Ask about this productRelated genes to: HIST1H1E Blocking Peptide
- Gene:
- HIST1H1E NIH gene
- Name:
- histone cluster 1 H1 family member e
- Previous symbol:
- H1F4
- Synonyms:
- H1.4, H1e, H1s-4
- Chromosome:
- 6p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-31
- Date modifiied:
- 2016-10-05
Related products to: HIST1H1E Blocking Peptide
Related articles to: HIST1H1E Blocking Peptide
- Triple-positive diffuse large B-cell lymphoma (TP-DLBCL), co-expressing CD10, BCL6 and MUM1, represents a rare subset with potential associations with IRF4 rearrangements. This study investigated the clinicopathological spectrum and frequency of IRF4 rearrangements in TP-DLBCL and characterised large B-cell lymphoma with IRF4 rearrangement (LBCL-IRF4-R) in a Korean population. - Source: PubMed
Publication date: 2026/05/06
Na SeiLee Ki RimJeon Yoon KyungKim HyungjinLee Jeong-OkLee Ji YunKim Sang-AYun HongseokPaik Jin Ho - Mouse mammary epithelial cells possess a remarkable ability to regenerate the entire mammary gland through precisely regulated differentiation, involving complex molecular, morphological, and functional changes. Here, we performed comprehensive transcriptomic profiling of HC11 mouse mammary epithelial cells undergoing lactogenic differentiation using RNA sequencing and integrative bioinformatics. We identified 566 differentially expressed genes, reflecting extensive transcriptional reprogramming and activation of biosynthetic, metabolic, and secretory programs. Strong up-regulation of terminal and lactogenic differentiation markers, including Wap, Csn2, Lpl, Cd36, Lalba, Btn1a1, Xdh, Gata3, and Cebpb, signified maturation into a secretory phenotype. Functional evaluation via gene set enrichment analysis revealed transcriptional enrichment of mTOR, prolactin, insulin, ErbB, and autophagy-associated pathways, consistent with anabolic readiness and terminal differentiation. Conversely, p53, Wnt, and FoxO pathways were down-regulated, marking a transition from proliferation to differentiation. Transcription factors (FoxO1, Zbtb16, and Srebf1) and epigenetic regulators (Gadd45a and Hist1h1e) exhibited dynamic changes, underscoring coordinated transcriptional and chromatin remodeling. Gene set enrichment and protein-protein interaction analyses identified 10 hub genes, Agt, Ccnd1, Igf1, Mki67, Myc, Calm4, Rasgrp1, Cd69, Il6, and Pecam1, as central drivers of differentiation. Clustering of uniquely regulated genes further implicated roles in milk synthesis, protease activity, and lineage stabilization. Together, these findings define a transcriptional framework for lactogenic differentiation in the HC11 cell line model and provide a basis for future mechanistic studies. - Source: PubMed
Publication date: 2026/05/04
Ahmad WaqarPanicker Neena GopinathanRizvi Tahir AMustafa Farah - Oxidative stress correlates with the development and prognosis of lung adenocarcinoma (LUAD). This study, on the basis of oxidative stress-related genes (OSRGs), commences to identify molecular subtypes and develop prognostic model for LUAD. - Source: PubMed
Publication date: 2026/03/19
Zhang WeiranZhao XiaojiangWang YuhangLi Xin - Rahman syndrome (HIST1H1E-related neurodevelopmental syndrome, OMIM #617537) is a rare autosomal-dominant condition caused by truncating variants in the C-terminal domain of the HIST1H1E gene. It is characterized by macrocephaly, hypotonia, craniofacial anomalies, and multisystem anomalies. Although multisystem involvement has been increasingly described, respiratory manifestations remain sparsely documented. We report a female infant with mosaic HIST1H1E truncation (c.435dupC; p.Thr146Hisfs*50) who presented with severe mixed sleep apnea secondary to laryngomalacia, requiring two airway surgeries and multidisciplinary management. Despite surgical intervention, polysomnography demonstrated persistent mixed apneas, suggesting both structural and central components. Brain MRI revealed nonspecific ischemic changes that could contribute to the neurological phenotype. To contextualize this observation, we reviewed 70 published cases of Rahman syndrome. Respiratory involvement was reported in only 13.5% (neonatal respiratory distress), 2.8% (upper-airway anomalies), and 1.4% (sleep-disordered breathing), frequencies comparable to those in the general population, although most reports lacked systematic respiratory evaluation. These findings suggest that respiratory morbidity may be under-evaluated rather than absent in Rahman syndrome. The combination of hypotonia, craniofacial restriction, and possible brain-stem dysregulation provides a plausible pathophysiologic substrate for both central and obstructive apnea. We recommend considering airway assessment and polysomnography in affected individuals presenting with stridor, desaturations, or sleep-related breathing difficulties. This case further expands the phenotypic spectrum of HIST1H1E-related disorders and represents the first documented example of mosaicism associated with this condition. - Source: PubMed
Publication date: 2025/12/08
Barakat NadaChampagne MarjolaineBergeron MathieuDodin PhilippeRoumeliotis Nadia - HIST1H1E Syndrome is a rare autosomal dominant disorder resulting from a heterozygous variation in the H1-4 gene located on chromosome 6p22.2. Mental retardation, recognizable facial features, skeletal abnormalities and overgrowth are the main clinical manifestations of this syndrome. A 17-year-old male presented to the pediatric endocrinology clinic due to short stature. He had a characteristic facial appearance with neurodevelopmental delay. Genetic analysis revealed a heterozygous pathogenic variation in the H1-4 gene located on chromosome 6p22.2 which confirmed his diagnosis of HIST1H1E syndrome. In our case, distinguished by the co-occurrence of short stature and obesity accompanying central hypothyroidism and growth hormone (GH) deficiency due to hipoplastic pituitary gland, which differs from the somatic overgrowth characterizing this syndrome.These is the second reported HIST1H1E syndrome case with hyposecretion of multiple pituitary hormones caused by hypoplasia in the pituitary gland. - Source: PubMed
Publication date: 2025/05/30
Altun İlaydaBayramoğlu ElvanKarakaş HasanVelioğlu Haşlak GökçeUçar MertTuran HandeEvliyaoğlu Olcay