Human IGF2BP2 Protein
- Known as:
- Human IGF2BP2 Protein
- Catalog number:
- 10003-H01H
- Product Quantity:
- 50μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human IGF2BP2 Protein
Related genes to: Human IGF2BP2 Protein
- 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: Human IGF2BP2 Protein
Related articles to: Human IGF2BP2 Protein
- This study aimed to investigate the effects of the Total Flavonoids from Rhizoma Drynaria (TFRD) on METTL3-mediated m6A methylation and osteogenic-angiogenic coupling during the repair of large bone defects and to elucidate its role in bone remodeling under the Masquelet technique. - Source: PubMed
Publication date: 2025/11/14
Wu JieZeng JingqiWu RuizheJin HuiMa HuaiyuXu HaoranLi YueTan LeiSun ShaoqiuWang Fan - Hepatocellular carcinoma (HCC) is a common and serious type of malignant tumor with an unfavorable prognosis, partly attributed to the prevalence of hepatitis B virus (HBV) infection. However, the molecular mechanism underlying HBV-HCC are not yet fully understood. Here, we found that Kruppel-like factor 16 (KLF16) was significantly upregulated in HBV-HCC and KLF16 knockdown suppressed the growth and metastasis of HBV-infected HCC cells. Hepatitis B virus X protein (HBx)-mediated N6-methyladenosine (m6A) modification of KLF16 mRNA promoted the binding of insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) and IGF2BP3, thereby enhancing the stability of KLF16 mRNA. Furthermore, KLF16 was found to promote the transcription of chromosome 12 open reading frame 49 (C12orf49), which in turn increased programmed death-ligand 1 (PD-L1) expression by competitively binding to speckle-type POZ protein (SPOP) and blocking SPOP-mediated ubiquitination and degradation of PD-L1. HBx contributed to immune escape in HBV-HCC through the KLF16-C12orf49-PD-L1 axis. Importantly, inhibiting KLF16 significantly improved the efficacy of anti-PD-L1 therapy in HBV-HCC. Collectively, our study reveals the newly identified HBx-KLF16-C12orf49-PD-L1 axis and its role in promoting growth and immune evasion in HBV-HCC, offering a promising target for clinical interventions in HBV-HCC treatment. - Source: PubMed
Publication date: 2025/11/14
Chen WenbiaoLin ChenhongWang LuolinYu ZhichaoXu YuxiuxiuZhang MinhaiWang LishengYao Jun - Tuberous sclerosis complex (TSC) is an autosomal dominant disorder caused by inactivating mutations in TSC1 or TSC2 gene, leading to mTORC1 hyperactivation. However, mTORC1-independent mechanisms in this disorder remain poorly understood. In the study, excess glycogen storage was found in Tsc1 cells, Tsc1 and Tsc1 mice, as well as in Tsc2 cells, Tsc2 and Tsc2 mice, with more pronounced accumulation in models with TSC2 defects. Mechanistically, the deficiency of TSC1 or TSC2 gene caused redundant uncomplexed-TSC2 or TSC1 protein, respectively. Strikingly, only uncomplexed-TSC1 downregulated the histone demethylase KDM5A, which in turn increased H3K4me3 levels at the METTL3 promoter to enhance its expression. The upregulated mA "writer" protein METTL3 cooperated with the "reader" protein IGF2BP2 to stabilize GYS2 mRNA, causing the upregulation of GYS2 resulting in the glycogen storage. Thus, our study uncovered a novel mTORC1 independent pathway (TSC1-KDM5A-METTL3-IGF2BP2-GYS2) that underlies the excess glycogen storage, and that synergy of mTORC1-dependent and independent pathways leads to the more pronounced glycogen storage with TSC2 defects compared to those with TSC1 defects, reflecting the more severer clinical phenotypes in TSC patients with TSC2 mutations. Importantly, the restoration of glycogen homeostasis and significant amelioration of liver lesion in TSC2 defect models after the combination treatment of pharmacological inhibitors targeting mTORC1 and METTL3, unveil a potential clinic intervention for TSC patients to whom mTORC1 inhibitors are less effective or even ineffective. - Source: PubMed
Publication date: 2025/11/14
Yue XiaoqiaoZhang YanpingZhao NaLang TaoChen GuangxinXiong QiuhongGao LeiWang WenjingLi PingWu Changxin - This study delineates a hierarchical signaling axis driving gastric cancer (GC) progression through integrated transcriptomic and functional analyses. Single-cell sequencing and TCGA data identified CSF2 as a key oncogene, with elevated expression correlating with poor prognosis. Mechanistically, the transcription factor HES1 directly activates IGF2BP2 transcription, as confirmed by chromatin immunoprecipitation and dual-luciferase assays. IGF2BP2 subsequently stabilizes CSF2 mRNA via N6-methyladenosine (mA) modification, validated through RNA immunoprecipitation and mRNA decay kinetics. Functional interrogation revealed that the HES1-IGF2BP2-CSF2 axis promotes GC cell growth, motility, and infiltrative capacity while inhibiting apoptosis. Critically, this axis orchestrates glycolytic reprogramming, evidenced by upregulated HK2/PKM2/LDHA expression, increased lactate/ATP production, and enhanced glycolytic flux. In vivo xenografts demonstrated accelerated tumor growth upon axis activation, with immunohistochemistry showing elevated Ki67 and reduced apoptosis. These results establish a novel signaling cascade wherein HES1 transcriptionally integrates IGF2BP2-mediated mA epitranscriptomics and metabolic rewiring to fuel GC aggressiveness. - Source: PubMed
Publication date: 2025/11/08
Du JunLi LeiChen BanglingChen YuzhongWang QingkangMa Jiachi - Epigenetic dysregulation plays a critical role in colorectal cancer (CRC) progression. Our study investigated the role of FAM111B in tumorigenic phenotypes and ferroptosis in CRC and the mechanisms by which epigenetic alterations influence FAM111B expression. Bioinformatics analyses revealed FAM111B expression and predicted the association between IGF2BP2 and FAM111B or ELF1. The influence on cell phenotypes was determined by assessing cell proliferation, migration, apoptosis and ferroptosis. Mechanism analyses were performed using luciferase reporter and ChIP assays. Subcutaneous xenografts were used to evaluate the role in vivo. FAM111B, IGF2BP2 and ELF1 were upregulated in CRC tumours and cell lines. FAM111B downregulation inhibited cell proliferation and migration while inducing apoptosis and ferroptosis. IGF2BP2 increased FAM111B expression by stabilising its mRNA, and ELF1 transcriptionally upregulated IGF2BP2. Moreover, ELF1 modulated FAM111B expression through IGF2BP2. ELF1 knockdown suppressed cell proliferation and migration while triggering apoptosis and ferroptosis, which could be abolished by reintroduction of IGF2BP2 or FAM111B. Additionally, ELF1 depletion diminished the in vivo tumorigenicity of HCT116 cells. The ELF1/IGF2BP2/FAM111B cascade drives CRC progression and ferroptosis resistance. Targeting this cascade may provide a therapeutic avenue for CRC treatment. - Source: PubMed
Yin DianCao LiliHua MeiChen Ying