Ask about this productRelated genes to: TFDP1 Blocking Peptide
- Gene:
- TFDP1 NIH gene
- Name:
- transcription factor Dp-1
- Previous symbol:
- -
- Synonyms:
- Dp-1, DRTF1, DP1, DILC
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 1995-02-02
- Date modifiied:
- 2016-01-29
Related products to: TFDP1 Blocking Peptide
Related articles to: TFDP1 Blocking Peptide
- Systemic lupus erythematosus (SLE) is a chronic autoimmune disease influenced by multiple genetic and environmental factors.. This study used bioinformatics to identify new diagnostic biomarkers and explore the pathogenesis of SLE. - Source: PubMed
Publication date: 2026/05/11
Pan QingboYu XuliangZhu JinZheng Xiaojin - The inflammation-intestinal metaplasia (IM)-carcinoma cascade has been proposed as a framework for gastric cancer (GC) development, yet the cell-level heterogeneity and microenvironmental remodeling underlying this progression remain poorly characterized. Here, we constructed a single-cell transcriptomic atlas by integrating scRNA-seq data from chronic gastritis (superficial, CGS), IM, cancer-adjacent, and tumor tissues through a unified analytical pipeline. Seven major cell lineages were resolved. Relative to CGS, IM and GC tissues exhibited a progressive contraction of epithelial compartments accompanied by expansion of immune and stromal populations. Copy number variation (CNV) inference identified two tumor-restricted malignant epithelial subgroups-one biased toward differentiation and the other enriched for inflammatory and epithelial-mesenchymal transition (EMT) signatures-as well as putative proto-malignant intermediates that coexisted with phenotypically normal epithelium. Cell-cell communication analysis indicated broadly augmented crosstalk between epithelial cells and T cells, myeloid cells, and fibroblasts, with prominent involvement of a CD44-extracellular matrix (ECM) axis. Pseudotime trajectory analysis placed malignant epithelium at late positions along gastric and pyloric mucosal cell differentiation backbones, coinciding with increasing CNV burden and enrichment of stem-like transcriptional programs. Gene regulatory network analysis revealed coordinated activity of lineage-specification modules (HNF4/CDX, NR1H4/ESRRA), proliferative regulons (MYC/TFDP1), and inflammatory/EMT-associated programs (FOSL1/REL/NF-κB). In independent cohorts, elevated expression of several malignant-epithelium-associated transcription factors-including HNF4A, KLF3, FOSL1, TCF7L2, BCL3, RELB, ONECUT2, and MAF-correlated with unfavorable overall survival. Collectively, these findings provide single-cell-resolution evidence consistent with the proposed three-stage model of gastric carcinogenesis and highlight candidate transcriptional regulators warranting further investigation as potential early-detection biomarkers. - Source: PubMed
Publication date: 2026/04/22
Li XiulanGuo MengqiWen YunhanLong Bo - Hypoxia-inducible factors (HIFs) are transcriptional regulators that orchestrate the canonical response to low-oxygen tension in animal cells. Vertebrates possess three HIF-α isoforms, which arose from two gene duplication events of the ancestral HIF-1α gene. Here, we examined whether the HIF gene family (HIF-1α, HIF-2α, HIF-3α, and HIF-1αN inhibitor) shows evidence of positive selection in hypoxia-tolerant reptiles (Testudines), compared evolutionary patterns within the family, and assessed the transcriptional response to hypoxia in primary cells derived from a hypoxia-tolerant ( ) and a non-tolerant ( ) reptile. We found that HIF-1α, HIF-2α, and HIF-1αN are highly conserved across reptiles, whereas HIF-3α is under positive selection in Testudines. We also identified multiple novel regulatory motifs unique to Testudines. Transcriptional signatures of hypoxia exposure indicated stark differences between lizards and turtles. Whereas lizard cells exhibited a canonical response to hypoxia, characterized by enriched cell-survival pathways, sea turtle cells exhibit a robust, distinctive transcriptional response involving enriched pathways related to protein synthesis, quality maintenance, and mitochondrial integrity. Surprisingly, cis-regulatory element analysis did not show HIFs as key regulators of the transcriptional response in either species. Instead, TFDP1 in lizard cells and E2F1 in sea turtle cells emerged as potential key regulators. TFDP1 regulates the cell cycle, specifically DNA synthesis and cell cycle progression, while E2F regulates DNA-damage response, apoptosis, metabolism, and fatty acid biosynthesis. These results suggest that the reptilian response to hypoxia is shaped by transcriptional plasticity, while highlighting key regulatory mechanisms driving hypoxic adaptation in sea turtle cells. However, positive selection of HIF-3α and novel HIF motifs suggest a combined, but yet to be uncovered, contribution of regulatory and coding sequence evolutionary mechanisms shaping hypoxia tolerance in Testudines. - Source: PubMed
Publication date: 2026/01/10
Arango B GabrielaSelleghin-Veiga GiovannaMoreno-Santillán Diana DanielaEnsminger David CVázquez Juan ManuelTarvin RebecaNery MarianaGodard-Codding Céline AVázquez-Medina José Pablo - Esophageal squamous cell carcinoma (ESCC) exhibits marked heterogeneity and poor prognosis, but the contribution of stemness‑related tumor cells remains unclear. Using single‑cell RNA sequencing, we identified eight tumor subpopulations in ESCC, among which one cluster displayed prominent stem‑like and proliferative features with high expression of MKI67, STMN1, and UBE2C. Based on its marker genes, we established a stemness‑associated scoring model (SASM). Validation in independent TCGA and GSE53624 cohorts confirmed that higher SASM scores predicted shorter overall survival and reduced immune infiltration, particularly of CD8⁺ T cells. SASM scores were positively correlated with tumor mutational burden (TMB), and patients with high SASM and low TMB exhibited the poorest outcomes. Further analysis identified TFDP1 as a key gene associated with SASM and adverse prognosis, which was upregulated in tumor tissues and promoted ESCC cell proliferation in vitro. Overall, our study delineates stemness‑related tumor heterogeneity in ESCC, proposes a prognostic scoring system with immunological relevance, and highlights TFDP1 as a potential therapeutic target. - Source: PubMed
Publication date: 2026/01/06
Ye WeiSu WeiLei ChangHuang ChenjunDu Mingjun - Noncystic fibrosis (non-CF) bronchiectasis is a chronic respiratory disease characterized by irreversible bronchial dilation, with an increasing global prevalence and substantial clinical burden. Despite the advances in symptomatic management, the underlying molecular mechanisms remain poorly understood. Transcription factor DP-1 () and cell division cycle protein 27 (), which are implicated in tumorigenesis and cell cycle regulation, have not been explored in bronchiectasis. - Source: PubMed
Publication date: 2025/12/25
Hong Kang-KangLi Guo-ShengHe Rong-QuanHuang Zhi-GuangFeng Yi-ZhiKong Jin-LiangLi Lao-Dong