scholarly journals BMP and Notch Signaling Pathways differentially regulate Cardiomyocyte Proliferation during Ventricle Regeneration

2021 ◽  
Vol 17 (9) ◽  
pp. 2157-2166
Author(s):  
Wenyuan Wang ◽  
Ye-Fan Hu ◽  
Meijun Pang ◽  
Nannan Chang ◽  
Chunxiao Yu ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Signaling Pathways ◽  
Cardiomyocyte Proliferation

scholarly journals Dominant Enhancers of Egfr in Drosophila melanogaster: Genetic Links Between the Notch and Egfr Signaling Pathways

Genetics ◽  
1997 ◽  
Vol 147 (3) ◽  
pp. 1139-1153 ◽  
Author(s):  
James V Price ◽  
Edward D Savenye ◽  
David Lum ◽  
Ashton Breitkreutz
Keyword(s):  
Notch Signaling ◽  
Signaling Pathways ◽  
Growth Factor Receptor ◽  
Compound Eyes ◽  
Egfr Signaling ◽  
Wing Vein ◽  
Developmental Context ◽  
Epidermal Growth ◽  
Hypomorphic Alleles ◽  
Complex Signaling

The Drosophila epidermal growth factor receptor (EGFR) is a key component of a complex signaling pathway that participates in multiple developmental processes. We have performed and F1 screen for mutations that cause dominant enhancement of wing vein phenotypes associated with mutations in Egfr. With this screen, we have recovered mutations in Hairless (H), vein, groucho (gro), and three apparently novel loci. All of the E(Egfr)s we have identified show dominant interactions in transheterozygous combinations with each other and with alleles of N or Su(H), suggesting that they are involved in cross-talk between the N and EGFR signaling pathways. Further examination of the phenotypic interactions between Egfr, H, and gro revealed that reductions in Egfr activity enhanced both the bristle loss associated with H mutations, and the bristle hyperplasia and ocellar hypertrophy associated with gro mutations. Double mutant combinations of Egfr and gro hypomorphic alleles led to the formation of ectopic compound eyes in a dosage sensitive manner. Our findings suggest that these E(Egfr)s represent links between the Egfr and Notch signaling pathways, and that Egfr activity can either promote or suppress Notch signaling, depending on its developmental context.

scholarly journals Mesenchymal stem cells regulate maintenance of neural stem cells through VEGFR2 and Notch signaling pathways

Cell Research ◽  
2008 ◽  
Vol 18 (S1) ◽  
pp. S59-S59
Author(s):  
Zhifeng Deng ◽  
Zhumin Liu ◽  
Wei Tu ◽  
Yang Wang ◽  
Yuanlei Lou
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Neural Stem Cells ◽  
Notch Signaling ◽  
Signaling Pathways

MiRNA expression analysis during normal zebrafish development and following inhibition of the Hedgehog and Notch signaling pathways

2007 ◽  
Vol 236 (8) ◽  
pp. 2172-2180 ◽  
Author(s):  
Elizabeth J. Thatcher ◽  
Alex S. Flynt ◽  
Nan Li ◽  
Jonathan R. Patton ◽  
James G. Patton
Keyword(s):  
Notch Signaling ◽  
Signaling Pathways ◽  
Expression Analysis ◽  
Mirna Expression ◽  
Zebrafish Development

scholarly journals The Impact of Drosophila Awd/NME1/2 Levels on Notch and Wg Signaling Pathways

2020 ◽  
Vol 21 (19) ◽  
pp. 7257
Author(s):  
Giulia Serafini ◽  
Giorgia Giordani ◽  
Luca Grillini ◽  
Davide Andrenacci ◽  
Giuseppe Gargiulo ◽  
...  
Keyword(s):  
Cell Death ◽  
Notch Signaling ◽  
Signaling Pathways ◽  
Target Genes ◽  
Wing Disc ◽  
Amino Terminal ◽  
Disc Cells ◽  
Function Blocks ◽  
The Impact ◽  
Dose Dependent

Awd, the Drosophila homologue of NME1/2 metastasis suppressors, plays key roles in many signaling pathways. Mosaic analysis of the null awdJ2A4 allele showed that loss of awd gene function blocks Notch signaling and the expression of its target genes including the Wingless (Wg/Wnt1) morphogen. We also showed that RNA interference (RNAi)-mediated awd silencing (awdi) in larval wing disc leads to chromosomal instability (CIN) and to Jun amino-terminal kinases (JNK)-mediated cell death. Here we show that this cell death is independent of p53 activity. Based on our previous finding showing that forced survival of awdi-CIN cells leads to aneuploidy without the hyperproliferative effect, we investigated the Wg expression in awdi wing disc cells. Interestingly, the Wg protein is expressed in its correct dorso-ventral domain but shows an altered cellular distribution which impairs its signaling. Further, we show that RNAi-mediated knock down of awd in wing discs does not affect Notch signaling. Thus, our analysis of the hypomorphic phenotype arising from awd downregulation uncovers a dose-dependent effect of Awd in Notch and Wg signaling.

scholarly journals Exosome-Derived LINC00960 and LINC02470 Promote the Epithelial-Mesenchymal Transition and Aggressiveness of Bladder Cancer Cells

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1419
Author(s):  
Cheng-Shuo Huang ◽  
Jar-Yi Ho ◽  
Jung-Hwa Chiang ◽  
Cheng-Ping Yu ◽  
Dah-Shyong Yu
Keyword(s):  
Bladder Cancer ◽  
Notch Signaling ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Low Grade ◽  
High Grade ◽  
Mesenchymal Transition ◽  
Bladder Cancer Cells

Exosomes are essential for several tumor progression-related processes, including the epithelial–mesenchymal transition (EMT). Long non-coding RNAs (lncRNAs) comprise a major group of exosomal components and regulate the neoplastic development of several cancer types; however, the progressive role of exosomal lncRNAs in bladder cancer have rarely been addressed. In this study, we identified two potential aggressiveness-promoting exosomal lncRNAs, LINC00960 and LINC02470. Exosomes derived from high-grade bladder cancer cells enhanced the viability, migration, invasion and clonogenicity of recipient low-grade bladder cancer cells and activated major EMT-upstream signaling pathways, including β-catenin signaling, Notch signaling, and Smad2/3 signaling pathways. Nevertheless, LINC00960 and LINC02470 were expressed at significantly higher levels in T24 and J82 cells and their secreted exosomes than in TSGH-8301 cells. Moreover, exosomes derived from LINC00960 knockdown or LINC02470 knockdown T24 cells significantly attenuated the ability of exosomes to promote cell aggressiveness and activate EMT-related signaling pathways in recipient TSGH-8301 cells. Our findings indicate that exosome-derived LINC00960 and LINC02470 from high-grade bladder cancer cells promote the malignant behaviors of recipient low-grade bladder cancer cells and induce EMT by upregulating β-catenin signaling, Notch signaling, and Smad2/3 signaling. Both lncRNAs may serve as potential liquid biomarkers for the prognostic surveillance of bladder cancer progression.

scholarly journals C1q/tumor necrosis factor‐related protein‐3 improves renal fibrosis via inhibiting notch signaling pathways

2019 ◽  
Vol 234 (12) ◽  
pp. 22352-22364
Author(s):  
Xinpan Chen ◽  
Yiru Wu ◽  
Zongli Diao ◽  
Xue Han ◽  
Dishan Li ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Notch Signaling ◽  
Signaling Pathways ◽  
Renal Fibrosis ◽  
Tumor Necrosis ◽  
Related Protein ◽  
Necrosis Factor
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