TFDP1 antibody - N-terminal region (P100820_P050)
- Known as:
- TFDP1 (anti-) - N-terminal region (P100820_P050)
- Catalog number:
- p100820_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TFDP1 antibody - N-terminal region (P100820_P050)
Related genes to: TFDP1 antibody - N-terminal region (P100820_P050)
- 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 antibody - N-terminal region (P100820_P050)
Related articles to: TFDP1 antibody - N-terminal region (P100820_P050)
- 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 - Hepatocellular carcinoma (HCC) is the ultimate result of long-term chronic hepatitis B. Molecular interactions among parenchymal, non-parenchymal, and immune cells in the liver tumor microenvironment (TME) influence the progression of the disease by sharing molecules such as protein, nucleic acids (DNA, coding and non-coding RNAs), lipids, and others through extracellular vesicles (EVs). This study has examined the influence of Hepatitis B virus (HBV) on the enrichment of proteins in the HCC cell-derived EVs and . - Source: PubMed
Publication date: 2025/12/05
Dey IndrashishDas AnusmritiDas SubhasSaha SohamChowdhury AbhijitDatta SimantiBanerjee Soma - Renal cell carcinoma (RCC) is often associated with metabolic disorders such as type 2 diabetes mellitus (T2DM) and hypertension. While existing research has established connections between these metabolic conditions and RCC, the underlying mechanisms driving RCC followed by pancreatic metastasis remain incompletely understood. Therefore, our study aimed to investigate the complex interplay between metabolic disorders (type 2 diabetes and hypertension) and malignancies (renal cell carcinoma and pancreatic cancer). To investigate the hidden link, we performed an integrative transcriptomic analysis. The analysis focuses only on T2DM and hypertension to identify a connection with the RCC pathway. Our analysis revealed that 190 significantly upregulated genes, of which MET emerged as a master regulator in RCC, while KRAS was the key regulator in pancreatic cancer. Furthermore, we identified key microRNAs (has-mir-1-3p, has-mir-16-5p, and has-mir-455-3p) and transcription factors (MBD1, TFDP1, and KLF9) regulate these targets. Additionally, we identified and validated CDC42, PTPN11, TGFB3, and MET as potential prognostic or theragnostic biomarkers. MET, KRAS, and PIK3CD emerged as the most promising therapeutic targets against a panel of 28 repurposable inhibitory drugs. The genetic and immune association suggested that CD8 + T cells are the key immune infiltrate significantly associated with poor survival outcomes in RCC and pancreatic cancer patients. Mutational analysis further highlighted the significance of KRAS G12C, G12V, and G12D mutations, which were common between RCC and pancreatic metastasis. Our study provides critical insights into the statistically significant associations between metabolic disorders and malignancies, emphasizing the potential of tailored therapies alongside shared therapies in managing RCC and its progression to pancreatic metastasis. - Source: PubMed
Publication date: 2025/11/29
Islam K M TanjidaKhanam RoksanaRoy AnindaMohiuddin Ramisa BintiAkter JannatiHaque SamiaAl Ashik Sheikh AbdullahSarker SaborniMohiuddin A K MMahmud Shahin