Ask about this productRelated genes to: SPDEF Blocking Peptide
- Gene:
- SPDEF NIH gene
- Name:
- SAM pointed domain containing ETS transcription factor
- Previous symbol:
- -
- Synonyms:
- PDEF, bA375E1.3
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-27
- Date modifiied:
- 2016-10-05
Related products to: SPDEF Blocking Peptide
Related articles to: SPDEF Blocking Peptide
- Gene mutations and altered epigenetic regulation of gene expression are characteristic features of malignant neoplasms. Combinations of these abnormalities form molecular features of individual tumors. In the large-scale Dependency Map (DepMap) project, the broad panels of human tumor cell lines are being tested for sensitivity to single gene inactivation. Using DepMap data, we have previously identified a set of genes termed supertargets, the deletion of which significantly reduced the survival of cells of a particular tissue origin while minimally impairing the unrelated cell lines. In the present study, we determined the factors of viability (inhibition of proliferation or death) of cell lines in which the supertarget genes have been deleted. We found that, in 79 % of cases, the reduced survival may be caused by epigenetic changes of gene expression. In the remaining 21 % of cases, it is associated with altered gene structure. Three groups containing different types of gene expression alterations can be distinguished. In the first group, the reduced cell survival correlated with a higher expression of the supertarget gene (e. g., SOX10 and HNF1B). In the second group, a gene different from the deleted supertarget was overexpressed (gene pairs: FOXA1 and SPDEF, TP63 and SERPINB13, etc.). The third group was characterized by correlations between low expression of a certain gene and tumor cell sensitivity (e. g., FAM126A and FAM126B, SMARCA2 and SMARCA4). The genetic changes included GOF mutations (KRAS, BRAF genes, etc.), LOF mutations (STAG1, SMARCA2 genes, etc.), gene fusions (BCR-ABL1, PAX3-FOXO1, etc.), and amplification (CPM, BEST3, etc.). Therefore, many different molecular mechanisms act as predictors of tumor cell response to inhibition of supertarget genes. - Source: PubMed
Chetverina D AKozelchuk N YLomaev D VShtil A AErokhin М M - Mucin 5AC (MUC5AC) is a mucin that forms a gel on the surface of the airway epithelium, and its hyperproduction plays a pathological role in chronic inflammatory airway diseases. Short-chain fatty acids (SCFAs), microbial fermentation products of dietary fiber in the gut, have been shown to significantly impact the development of allergic airway disease. Nonetheless, little is known about whether and how SCFAs influence the function of airway epithelial cells. In this study, we investigated the direct effects of SCFAs, especially butyrate, on MUC5AC production and the underlying mechanisms. - Source: PubMed
Jo Sang HeeBae IkhyeonSim Myeong SeongKim Hye JeongKim ChunChung Il YupChang Hun Soo - Excessive mucus production in the airways is a key pathogenic characteristic of chronic respiratory conditions, including bronchial asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF). The etiology is intricate, encompassing various factors such as aberrant activation of inflammatory signaling pathways, deregulation of mucin gene expression, modified rheological characteristics of mucus, and impairment of the ciliary clearance mechanism. Nonetheless, the current evidence is disjointed, and a thorough and systematic synthesis is still absent. - Source: PubMed
Publication date: 2026/03/09
Ying WeilinJing XinChen LingZhang JingYue LiZhang Boda - The porcine endometrium undergoes dynamic cellular remodeling across the estrous cycle, yet epithelial heterogeneity and differentiation trajectories remain incompletely characterized. In this study, a single-cell transcriptomic atlas of the endometrial epithelium during the follicular and luteal phases in Meishan pigs was generated using high-resolution single-cell RNA sequencing. Canonical epithelial cell types were identified, including glandular epithelium (GE), secretory glandular epithelium (secretory GE), luminal epithelium (LE), ciliated epithelium, as well as an epithelial stem cell subpopulation marked by ALDH1A3 and LGR5 and a progenitor subpopulation marked by ALDH1A1. During the follicular phase, the epithelium was primarily composed of ALDH1A3+LGR5+ stem cells and ALDH1A1+ progenitor cells, whereas GE, secretory GE, and LE predominated during the luteal phase. Integrated trajectory inference and RNA velocity analyses suggested a continuous differentiation trajectory from ALDH1A3+LGR5+ stem cells through ALDH1A1+ progenitors toward GE. Gene expression patterns indicated that glandular epithelial formation was associated with activation of transcriptional regulatory programs and increased mitochondrial respiratory activity. In contrast, differentiation toward the secretory glandular epithelial lineage was characterized by early activation of stress-response pathways, secretion-related genes, and specific metabolic programs. Several transcription factors, including ZFP36L1, TRPS1, and KLF6, were associated with glandular differentiation, whereas MBD4, CREB3L4, ZNF524, SPDEF, USF1, XBP1, and MLX were predicted to contribute to glandular secretory function. These genes showed significant associations with sow reproductive traits in a phenome-wide association study. Overall, this study provides a single-cell framework for understanding epithelial dynamics in the porcine endometrium across the estrous cycle. - Source: PubMed
Jiang NengjingChen YuejiaYin YanzhenXiao WeiXiao XuemeiMa JinfengLiao XingLiu QianJin XuexiaXu BinBinWang JingZhou TengbinZhao QingboLi PinghuaHuang Ruihua - Triple-negative breast cancer (TNBC), particularly the androgen receptor-low (AR-low) subtype, is one of the most aggressive and hard-to-treat forms of BC, characterized by a high index of proliferation, chromosomal instability (CIN), and high prevalence of TP53 mutations. These features fuel therapy resistance, metastases, and poor clinical outcomes. An integrated framework describing the dysregulated molecular networks that support the pathobiology of AR-low TNBC is lacking. Multiple published studies in breast cancer have previously proposed mechanistic links between TP53 loss, AR-low states, and heightened FOXM1-driven G2/M transcriptional programs, potentially via deregulation of E2F activity, chromatin-associated co-regulators (e.g., ATAD2), and disruption of repressive networks involving p53-p21-DREAM and SPDEF. Additional reports suggest that FOXM1-associated circuitry may be reinforced by chromatin regulators such as WDR5 and by mitotic/spindle factors such as ASPM, including through feedback interactions and condensate-associated transcriptional organization. We previously showed that FOXM1, a master regulator transcription factor, is upregulated and is a biomarker of poor prognosis in AR-low TNBC. In this study, we filtered a set of "TNBC core genes" known to promote transcriptional chaos downstream of FoxM1. We identified a set of 15 cell cycle regulators-including mitotic kinesin motors (KIF14, KIF11, KIF4A, KIF2C, and KIF20A), centromeric proteins (CENPA, CENPO, CENPL, CENPF, and OIP5), and regulators of proteolysis (UBE2C, UBE2S, UBE2T, PSMD14, and TUBA1B). These 15 genes, which were ranked highly among genes overexpressed in TNBC featured prominently in gene signatures of chromosomal instability and were also overexpressed among AR-low TNBCs and TP53-mutant breast tumors. We show that expression of each of these 15 genes correlates positively with proliferation markers (Ki67, PCNA, and MCM2) in TNBC, and that the overexpression of this gene set is associated with shorter relapse-free survival and distinct immune/stromal infiltration patterns. In light of prior work, our findings point to a FOXM1-associated 15-gene signature enriched in AR-low TNBC and associated with the high-proliferation and high-CIN phenotypes of this clinically challenging tumor type. This 15-gene set represents an actionable vulnerability with therapeutic potential for AR-low TNBC and provides a framework for rethinking how to manage highly proliferative, genomically unstable BCs. - Source: PubMed
Publication date: 2026/02/14
Rida PadmashreeAndreae RaphaelBikhazi NoahJackson BeneciaWang IvanJinna Nikita