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
- Sublethal heat stress exacerbates hepatocellular carcinoma (HCC) by promoting recurrence and metastasis. This study aimed to investigate the molecular mechanisms by which sublethal heat stress enhances HCC progression to improve therapeutic strategies and patient outcomes in HCC management. - Source: PubMed
Publication date: 2026/09/17
Chen JieTan YanXie WeiShi LeiQuan HuXiao HuaLiu JiaMao XianhaiChen PanLuo Jia - Oral squamous cell carcinoma (OSCC) is a malignant tumor arising from the oral mucosa and is highly prevalent in Southeast Asia and the Pacific region. Recurrence and metastasis significantly contribute to poor clinical outcomes, highlighting the importance of understanding the underlying molecular mechanisms. Circular RNAs (circRNAs), a class of covalently closed non-coding RNAs, have emerged as key regulators of tumor development and progression. However, their roles in OSCC remain largely unexplored. In this study, we identified for the first time that circRHBDD1(4,5) (hsa_circ_0058493, a 656-nt circRNA generated by back-splicing of exons 4 and 5 of the RHBDD1 gene) is markedly upregulated in OSCC and promotes tumor cell proliferation, invasion, and metastasis. Mechanistically, circRHBDD1(4,5) functions as a molecular scaffold that brings IGF2BP2 and DKK1 mRNA into close proximity, thereby facilitating the mA-dependent recognition of DKK1 mRNA by IGF2BP2, which is mediated by WTAP. This interaction enhances DKK1 mRNA stability, leading to increased DKK1 expression and subsequent activation of the PI3K-AKT signaling pathway, thereby driving the malignant progression in OSCC. Collectively, our findings highlight the critical role of the circRHBDD1(4,5)/IGF2BP2/DKK1 axis in OSCC pathogenesis and provide a potential foundation for developing novel targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/09/11
Ren DaixiZhang JiarongHuang MaoWu JieYang MeiLiu YixuanXiang PingjuanQu HongkeWang DanGe JunshangYan QijiaShi LeiXiang BoXiong WeiLi GuiyuanFan ChunmeiZeng Zhaoyang - Cerebral ischemia-reperfusion injury (CIRI) is a leading cause of neurological disability with few effective therapeutic strategies, and ferroptosis has been proven to participate in CIRI progression while its upstream regulatory mechanisms remain poorly defined. Herein, we performed transcriptomic analysis on GSE162072 and GSE58720 datasets, and constructed mouse tMCAO/R and neuronal OGD/R models to recapitulate CIRI. Multiple assays including Longa scoring, TTC staining, H&E staining and Evans blue assay were applied to evaluate neurological function, cerebral infarction, histopathology and blood-brain barrier (BBB) integrity. We also quantified ferroptosis-related markers and detected m6A modification, RNA-protein interaction and mRNA stability via commercial kits, dot blot, MeRIP-qPCR, RIP-qPCR and actinomycin D assays. The results revealed that SLC39A14 was markedly upregulated in CIRI, accompanied by neuronal ferroptosis activation. Knockdown of SLC39A14 alleviated iron overload, lipid peroxidation and ferroptotic neuronal death both in vitro and in vivo. Mechanistically, the m6A reader IGF2BP2 was elevated in CIRI, which directly bound SLC39A14 mRNA to improve its stability and sustain its expression. In vivo AAV-mediated SLC39A14 silencing reduced infarct volume, maintained BBB integrity and relieved neurological deficits. Collectively, IGF2BP2 facilitates CIRI development by driving neuronal ferroptosis through m6A-dependent regulation of SLC39A14 mRNA stability, which may serve as a promising therapeutic target for CIRI. - Source: PubMed
Publication date: 2026/09/09
Wang HainingHan BaichaoXu ChenZhong DiChen Hongping - Acute myeloid leukemia (AML) progression relies on complex crosstalk with the bone marrow microenvironment, particularly M2 macrophage polarization. Exosomes mediate intercellular communication, while N6-methyladenosine (m6A) modifications drive tumor malignancy. However, the role of exosomal m6A regulators in coordinating AML progression and macrophage polarization remains unclear. - Source: PubMed
Publication date: 2026/09/09
Shang ZhenZhou MiYan SijiaSu ShuaiZheng RubingWang YuXiao Yi - - Source: PubMed
Publication date: 2026/09/05
Li TingHu Pei-ShanZuo ZhixiangLin Jin-FeiLi XingyangWu Qi-NianChen Zhan-HongZeng Zhao-LeiWang FengZheng JianChen DemengLi BoKang Tie-BangXie DanLin DongxinJu Huai-QiangXu Rui-Hua