PAPPA antibody
- Known as:
- PAPPA (anti-)
- Catalog number:
- 10-1957
- Product Quantity:
- 200 ul
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- PAPPA antibody
Related genes to: PAPPA antibody
- Gene:
- PAPPA NIH gene
- Name:
- pappalysin 1
- Previous symbol:
- -
- Synonyms:
- PAPP-A, PAPPA1, IGFBP-4ase, PAPA, ASBABP2, DIPLA1
- Chromosome:
- 9q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-25
- Date modifiied:
- 2016-03-29
- Gene:
- PAPPA-AS1 NIH gene
- Name:
- PAPPA antisense RNA 1
- Previous symbol:
- PAPPAS
- Synonyms:
- PAPPA-AS, DIPAS, TAF4B, TAF2C2, TAFII105, NCRNA00156
- Chromosome:
- 9q33.2
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2008-09-22
- Date modifiied:
- 2014-11-19
Related products to: PAPPA antibody
Related articles to: PAPPA antibody
- Hypertrophic scar (HTS) is a complicated pathological process induced mainly by burns and wounds, with abnormal proliferation of fibroblasts and the transformation of fibroblasts to myofibroblasts. PAPPA-AS1, a differentially expressed long noncoding RNA (lncRNA) in the HTS tissues, attracted our interests in its potential role and mechanism in the development and process of HTS. In the present study, the regulatory effect of lncRNA PAPPA-AS1 on the Toll-like receptor 4 (TLR4) signal pathway, as well as the molecular mechanism, was investigated. Bioinformatics analysis was utilized to screen the differentially expressed lncRNAs in HTS tissues. PAPPA-AS1 was significantly upregulated in both HTS tissues and hypertrophic scar fibroblast (HTsFb) cells. The expression levels of TLR4, MyD88, TGF-1, collagen I, collagen III, and -SMA were greatly elevated in HTsFb cells. By knocking down PAPPA-AS1, the proliferation of HTsFb cells, TLR4, and TGF-1 signal pathway and the expression of fibrosis markers both in HTsFb cells and HTS tissues were suppressed. It was accompanied by the alleviated pathological state in the HTS tissues, which were significantly reversed by cotransfecting with the pcDNA3.1-TLR4 vector. Positive correlation and interaction were observed between PAPPA-AS1 and TAF15 and between TAF15 and the promoter of TLR4, respectively. In conclusion, lncRNA PAPPA-AS1 might induce the development of HTS by upregulating TLR4 through interacting with TAF15. - Source: PubMed
Publication date: 2021/07/03
Fan PengjuWang YongjieLi JingjingFang Man - Pernicious placenta previa with placenta percreta (PP) is a catastrophic condition during pregnancy. However, the underlying pathogenesis remains unclear. In the present study, the placental tissues of normal cases and PP tissues of pernicious placenta previa cases were collected to determine the expression profile of protein-coding genes, miRNAs, and lncRNAs through sequencing. Weighted gene co-expression network analysis (WGCNA), accompanied by miRNA target prediction and correlation analysis, were employed to select potential hub protein-coding genes and lncRNAs. The expression levels of selected protein-coding genes, Wnt5A and MAPK13, were determined by quantitative PCR and immunohistochemical staining, and lncRNA PTCHD1-AS and PAPPA-AS1 expression levels were determined by quantitative PCR and fluorescence in situ hybridization. The results indicated that 790 protein-coding genes, 382 miRNAs, and 541 lncRNAs were dysregulated in PP tissues, compared with normal tissues. WGCNA identified coding genes in the module (ME) black and ME turquoise modules that may be involved in the pathogenesis of PP. The selected potential hub protein-coding genes, Wnt5A and MAPK13, were down-regulated in PP tissues, and their expression levels were positively correlated with the expression levels of PTCHD1-AS and PAPPA-AS1. Further analysis demonstrated that PTCHD1-AS and PAPPA-AS1 regulated Wnt5A and MAPK13 expression by interacting with specific miRNAs. Collectively, our results provided multi-omics data to better understand the pathogenesis of PP and help identify predictive biomarkers and therapeutic targets for PP. - Source: PubMed
Publication date: 2020/10/21
Jiang QingyuanDai LeiChen NaLi JunshuGao YanZhao JingDing LiXie ChengbinYi XiaolianDeng HongxinWang Xiaodong