SPDEF antibody - N-terminal region (ARP31841_T100)
- Known as:
- SPDEF (anti-) - N-terminal region (ARP31841_T100)
- Catalog number:
- arp31841_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SPDEF antibody - N-terminal region (ARP31841_T100)
Related genes to: SPDEF antibody - N-terminal region (ARP31841_T100)
- 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 antibody - N-terminal region (ARP31841_T100)
Related articles to: SPDEF antibody - N-terminal region (ARP31841_T100)
- Characterized by cytoplasmic lipid accumulation and fatty-acid metabolic reprogramming, clear cell renal cell carcinoma (ccRCC) is closely related to tumor progression and invasion. The impact of SPDEF, an ETS transcription factor, in ccRCC and its involvement in lipid metabolism remain unclear. - Source: PubMed
Publication date: 2026/06/09
Zhang PuYu WanliLuo HuiwenWang DecaiLi MingzeWang TingGuo YihongXiong WeiGong BoHe Yu - Necrotizing enterocolitis (NEC) is the most deadly gastrointestinal disease in preterm neonates, with up to 50% mortality. There is no cure for NEC. Enhancing our understanding of intestinal epithelial cell (IEC) responses to NEC will provide novel therapeutic targets. The RNA-binding protein insulin-like growth factor 2 mRNA binding protein 1 (IMP1) plays roles in intestinal development and repair. Notably, roles for IMP1 in NEC are unknown. Intestinal goblet cells produce protective mucus, and their function depends on the transcription factor Spdef. Evidence suggests that goblet cell mucus glycosylation affects barrier function and inflammation. We aimed to define the role of IMP1 in NEC damage response using neonatal human enteroids and a NEC-like intestinal injury model. At post-natal day 3, wild-type mice or littermates with IEC-specific Imp1 overexpression () or loss () were assigned to control or NEC groups. NEC was induced with stress, formula feeding, bacterial exposure, and hypoxia. Imp1 effects on NEC response were assessed using RNA sequencing, western blotting, immunostaining, and a cytokine array. We found that pro-inflammatory bacteria induced expression in neonatal human enteroids. During NEC, mice exhibit more severe intestinal damage and priming for lytic cell death. Elevated Imp1 levels were linked to a Spdef transcriptional signature and in silico analysis predicted Imp1 binding to and mucus glycosylation mediator mRNAs. Functionally, Imp1 increased fucosylation in the intestinal epithelium. Collectively, results suggest that Imp1 primes the intestine for lytic death and promotes the production of fucosylated mucus, changes which could alter the damage response. - Source: PubMed
Publication date: 2026/06/04
Swift Kevin AShumway Alexandria JAloia MollyHedges MadelinePung RachelLiu MoqingRodriguez Santiago CariamShanahan Michael TDrake AlexanderHakar Melanie HSelesner LeighKuhn MadelineYung ClaireSethupathy PraveenAndres Sarah F - Endometritis is linked to adverse reproductive outcomes, but epithelial programs in disease initiation and persistence remain unclear. We aimed to systematically define inflammation-associated epithelial states and regulation in endometritis using single-cell analysis. - Source: PubMed
Publication date: 2026/05/14
Tian ChengziLi Zaiyi - 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