöring MarcusLiebisch GerhardBoth SimonGasparoni GillesBickelmann CarolineRobertson HanahDahlem CharlotteWalter JörnHelms VolkhardLaschke Matthias WAmpofo EmmanuelHoppstädter JessicaKiemer Alexandra K - Lung adenocarcinoma (LUAD) progression is strongly shaped by tumor-associated macrophages (TAMs), yet the post-transcriptional mechanisms that sustain matrix-remodeling TAM states remain incompletely understood. Here, circRNA profiling of LUAD TAMs versus normal tissue-resident macrophages identified circSMAD4 (hsa_circ_0047713) as a consistently TAM-enriched circRNA associated with advanced clinicopathological features and unfavorable survival. circSMAD4 exhibited canonical circular properties, including a validated back-splice junction, RNase R resistance, and enhanced transcript stability. Functionally, circSMAD4 knockdown in human and murine macrophages attenuated tumor education, shifted macrophages away from an M2-like phenotype, and weakened their ability to promote LUAD-cell proliferation, invasion, and EMT-like changes in co-culture. In syngeneic orthotopic lung and experimental metastasis models, circSMAD4-depleted macrophages restrained tumor growth and reduced metastatic burden. Mechanistically, cytoplasmic circSMAD4 acted as a ceRNA to sequester miR-562 and relieve repression of COL4A1. In parallel, circSMAD4 formed a specific ribonucleoprotein complex with the m6A reader IGF2BP2, facilitating IGF2BP2 association with COL4A1, ACTA2, and SPI1 transcripts and enhancing their m6A-dependent stability. Together, these dual branches converge on a matrix-remodeling output, positioning circSMAD4 as a post-transcriptional hub that reinforces protumor TAM programs in LUAD and a potential target for microenvironment-directed therapy. - Source: PubMed
Publication date: 2026/03/26
Yu ZhengweiWang XinyueZheng YiqianHe YifanLin JiayuXiao YueMo BinXie HaoyuHang SitongGao XiaXu PeiLiu YihaoXiao Haibo - Dysregulation of N6-methyladenosine (m6A) RNA methylation plays a crucial role in colorectal cancer (CRC) development. Despite the established oncogenic role of methyltransferase-like 3 (METTL3) in CRC, the mechanisms behind its tumor-promoting functions are not fully understood. - Source: PubMed
Publication date: 2026/04/02
Ren HongtaoWang MincongMa XiulongAn LeiGuo YuyanMa Hongbing - - Source: PubMed
Publication date: 2026/03/31
Yi RanWu RuifanJiang Qingyan