HNRPUL1 Blocking Peptide
- Known as:
- HNRPUL1 Blocking Peptide
- Catalog number:
- 33r-5262
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- HNRPUL1 Blocking Peptide
Related genes to: HNRPUL1 Blocking Peptide
- Gene:
- HNRNPUL1 NIH gene
- Name:
- heterogeneous nuclear ribonucleoprotein U like 1
- Previous symbol:
- HNRPUL1
- Synonyms:
- E1B-AP5, E1BAP5, FLJ12944
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-11
- Date modifiied:
- 2016-04-26
Related products to: HNRPUL1 Blocking Peptide
Related articles to: HNRPUL1 Blocking Peptide
- hnRNPUL1 is a nuclear RNA-binding protein involved in both pre-mRNA splicing and DNA double-strand break repair. Using AlphaFold, we show that hnRNPUL1 has a central folded region consisting of tightly juxtaposed SPRY and dead polynucleotide kinase (dPNK) domains flanked by intrinsically disordered regions (IDRs). The dPNK domain binds both nucleotides and RNA. Remarkably, polynucleotide kinase activity can be reactivated with a single amino acid substitution. Mutations altering nucleotide binding also change the ability of the entire protein to bind RNA and regulate homotypic versus heterotypic protein interactions driven by the IDRs. A mutation that prevents nucleotide binding also destabilizes the protein. In a small number of amyotrophic lateral sclerosis patients, we identify rare coding variants in the gene, which alter the ability of hnRNPUL1 to bind nucleotides, RNAs, and FUS. Together, these data establish that hnRNPUL1 utilizes its dPNK domain to regulate interactions with itself, RNA, and other proteins. - Source: PubMed
Publication date: 2026/03/14
Apostol Carmen VLi AngDaniels PeterGriffith LlywelynCooper-Knock JohnathanAguilar-Martinez ElisaYonchev Ivaylo DWhelan Ashleigh G RShaw Pamela JSudbery Ian MWilson Stuart A - Hemoglobinopathies are the most common monogenic genetic disorders, primarily managed through blood transfusions or bone marrow transplantation. Clinical severity other than mutational effect not well investigated and still unknown. This study aims to identify dysregulated molecular pathways in red blood cells contributing to thalassemia severity. From a cohort of 285 hemoglobinopathy patients, 10 age-matched individuals with identical compound heterozygous mutations (IVS 1-5 G>C and CD 26 G>A) were screened. Five had severe thalassemia requiring regular transfusions, while five had a non-severe form requiring fewer transfusions. RNA sequencing and proteome analysis were conducted on isolated RBCs, through Novaseq and Orbitrap MS platform respectively. Bioconductor-R and different bioinformatics tools were utilized subsequently. Integrated transcriptome-proteome analysis revealed a global loss of mRNA-protein concordance. CDK11A and MCTS1 lost positive correlation, whereas RLP38 and H3C1 showed compensatory overtranslation, linked to transcription factors regulating erythropoiesis. In TDT, WNK3, HNRNPUL1, COPS7A, and HTATSF1 displayed discordant expression, indicating post-transcriptional aberrations. PTR analysis showed reduced cytoskeletal (ankyrin, spectrin) expression, elevated chaperone activity, ferroptosis markers (FTH1, FTL, HMOX1), and suppressed autophagy. Collectively, these multilayered alterations-splicing dysfunction, post-transcriptional deregulation, ferroptosis, autophagy suppression, oxidative stress, and cytoskeletal fragility-underlie the greater disease severity observed in TDT compared with NTDT. - Source: PubMed
Publication date: 2026/01/30
Mitra NibeditaBhattacharyya UpasanaChowdhury Prosanto KumarPal ArijitKorwar ArvindBhattacharjee SamsidhhiBasu Anupam - MEF2D gene related fusions, define a unique B-cell precursor acute lymphoblastic leukemia (BCP-ALL) with poor prognosis. In this study, we performed single-cell RNA sequencing (scRNA-seq) on three MEF2D fusion cases and collected transcriptomic data of 81 BCP-ALL cases with MEF2D fusions from public datasets. By comparing scRNA-seq profiles with those of normal bone marrow cells and other BCP-ALL subtypes, we identified a characteristic pre-B cell developmental arrest specific to the MEF2D subtype. Single-cell analyses indicated a pronounced reduction of major histocompatibility complex (MHC) expression, suggesting a potential mechanism of immune evasion, which could be further corroborated by cell-cell communication analysis. Bulk RNA-seq data verified the downregulation of MHC molecules in MEF2D subtype, which was consistent with the downregulation of CIITA, the transactivator of MHC molecules. Knockdown of the MEF2D-HNRNPUL1 fusion in the Kasumi-7 cell line led to the upregulation of MHC molecules. ChIP-seq data of the Kasumi-7 cell line showed that the MEF2D::HNRNPUL1 fusion protein directly bound to the region next to an intronic enhancer sequence of CIITA, indicating a MEF2D-CIITA-MHC potential pathogenic mechanism. This study offers a comprehensive analysis of MEF2D-fusion cases, detailing the fusion features and functional alterations, thus providing insights for future investigations. - Source: PubMed
Publication date: 2026/01/12
Zhang WeinaLiu YongjingXiao XinhuaZheng QingqingXie YaliLi JinpingZeng TaoWang YuliangJiang HuaHuang Jinyan - B-cell acute lymphoblastic leukemia harboring MEF2D-translocations represents an aggressive subtype with poor prognosis. MEF2D fusion proteins drive leukemogenesis super enhancer mediated transcriptional dysregulation, making them promising target for epigenetic intervention. BET proteins, especially BRD4, are key regulators of oncogenic enhancer activity. Here, we explored the potential of BET protein inhibition as a targeted therapeutic strategy in MEF2D-HNRNPUL1 translocated B-ALL. Our study revealed that BET inhibitor inhibited proliferation and triggered apoptosis in leukemic cells, by targeting pre-BCR genes in addition to previously demonstrated targets, c-myc and IL-7R. A novel finding is that BET inhibitor induces DNA damage by downregulating DNA repair genes. These findings highlight that anti-leukemic activity of BET inhibitors offers a promising strategy to improve outcomes in this high-risk leukemia subtype. - Source: PubMed
Publication date: 2026/01/16
Chauhan AditiSingh KulwantChaturvedi Chandra PrakashRai Ambak Kumar - High-grade serous ovarian carcinoma (HGSOC) accounts for 70% of all ovarian cancer cases and 80% of related deaths. TP53 mutations are common; however, other driving genetic factors are not well understood. In this study, we used RNA sequencing to explore the genetic background of HGSOC in patients with unclear profiles. - Source: PubMed
Publication date: 2025/09/29
Masago KatsuhiroSasaki EiichiFujita YasukoFujita ShiroHorio YoshitsuguKuroda HiroakiOgasawara AikoTatsuno KenjiAburatani HiroyukiOda KatsutoshiHasegawa KoseiMatsushita Hirokazu