HNRPLL Blocking Peptide
- Known as:
- HNRPLL Blocking Peptide
- Catalog number:
- 33r-8037
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- HNRPLL Blocking Peptide
Related genes to: HNRPLL Blocking Peptide
- Gene:
- HNRNPLL NIH gene
- Name:
- heterogeneous nuclear ribonucleoprotein L like
- Previous symbol:
- HNRPLL
- Synonyms:
- -
- Chromosome:
- 2p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-30
- Date modifiied:
- 2016-10-05
Related products to: HNRPLL Blocking Peptide
Related articles to: HNRPLL Blocking Peptide
- : Heterogeneous nuclear ribonucleoprotein L-like (HNRNPLL) is an RNA-binding protein involved in alternative splicing and immune regulation; however, its role in liver hepatocellular carcinoma (LIHC) remains unclear. : We performed integrative multi-omics analyses using data from TCGA, GEO, and the Human Protein Atlas to evaluate the expression patterns, prognostic value, and potential biological functions of HNRNPLL. Functional enrichment and immune-related analyses were conducted to explore associated pathways. Experimental validation was performed in LIHC cell lines using Western blotting, RT-qPCR, CCK-8, colony formation, and Transwell assays, along with a xenograft mouse model. : HNRNPLL was significantly upregulated in LIHC at both transcriptomic and proteomic levels and was associated with advanced clinicopathological features and poor overall survival. Multivariate Cox regression analysis identified HNRNPLL as an independent prognostic factor. Enrichment analyses suggested that HNRNPLL-related genes are mainly involved in cell cycle regulation, mitotic progression, epithelial-mesenchymal transition, and immune-related pathways. In addition, HNRNPLL expression was correlated with immune cell infiltration, tumor mutational burden, microsatellite instability, ferroptosis-related genes, and m6A methylation regulators. Functional experiments demonstrated that HNRNPLL knockdown suppressed proliferation, migration, and invasion of liver cancer cells and inhibited tumor growth in vivo. : These findings suggest that HNRNPLL may act as a potential regulator of LIHC progression and is associated with tumor-related biological processes and immune features. HNRNPLL may serve as a candidate biomarker for prognosis and a potential therapeutic target in LIHC, although further mechanistic studies are required. - Source: PubMed
Publication date: 2026/03/31
Wang XiaojingLi BinLi KunWan DanLiu Nanbin - The transcription factor IKAROS, encoded by IKZF1, is crucial for lymphocyte development and differentiation. Germline heterozygous IKZF1 mutations cause B cell immunodeficiency, but also affect T cells. Patients with IKZF1 haploinsufficiency (HI) or dimerization-defective (DD) variants show reduced naive and increased memory T cells, while dominant-negative (DN) mutations result in the opposite phenotype. Gain-of-function patients display variable patterns. To investigate IKAROS's role in shaping the human naive/memory T cell phenotype, we performed IKAROS immunomodulation and knockdown experiments and analyzed early T cell development in an artificial thymic organoid (ATO) system using CD34+ cells from patients with representative IKZF1 variants. IKAROS inhibition by lenalidomide or silencing by small hairpin RNA directly altered expression of HNRNPLL, the master regulator of CD45 isoform splicing that defines CD45RA+/naive and CD45RO+/memory phenotypes. In the ATO system, IKAROS-DN precursor cells were blocked at the CD4-CD8-/double-negative stage and retained a CD45RA+ phenotype, whereas IKAROS-HI cells inefficiently reached the CD4+CD8+/double-positive stage and partially transitioned from CD45RA to CD45RO. Analysis of public gene expression data showed high HNRNPLL expression in double-positive thymic cells, beyond the stages affected by IKZF1 DN and HI mutations. Collectively, these findings indicate that IKAROS regulates early and late T cell development by mechanisms, including HNRNPLL modulation. - Source: PubMed
Publication date: 2025/12/22
Stoddard JenniferKuehn Hye SunTagirasa RavichandraBosticardo MaritaPala FrancescaNiemela Julie EGil Silva Agustin AAmini KaylaAnaya EduardoFramil Seoane MarioBouso CarolinaDimitrova DimanaKanakry Jennifer AAlsina LaiaOleastro MatiasHolland Steven MFleisher Thomas AWasserman Richard LNotarangelo Luigi DRosenzweig Sergio D - The programmed cell death 1 (PD-1) is an immune checkpoint that mediates immune evasion of tumors. Alternative splicing (AS) such as intron retention (IR) plays a crucial role in the immune-related gene processing and its function. However, it is not clear whether encoding PD-1 exists as an IR splicing isoform and what underlying function of such isoform plays in tumor evasion. - Source: PubMed
Publication date: 2025/03/06
Zang HaojingLiu TongfengWang XiaodongCheng ShuwenZhu XiaofengHuang ChangDuan LiqiangZhao XujieGuo FangWang XuetongZhang ChangYang FacaiGu YinminHu HongboGao Shan - Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer known for its high rate of early metastasis, necessitating the discovery of the underlying mechanisms. Herein, we report that heterogeneous nuclear ribonucleoprotein L-like (hnRNPLL) expression significantly increases at the invasion forefront in PDAC and is associated with early metastasis and poor prognosis. Our findings revealed that hnRNPLL knockdown resulted in extensive exon skipping (ES) events. In particular, we identified myoferlin (MYOF), a member of the ferlin family involved in membrane processes, as a functional splicing target of hnRNPLL. hnRNPLL depletion stimulates MYOF exon 17 retention to reduce the short isoform of MYOF (MYOFb) and inhibit metastasis. In contrast, hnRNPLL or MYOFb overexpression promoted pancreatic cancer cell migration and invasion. These results suggest that hnRNPLL is a critical factor for early PDAC metastasis. hnRNPLL and MYOFb may be potential therapeutic targets for PDAC. - Source: PubMed
Publication date: 2024/12/30
Chen XianghanGong RuiningWang LiliLei KeLiu XiaolanWang JigangSun MingyueSaluja Ashok KumarYu QianRen He - Alternative splicing contributes to complex traits, but whether this differs in trait-relevant cell types across diverse genetic ancestries is unclear. Here we describe cell-type-specific, sex-biased and ancestry-biased alternative splicing in ~1 M peripheral blood mononuclear cells from 474 healthy donors from the Asian Immune Diversity Atlas. We identify widespread sex-biased and ancestry-biased differential splicing, most of which is cell-type-specific. We identify 11,577 independent cis-splicing quantitative trait loci (sQTLs), 607 trans-sGenes and 107 dynamic sQTLs. Colocalization between cis-eQTLs and trans-sQTLs revealed a cell-type-specific regulatory relationship between HNRNPLL and PTPRC. We observed an enrichment of cis-sQTL effects in autoimmune and inflammatory disease heritability. Specifically, we functionally validated an Asian-specific sQTL disrupting the 5' splice site of TCHP exon 4 that putatively modulates the risk of Graves' disease in East Asian populations. Our work highlights the impact of ancestral diversity on splicing and provides a roadmap to dissect its role in complex diseases at single-cell resolution. - Source: PubMed
Publication date: 2024/12/03
Tian ChiZhang YuntianTong YihanKock Kian HongSim Donald YuhuiLiu FeiDong JiaqiJing ZhixuanWang WenjingGao JunbinTan Le MinHan Kyung YeonTomofuji YoshihikoNakano MasahiroBuyamin Eliora ViolainSonthalia RadhikaAndo YoshinariHatano HiroakiSonehara Kyuto Jin XinLoh MarieChambers JohnHon Chung-ChauChoi MurimPark Jong-EunIshigaki KazuyoshiOkamura TomohisaFujio KeishiOkada YukinoriPark Woong-YangShin Jay WRoca XavierPrabhakar ShyamLiu Boxiang