HNRNPH1 (Heterogeneous Nuclear Ribonucleoprotein H1)

Moreover, combined treatment with a 5'tiRNAGly-GCC inhibitor and doxorubicin hydrochloride significantly suppresses ATC progression in vivo. Thus, decreased DNMT2 expression facilitates ATC development by promoting the production of 5'tiRNAGly-GCC. Our findings also highlight the considerable therapeutic potential of targeting 5'tiRNAGly-GCC in the treatment of ATC.

Furthermore, the myelin-enhancing drug benztropine rescues myelination, restores myelin-related gene expression, and ameliorates cognitive deficits, highlighting the role of hnRNPH2 P213L-induced myelin abnormalities in the pathogenesis of ID. Mechanistically, the P213L mutation disrupts the interaction between hnRNPH2 and its target transcripts, leading to the downregulation of myelination-related genes. Collectively, these findings reveal a critical mechanistic connection between myelin dysfunction and ID, thereby offering potential therapeutic insights for X-linked neurodevelopmental disorders.

These findings provide the first insight into the role of hnRNPH1/H2 as critical drivers of melanoma immunogenicity and suggest their potential as novel therapeutic targets for enhancing melanoma treatment outcomes. This study underscores the impact of post-transcriptional regulation on the immune environment in melanoma and in cancer in general.

In APL, the PML/RARα fusion protein inhibited PU.1-dependent transactivation of lnc-SPI1U by hijacking the SE region that overlapped with lnc-SPI1U locus. Our study provides mechanistic insight into how SE-lncRNAs contribute to the precise regulation of transcription factor activity during myeloid differentiation.

This was the first study to evaluate the performance of whole RNA-seq in fusion detection in patients with acute leukemia in Korea. Incorporating RNA-seq into diagnostic workflows may facilitate earlier and more precise therapeutic decisions and improve prognostic assessment in patients with acute leukemia.

Depletion of HNRNPH1 alters the expression of specific protein-coding EIF4G1 transcript variants. HNRNPH1 mediates the inclusion of an AURKA 5'UTR exon that enhances protein expression.

Additionally, this review summarizes the current therapeutic strategies targeting hnRNPH1, discusses the associated challenges, outlines optimization approaches, and considers future research directions. Overall, this review aims to deepen our understanding of hnRNPH1 biology and inspire the development of novel diagnostic and therapeutic interventions.

We verified the key role of HSP90AB1, HNRNPH1, and MAP1LC3B in LUAD, and revealed a possible regulatory mechanism, namely, HNRNPH1 could inhibit the development of LUAD by promoting autophagy through the HSP90AB1/MAP1LC3B axis. These findings may offer new insights for improving the treatment and prognosis of LUAD.

However, that immunosuppression may be tempered by AhR control of MHC expression. Given the multiple roles of JAK/STAT signaling in the immune system, the results also suggest multiple levels on which the AhR may affect tumor immunity.

In our review, Only 1 adult case of AML has been reported so far. To summarize the 5 cases in the studies, the HNRNPH1::ERG positive AML cases had a significantly higher blast cell counts and more frequently companied with rare gene mutations, which characterized poorer prognosis and lower remission in adult HNRNPH1::ERG positive AML.

Additionally, PDO and CDX models indicated that tilfrinib, an inhibitor targeting PTK6, could inhibit CRC growth. Overall, our findings reveal the novel PTK6-HNRNPH1-NBR1 regulatory autophagy axis and provide a potential therapy target for CRC.

The CSF3/CSF3R pathway may contribute to immunosuppression in GC by upregulating LILRB2 and its ligands, with heterogeneous nuclear ribonucleoprotein H1 playing a regulatory role.