Ask about this productRelated genes to: HNRPH1 antibody
- Gene:
- HNRNPH1 NIH gene
- Name:
- heterogeneous nuclear ribonucleoprotein H1
- Previous symbol:
- HNRPH1
- Synonyms:
- hnRNPH
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2017-01-12
Related products to: HNRPH1 antibody
Related articles to: HNRPH1 antibody
- Mutations in cause an X-linked disorder characterized by developmental delay, intellectual disability, motor and gait disturbances, and seizures. Murine models that reproduce key clinical features of -related neurodevelopmental disorder suggest that it may result from a toxic gain of function of the mutant protein or a complex loss of normal HNRNPH2 function with impaired compensation by its paralog, HNRNPH1. In this study, we tested gapmer antisense oligonucleotides (ASOs) that target murine in a non-allele-specific manner. The lead ASO reduced messenger RNA (mRNA) and protein expression while inducing compensatory up-regulation of expression in both wild-type and mutant mouse brains. A single intracerebroventricular injection of the ASO into neonatal mutant mice rescued molecular and audiogenic seizure phenotypes and improved certain motor and cognitive phenotypes. ASO treatment at the juvenile stage also rescued audiogenic seizures. In contrast, ASO administration did not alter survival, body weight, or the incidence of hydrocephalus. In human induced pluripotent stem cell-derived neurons, a human-specific research ASO reduced mRNA and up-regulated mRNA. Mechanistically, we found that expression is regulated by alternative splicing and that HNRNPH2 modulates this process. These findings provide a preclinical proof of concept for ASO therapy and offer insights into its underlying molecular mechanism. - Source: PubMed
Publication date: 2026/04/22
Korff AneYang XiaojingOzdemir OzanSamanta AnanyaWang Yong-DongPatni TusharLavado Alfonso JKavirayani Anoop MurthyOchaba JosephPowers BeritBennett C FrankKim Hong JooTaylor J Paul - Coexisting myocardial infarction (MI) and type 2 diabetes mellitus (T2DM) is a common condition. We aimed to investigate the association between MI and type 2 diabetes (T2D) with mitophagy-related differentially expressed genes (MRDEGs) and the impact thereof on disease progression. - Source: PubMed
Publication date: 2026/04/08
Yang YingWan FeiyanXu XuelianXu WeiJiang LingliPan Pei - Although glioblastoma (GBM) harbors multiple genetic abnormalities leading to cell cycle deregulation, a functional mitotic checkpoint is essential to prevent mitotic catastrophe and tumor cell death. Here, we identify the RNA-binding protein HNRNPH1 as a key post-transcriptional modulator of G2/M checkpoint-associated genes in GBM. HNRNPH1 is overexpressed in malignant cells, especially in the neural- and oligodendrocyte-progenitor-like state, and its expression levels are higher in non-hypoxic regions of the tumor. Knocking out HNRNPH1 causes aberrant splicing and downregulation of several genes involved in cell division. These molecular alterations are associated with G2/M cell cycle arrest, reduced cell proliferation, abnormal cell morphology, and increased nuclear fragmentation. Silencing HNRNPH1 in vivo inhibits the tumor growth of patient-derived GBM cell-originated intracranial xenografts and has significant survival benefits. Together, our results show the critical importance of HNRNPH1 in cell cycle progression and tumor growth, potentially impacting the development of novel strategies to treat GBM. - Source: PubMed
Publication date: 2026/03/24
Villa Genaro RAlimonti PaoloToker Joseph SPiranlioglu RaziyeKarkoski Mikayla AMazzetti DeboraBen Mrid RedaEl Guendouzi SaraLauinger AlexaChiocca Andrew NEl Fatimy RachidChiocca E AntonioMineo Marco - Complex tRNA methylation modifications collectively maintain the structural integrity and functional efficiency of tRNA. DNA methyltransferase 2 (DNMT2) regulates the m5C methylation status of tRNA, thereby reprogramming its structure and influencing cancer progression. However, the precise mechanisms through which DNMT2 affects tumor development via tRNA methylation remain insufficiently understood. In this study, we demonstrate that reduced DNMT2 expression promotes the progression of anaplastic thyroid carcinoma (ATC). Specifically, in ATC, DNMT2 catalyzes m5C38 methylation on three tRNAs: tRNA-Asp-GUC, tRNA-Gly-GCC, and tRNA-Val-AAC. Loss of DNMT2 leads to an increased abundance of 5'tiRNA, generated by ANG-mediated cleavage of m5C38-hypomethylated tRNA-Gly-GCC. This 5'tiRNA directly binds to hnRNPH1, resulting in a reduction of its protein levels. Moreover, combined treatment with a 5'tiRNA inhibitor and doxorubicin hydrochloride significantly suppresses ATC progression in vivo. Thus, decreased DNMT2 expression facilitates ATC development by promoting the production of 5'tiRNA. Our findings also highlight the considerable therapeutic potential of targeting 5'tiRNA in the treatment of ATC. - Source: PubMed
Publication date: 2026/02/21
Zhou RuixinLi BaizhaoCao MingyuWu ZhijingXia FadaLi Xinying - The progression of spermatogenesis is under dynamic transcriptional regulation. As a subunit of the transcription-export complex 2 (TREX-2), PCI domain-containing protein 2 (PCID2), participates in RNA processing. However, the physiological functions of PCID2 in spermatogenesis remain poorly understood. Here, we generate germline conditional knockout (Pcid2-SKO) mice using Stra8-Cre, and it is found that Pcid2-SKO mice are infertile, exhibit extensive germ cell apoptosis, impaired spermatogonial differentiation, and failure of meiosis initiation. Single-cell transcriptome analysis reveals developmental arrest at the transition from type A to type B spermatogonia in Pcid2-SKO mice. Gene Set Enrichment Analysis (GSEA) demonstrates a significant decrease in the enrichment of mRNA splicing pathway in Pcid2-SKO germ cells. IP-MS results indicate candidate proteins interacting with PCID2 are significantly enriched in RNA splicing pathway. Co-IP results indicate that PCID2 interacts with SNRPG, hnRNPH1 and SF3B1 to modulate alternative splicing in germ cells. Combining RNA sequencing and PCR identifies four key genes (Prpf3, Nek3, Dvl2, and Slc30a9) as splicing targets of PCID2. Collectively, PCID2 is essential for normal spermatogenesis and male fertility by regulating the alternative splicing (AS) of genes critical for cell cycle progression, spliceosome assembly, and mitochondrial homeostasis. This study provides novel insights into the molecular mechanisms underlying spermatogenesis and highlights the importance of AS in germ cell development. - Source: PubMed
Publication date: 2026/01/13
Zhu FeiyinZhang YingXi YuGong ChenjiaTang YanlinChen YidongYan LiyingQiao JieLiu Qiang