Ask about this productRelated genes to: KLF17 antibody
- Gene:
- KLF17 NIH gene
- Name:
- Kruppel like factor 17
- Previous symbol:
- ZNF393
- Synonyms:
- Zfp393, FLJ40160
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-03
- Date modifiied:
- 2016-06-03
Related products to: KLF17 antibody
Related articles to: KLF17 antibody
- DUX4 initiates the first wave of zygotic genome activation (ZGA) in the human embryo, and its misexpression in skeletal muscle causes facioscapulohumeral muscular dystrophy (FSHD). However, other factors that help regulate ZGA-like transcription in human development and disease are still not fully understood. Here we identify Krüppel-like factor 18 (KLF18) as a component of a DUX4 feed-forward network that is necessary for expression of and a subset of DUX4-regulated totipotency-associated genes. We mapped the genome-wide binding profile of KLF18 downstream from DUX4 and showed that its activity is influenced by DUX4 and chromatin accessibility. We found that in contrast to the rodent ortholog, human KLF18 has a predicted β-solenoid structure composed of a variable number of tandem repeats (VNTR) with multiple different structural variants in the human population. Expression of different KLF18 variants in combination with DUX4 showed similar transcriptional activity, whereas assessment of structural variants in individuals with FSHD1 showed inconsistent association with disease severity that requires further study as a modifier locus. Together, these findings establish the polymorphic transcription factor KLF18 as a critical component of a DUX4-initiated feed-forward network and a candidate locus for human diversity. - Source: PubMed
Publication date: 2026/04/15
Hamm Danielle CO'Donnell Aidan BBennett Sean RLemmers Richard J L Fvan der Vliet Patrick Jvan der Maarel Silvère MTapscott Stephen J - - Source: PubMed
Hu MFang N - A subset of epithelioid-to-spindle cell sarcomas remains difficult to classify due to lack of defining molecular alterations or pathologic features that do not fit neatly into a single tumor class. After identification of a primary mesenchymal neoplasm with EPS15L1::KLF17 gene fusion, we retrospectively collected 4 additional soft tissue tumors with EPS15L1 :: KLF17 or EPS15 :: KLF17 fusions. The cohort comprised 4 males and one female with age range of 5 to 64 years. The tumors arose in soft tissue of the extremities, head/neck, paraspinal region, and intra-abdominal mesentery. Two patients developed metastatic disease with one death from disease at 62 months; one showed late metastases at 5 and 11 years. Histologically, these were cellular neoplasms composed of epithelioid and spindled tumor cells with prominent cystic spaces and focal stromal sclerosis. All tumors demonstrated diffuse, strong MUC4 positivity (5/5) with cytokeratin (3/3), EMA (4/4), and S100 (3/4) expression. Whole transcriptome RNA sequencing identified EPS15L1 :: KLF17 fusions in 2 cases and EPS15 :: KLF17 fusions in 3 cases. RNA expression profiles, available in 2 cases, showed high expression of MUC4 and CD24. DNA methylation profiling revealed distinct epigenetic clustering, separate from EWSR1 :: KLF15 -rearranged soft tissue myoepithelial tumor, sclerosing epithelioid fibrosarcoma, low-grade fibromyxoid sarcoma, and other mesenchymal neoplasms. EPS15/EPS15L1 :: KLF17 -rearranged sarcoma has distinctive histologic findings, including diffuse MUC4 expression. Recognition is clinically important given its potential for late recurrence and metastasis. - Source: PubMed
Publication date: 2026/03/21
Malik FaizanVong MaiaDehner Carina AShi ZonggaoKaranian MariePissaloux DanielPinto Soniya NBlackburn Patrick RTran Quynh TOrr Brent AKoo Selene C - Embryonic genome activation (EGA) marks a critical developmental transition, yet its regulatory architecture remains incompletely defined. Here, we employed optimized low-input SLAM-seq (thiol(SH)-linked alkylation for the metabolic sequencing) to map the temporal hierarchy of nascent transcription during mouse EGA. We uncovered patterns of transcriptional priming characterized by pre-activated genes (PAGs) with permissive chromatin states, followed by pronounced accumulation of PAGs-encoded proteins in blastocysts, suggesting that EGA memory propagates from early transcriptional activation to later lineage commitment. Furthermore, Integrative analysis nominated two-cell nascent transcription factors (TFs) as candidate regulators of the first lineage specification. Functional investigations demonstrated KLF17 as a key TF linking EGA to the first lineage specification via regulation of PAGs transcription. KLF17 deficiency led to the failure of transcriptional activation in approximately half of PAGs at the two-cell stage. Our work provides a detailed framework for decoding mammalian EGA and offers insights into how embryonic transcriptional priming is coordinated with early cell fate specification. - Source: PubMed
Hu YueWang YuxiangYe MaoshengHe YuanlinOuyang ZhangyiRen ChaoMiao TianyinWang SiqiZhong OuLiu LiShu WenjieHuo Ran - Corneal fibrosis results in loss of corneal transparency and vision impairment. Dynamic chromatin accessibility is a key regulatory mechanism driving fibrotic process, allowing transcription factors to access specific DNA sequences to activate or shut down transcription of pro- and anti-fibrotic genes. Genome-wide chromatin accessibility profiling was employed to explore the epigenomic landscape in alkali-induced fibrosis in rabbit cornea to identify key fibrotic regulators. Chromatin accessible regions (peaks) were identified using MACS2 and annotated relative to genomic features using ChIPseeker. de novo motif enrichment was evaluated by HOMER. Differentially accessible regions (DARs) were quantified with csaw and edgeR followed by pathway enrichment analysis using clusterProfiler. Of the total 121,305 peaks identified across all samples, 5890 DARs (FDR<0.05) were identified exhibiting reduced accessibility. Distinct chromatin condensation was observed at promoter region in fibrotic (5 %) vs. naïve (15 %) corneas. Functional enrichment analysis revealed that cell cycle, metabolism and stress response regulation genes were the most affected. de novo motifs analysis identified motifs with high similarities to KLF17 (p = 1e), NRF2 (p = 1e), and ETV6 (p = 1e) as potential regulators of corneal fibrosis. The qRT-PCR evaluation of motifs in human corneal myofibroblasts showed low expression of KLF17 (p < 0.05) and NRF2 (p = 0.23), and elevated levels of ETV6 (p = 0.64) compared to fibroblast cells. ATAC-sequences are made available at the NCBI Gene Expression Omnibus (GEO accession no. GSE305524). Fibrosis triggers extensive epigenomic reprogramming, characterized by promoter-to-enhancer regulatory shifts and selective activation of fibrosis-associated transcriptional networks providing promising avenue for therapeutic interventions managing corneal fibrosis. - Source: PubMed
Publication date: 2025/12/24
Sood SwatiKumar RajnishSinha Nishant RMohan Rajiv R