Ask about this productRelated genes to: INPP5B antibody
- Gene:
- INPP5B NIH gene
- Name:
- inositol polyphosphate-5-phosphatase B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-14
- Date modifiied:
- 2016-10-05
Related products to: INPP5B antibody
Related articles to: INPP5B antibody
- Phosphorylated CTD Interacting Factor 1 (PCIF1) is the exclusive methyltransferase responsible for the N6,2-O-dimethyladenosine (m6Am) modification in mammalian mRNA. Our previous research identified PCIF1 as a potent tumor suppressor in glioma, demonstrating its ability to impair cell proliferation, induce G2/M phase arrest, and promote apoptosis. However, its role in glioma cell migration and invasion remains unclear. In this study, we investigate how PCIF1 regulates glioma cell migration and invasion. Overexpression of PCIF1 inhibits migration and invasion, whereas PCIF1 knockdown enhances these behaviors. Corresponding changes are observed in mesenchymal markers (Vimentin, β-catenin, Snail, Slug) and the epithelial marker T-cadherin, indicating that PCIF1 suppresses epithelial-to-mesenchymal transition (EMT)-mediated glioma invasion. Mechanistically, PCIF1 modulates the AKT pathway by promoting proteasomal degradation of AKT while increasing phosphorylated AKT (p-AKT) levels, revealing a complex regulatory mechanism. PCIF1 knockdown upregulates INPP5B, a lipid phosphatase, causing accumulation of PI(3,4)P2 and enhanced AKT activation. Conversely, PCIF1 overexpression increases PI(3,4,5)P3 production, elevating p-AKT levels. This bidirectional regulation suggests that PCIF1 influences phosphoinositide signaling and AKT activation. Our findings highlight PCIF1 as a key modulator of glioblastoma cell migration and invasion through phosphoinositide signaling, positioning it as a potential biomarker and therapeutic target in glioma. - Source: PubMed
Publication date: 2026/05/09
Musunuru Preethi PriyankaLi YihanZhou YuLiu GaiSha ZhuangHu ZhiyuanZhou JunboKonduru NaveenaMeng QingmingGao ShangfengYu Rutong - Migraine (MIG) frequently co-occurs with autoimmune diseases (ADs), but the shared genetic basis underlying this comorbidity remains unclear. - Source: PubMed
Publication date: 2026/05/03
Chen JunWu YameiLiu MeijunFan YihuaCao TianZhao LiangbinLong KunlanWang CixiaoWu LingLv LizeyuLi HaijunChen XingyueZhi LijiaHe YuchiTao Tian - Hepatic steatosis is a hallmark of alcohol-associated liver disease (ALD) and interacts with hepatic inflammation to drive disease progression. NF-κB-inducing kinase (NIK) has been established as a bridge linking inflammation to steatosis in ALD. Intriguingly, while hepatocyte-specific NIK deficiency attenuated ALD in the chronic-plus-binge model, it paradoxically exacerbated the disease under chronic ethanol exposure, suggesting a complex, context-dependent role for NIK. - Source: PubMed
Publication date: 2025/12/12
Zhang WenQi ManzhiZhao XiaojingZhong YingXu WeilongSheng LiangYang Liu - Genome-wide association studies have identified over 300 genomic loci associated with coronary artery disease (CAD) risk, but identifying functional variants remains challenging due to linkage disequilibrium. Here we show a comprehensive functional characterization of CAD-associated variants in primary vascular smooth muscle cells (SMCs). We performed lentivirus-based massively parallel reporter assays (lentiMPRAs) on 25,892 CAD-associated variants, testing their allele-specific enhancer activity in quiescent and proliferative SMCs. We identified 122 candidate variants with enhancer activity and allelic imbalance, including 23 variants showing condition-biased and 41 showing sex-biased effects. Integrating lentiMPRA with CUT&RUN epigenome profiling and expression quantitative trait loci data, we prioritized 49 functionally relevant variants. CRISPRi experiments on eight variants confirmed their regulatory effects on nine variant-gene pairs: rs35976034 (MAP1S), rs4888409 (CFDP1), rs73193808 (MAP3K7CL), rs67631072 (INPP5B/FHL3), rs1651285 (SNHG18), rs17293632 (SMAD3), rs2238792 (ARVCF) and rs4627080 (NRIP3). Our results fine-map the causal variants that confer CAD risk through their effects on vascular SMCs. - Source: PubMed
Publication date: 2025/10/07
Barbera NicolasLei LilyWallace AlexiaErin FarukPerry R Noahden Ruijter Hester MCivelek Mete - To elucidate the role of miRNAs in porcine muscle tissues, this study used Solexa high-throughput sequencing to identify and compare differentially expressed miRNAs in Landrace pigs and the Diannan small ear pigs. - Source: PubMed
Publication date: 2025/07/23
Xie YuxiaoCheng WenjieHao MeilinYi Lan-LanZhu Jun-HongZhao Yan-GuangZhao Sumei