Ask about this productRelated genes to: STOX2 Blocking Peptide
- Gene:
- STOX2 NIH gene
- Name:
- storkhead box 2
- Previous symbol:
- -
- Synonyms:
- DKFZp762K222
- Chromosome:
- 4q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-04-04
- Date modifiied:
- 2015-08-26
Related products to: STOX2 Blocking Peptide
Related articles to: STOX2 Blocking Peptide
- This study aims to identify key modules and targets during the transition from gastric precancerous lesions to gastric cancer by performing weighted gene co-expression network analysis (WGCNA) on gene microarray datasets from the Gene Expression Omnibus (GEO) database containing gastritis, gastric cancer and precancerous lesions, providing insights for early intervention in gastric cancer. - Source: PubMed
Publication date: 2025/11/25
Li HengLi WenYang ZhenLiu HaiyuZhang XiaopingZhao YufengGu Hao - The Taihu Dianzi pigeon is a breed native to China, and its special piebalding, crest, and polydactyly phenotypes are the result of artificial and natural selection. Here, we analyzed the genetic differences among three kinds of pigeons with different phenotypes at the genomic level. A selective sweep was conducted based on the fixation index () and nucleotide diversity () ratio, and the results revealed that was related to the formation of the distinctive piebalding of the Taihu Dianzi pigeon. Combined with the results of genome-wide association studies, we identified candidate genes associated with the crest ( and ) and polydactyly ( and ). The candidate genes identified in this study and their variants may be useful for understanding the genetic mechanism underlying the special phenotypes of the Taihu Dianzi pigeon. This study provides new insights into the genetic factors that may influence the formation of the special piebalding, crest, and polydactyly characteristics in pigeons. - Source: PubMed
Publication date: 2024/03/29
Zhang RuiMu ChunyuChang LinglingShen XinyueBu ZhuYang MingjunFu ShengyongTang QingpingLiu PeiyaoYang Xiaoming - The five lysyl-oxidase genes share similar enzymatic activities and contribute to tumor progression. We have knocked out the five lysyl-oxidase genes in MDA-MB-231 breast cancer cells using CRISPR/Cas9 in order to identify genes that are regulated by LOX but not by other lysyl-oxidases and in order to study such genes in more mechanistic detail in the future. Re-expression of the full-length cDNA encoding LOX identified four genes whose expression was downregulated in the knock-out cells and rescued following LOX re-expression but not re-expression of other lysyl-oxidases. These were the AGR2, STOX2, DNAJB11 and DNAJC3 genes. AGR2 and STOX2 were previously identified as promoters of tumor progression. In addition, we identified several genes that were not downregulated in the knock-out cells but were strongly upregulated following LOX or LOXL3 re-expression. Some of these, such as the DERL3 gene, also promote tumor progression. There was very little proteolytic processing of the re-expressed LOX pro-enzyme in the MDA-MB-231 cells, while in the HEK293 cells, the LOX pro-enzyme was efficiently cleaved. We introduced point mutations into the known BMP-1 and ADAMTS2/14 cleavage sites of LOX. The BMP-1 mutant was secreted but not cleaved, while the LOX double mutant dmutLOX was not cleaved or secreted. However, even in the presence of the irreversible LOX inhibitor β-aminoproprionitrile (BAPN), these point-mutated LOX variants induced the expression of these genes, suggesting that the LOX pro-enzyme has hitherto unrecognized biological functions. - Source: PubMed
Publication date: 2022/09/26
Liburkin-Dan TatyanaNir-Zvi InbalRazon HilaKessler OfraNeufeld Gera - A hydatidiform mole is a condition caused by abnormal proliferation of trophoblastic cells. MicroRNA miR-30a acts as a tumor suppressor gene in most tumors and participates in the development of various cancers. However, its role in hydatidiform moles is not clear. - Source: PubMed
Publication date: 2022/03/04
Guo ZhenzhenZhu ChenyuWang YouhuiLi ZhenWang LuFan JianhuiXu YuefeiZou NaKong YingLi DongSui Linlin - The production of a clinically useful engineered cartilage is an outstanding and unmet clinical need. High-throughput RNA sequencing provides a means of characterizing the molecular phenotype of populations of cells and can be leveraged to better understand differences among source cells, derivative engineered tissues, and target phenotypes. In this study, small RNA sequencing is utilized to comprehensively characterize the microRNA transcriptomes (miRNomes) of native human neonatal articular cartilage and human bone marrow-derived mesenchymal stem cells (hBM-MSCs) differentiating into cartilage organoids, contrasting the microRNA regulation of engineered cartilage with that of a promising target phenotype. Five dominant microRNAs are upregulated during cartilage organoid differentiation and disproportionately regulate transcription factors: miR-148a-3p, miR-140-3p, miR-27b-3p, miR-140-5p, and miR-181a-5p. Two microRNAs that dominate the miRNomes of hBM-MSCs, miR-21-5p and miR-143-3p, persist throughout the differentiation process and may limit the ability of these cells to differentiate into an engineered cartilage resembling target native articular cartilage. By using predictive bioinformatics tools and antagomir inhibition, these persistent microRNAs are shown to destabilize the mRNA of genes with known or potential roles in cartilage biology including , , , , , , , , and These results shed light on the extent to which only a few microRNAs contribute to the complex regulatory environment of hBM-MSCs for engineered tissues. Impact statement MicroRNAs are emerging as important controlling elements in the differentiation of human bone marrow-derived mesenchymal stem cells (hBM-MSCs). By using a robust bioinformatic approach and further validation , here we provide a comprehensive characterization of the microRNA transcriptomes (miRNomes) of a commonly studied and clinically promising source of multipotent cells (hBM-MSCs), a gold standard model of chondrogenesis (hBM-MSC-derived cartilage organoids), and an attractive target phenotype for clinically useful engineered cartilage (neonatal articular cartilage). These analyses highlighted a specific set of microRNAs involved in the chondrogenic program that could be manipulated to acquire a more robust articular cartilage-like phenotype. This characterization provides researchers in the cartilage tissue engineering field a useful atlas with which to contextualize microRNA involvement in complex differentiation pathways. - Source: PubMed
Publication date: 2021/10/25
Vail Daniel JSomoza Rodrigo ACaplan Arnold I