Ask about this productRelated genes to: ZNF254 antibody
- Gene:
- ZNF254 NIH gene
- Name:
- zinc finger protein 254
- Previous symbol:
- ZNF91L, ZNF539
- Synonyms:
- HD-ZNF1, BMZF-5
- Chromosome:
- 19p13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-28
- Date modifiied:
- 2014-11-18
Related products to: ZNF254 antibody
Related articles to: ZNF254 antibody
- Defining correlates of HIV rebound upon antiretroviral therapy (ART) interruption can advance HIV cure research. In this issue of Immunity, Ma et al. analyze immunophenotypes and transcriptomes from multiple clinical trials, linking T and NK cell subsets to delayed rebound and identifying DDIT4 and ZNF254 as HIV silencing factors. The antidiabetic drug metformin induces DDIT4 and silences HIV in vitro. - Source: PubMed
Lujan Ramon ABoritz Eli A - Focal cortical dysplasia (FCD) is a major cause of drug-resistant epilepsy and displays substantial clinical and histopathological heterogeneity, yet the cellular and molecular bases underlying this diversity remain poorly defined. Here, we performed single-nucleus RNA sequencing of 487,286 nuclei from 34 paired lesional cores and perilesional cortices across FCD I-III, generating a cell-type-resolved transcriptomic atlas of human FCD. Comparative analyses identified both shared and subtype-specific transcriptional alterations across neuronal, glial, and vascular compartments. Inhibitory interneurons and deep-layer projection neurons exhibited prominent dysregulation, whereas astrocytes and vascular cells showed coordinated activation of inflammatory, metabolic, and hypoxia-responsive pathways. Several genes displayed consistent subtype-associated expression patterns, including , , and in astrocytes, and in endothelial cells. These results link cell-type-specific transcriptional programs to histopathological heterogeneity across FCD subtypes, identify candidate tissue-detectable markers, and provide insight into nonneuronal contributions to epileptogenic cortical malformations. - Source: PubMed
Publication date: 2026/04/21
Fang ChuantaoLiu YiZhang XiaodanWang ZiwuGuo RongliangGuo JingjingLiu XianmingTan YanfengLu Hao-JieZhao RuiMeng GuilinQi Dashi - Gliomas comprise a heterogeneous group of central nervous system tumors in which gene fusions (GFs) are significant oncogenic drivers and emerging diagnostic and therapeutic biomarkers. In cancer diagnosis, GF detection largely relies on targeted short-read sequencing fusion panels, such as the Children's Hospital of Philadelphia (CHOP) Fusion Panel (FUSIP). While these panels are effective for detecting recurrent, well-characterized GFs, they are limited to predefined gene sets and cannot identify full-length transcripts. Here, we analyzed 49 high- and low-grade gliomas previously classified as fusion-negative by FUSIP using an untargeted whole-transcriptome RNA sequencing approach with Oxford Nanopore Technologies (ONT) long-read sequencing. This enabled transcriptome-wide fusion discovery of additional known and potentially novel oncogenic GFs beyond panel constraints. Long-read sequencing further allowed direct resolution of full-length fusion transcripts and their associated isoform structures. By integrating GF detection with isoform-level transcript analysis, we identified fusion-associated transcript isoforms with alternative splicing patterns that aligned near reported GF breakpoints, including :: and ::, which have not been reported in literature or existing fusion databases. To assess functional relevance, candidate GFs were evaluated using the model, with ventral nerve cord (VNC) morphology serving as a quantitative readout of fusion-induced disruption of glial regulation. VNC enlargement or elongation reflects abnormal glial growth or defects in brain tissue organization. Of the 15 candidate GFs subjected to experimental functional testing, 8 induced significant VNC abnormalities relative to wild-type controls, indicating fusion-specific disruption and oncogenic potential. Notably, :: and :: produced the most pronounced VNC phenotypes. Together, these findings demonstrate that untargeted transcriptome-wide GF discovery, coupled with long-read isoform-level analysis and functional validation, enables the identification and prioritization of potentially novel and clinically relevant GFs that are missed by standard targeted short-read fusion panels in glioma. - Source: PubMed
Publication date: 2026/03/17
Rybacki KarleenaCha Emily Na YoungDeutsch Hannah MGaudet EloiseAhsan Mian UmairXu FengChan JoeLi MarilynSong YuanquanWang Kai - Immunological mechanisms regulating HIV rebound after antiretroviral therapy (ART) interruption remain unclear. We examined relationships between host factors, HIV reservoir, and HIV time-to-rebound after analytical treatment interruption (ATI) by characterizing pre-ATI peripheral blood mononuclear cells (PBMCs) from 75 ART-suppressed people with HIV (PWH) using high-parameter methods. Across interventional (CLEAR, TEACH, and REDUC) and non-interventional (A5345) cohorts, delayed rebound was not associated with intact HIV. Cohort-specific immune effectors were associated with delayed rebound. RNA sequencing of CD4 T cells from A5345 revealed that the mTOR inhibitor DDIT4 and zinc finger protein ZNF254 were associated with delayed rebound. In vitro and in vivo studies demonstrated that DDIT4 and ZNF254 suppressed HIV expression. Metformin induced DDIT4 and suppressed HIV expression in primary cells and cells from ART-suppressed PWH, suggesting that this affordable diabetes drug could be repurposed to silence HIV. Our results support the pursuit of both immune- and HIV-silencing strategies to achieve ART-free HIV remission. - Source: PubMed
Publication date: 2026/03/20
Ma TongcuiGeorge Ashley FLi ZichongThomas ReubenYin KailinShin Min-GyoungMontano MauricioMatsui YusukeAshokkumar ManickamYoung KyrliaPrigann JuliaFrouard JulieLeddy SabrinaAdiba MaishaHerrde ChristinaLange Ulrike CFeschotte CedricNixon Douglas FBrowne Edward PArchin Nancie MLi Jonathan ZSmith DaveyDeeks StevenSøgaard Ole STolstrup MartinLee SulggiPillai Satish KAbdel-Mohsen MohamedPollard Katherine SSiliciano RobertOtt MelanieGreene Warner CRoan Nadia R - A significantly diverse clinical presentation of amyotrophic lateral sclerosis (ALS), even in its best-studied familial form, continues to hinder current efforts to develop effective disease-modifying drugs for the cure of this rapidly progressive, fatal neuromuscular disease. We have previously shown that clinical heterogeneity of sporadic ALS (sALS) could be explained, at least in part, by its polygenic nature as well as by the presence of mutated genes linked to non-ALS neurological diseases and genes known to mediate ALS-related pathologies. We hypothesized that a similar genetic framework could also be present in patients with familial ALS (fALS). To test this hypothesis, we conducted post-mortem genetic screening of an individual with fALS and a mutation in the gene. mutations are highly penetrant and are present in the majority of fALS patients. Genetic screening by whole exome sequencing (WES) on the next generation sequencing (NGS) Illumina platform (San Diego, CA, USA) followed by examination of the respective rare (minor allele frequency (MAF) ≤ 0.01) pathological/deleterious genetic variants yielded results consistent with our hypothesis of the presence of a complex genetic framework in fALS. Additional members of this genetic framework were identified when the low-frequency (0.01 < MAF < 0.05) pathological/deleterious genetic variants were analyzed with the low-frequency biallelic and variants, warranting a closer look at their potentially important role in fALS as genetic modifiers as well as their link to both neuromuscular disorders/ALS and cancer. Therefore, in addition to the current genetic screening using a standard panel of ALS-related genes, a supplementary screening by WES could be very beneficial for the development of personalized treatment of ALS patients as well as in search of the respective efficient disease-modifying drugs. - Source: PubMed
Publication date: 2024/12/19
Frolov AndreyD'sa ElizabethHenderson CamilleGuzman Miguel AHayat GhazalaMartin John R