HIST1H1E Pre-design Chimera RNAi
- Known as:
- HIST1H1E Pre-design Chimera RNAi
- Catalog number:
- H00003008-R01
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- HIST1H1E Pre-design Chimera RNAi
Related genes to: HIST1H1E Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: HIST1H1E Pre-design Chimera RNAi
- Circulating tumor DNA (ctDNA) analysis enables real‑time assessment of the tumor burden and genomic complexity in lymphomas. However, real‑world evidence across lymphoma subtypes is limited. - Source: PubMed
Publication date: 2026/08/19
Kim Jin JuKim Yu RiKim HongkyungKook Hye WonChung HaerimHwang Doh YuJang Ji EunCheong June-WonLee Seung-TaeChoi Jong RakShin SaeamKim Jin Seok - HIST1H1E syndrome is caused by frameshift variants in the gene; while strabismus and refractive errors have been previously reported, this is the first case describing optic and cerebellar atrophy in an affected individual to our knowledge. - Source: PubMed
Publication date: 2026/06/03
Lai Zinnia Sen YenO'Neil NicolaSiebert EzannColley StephenPanegyres Peter K - 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