Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:4.1.2.42 (
DTA
)
1,693
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A specialized subtype of trophoblast giant cells (TGCs) line the torturous sinusoids of the murine placental labyrinth, and can be distinguished from most other TGCs by the expression of Ctsq. We generated a transgenic mouse line expressing Cre recombinase from the Ctsq promoter. Crosses with Cre-inducible tdTomato reporter mice indicated Cre activity was restricted to the sinusoidal TGCs of the labyrinth, as well as the recently characterized channel TGCs. When crossed with Cre-inducible
DTA
transgenic mice, ablation of sinusoidal TGCs was achieved in double transgenic embryos, resulting in fetal growth restriction by
E16
.5, and embryonic lethality by term.
...
PMID:Genetic ablation of placental sinusoidal trophoblast giant cells causes fetal growth restriction and embryonic lethality. 2609 29
Coordinated cardiomyocyte growth, differentiation, and morphogenesis are essential for heart formation. We demonstrate that the bHLH transcription factors Hand1 and Hand2 play critical regulatory roles for left ventricle (LV) cardiomyocyte proliferation and morphogenesis. Using an LV-specific Cre allele (Hand1LV-Cre), we ablate Hand1-lineage cardiomyocytes, revealing that
DTA
-mediated cardiomyocyte death results in a hypoplastic LV by E10.5. Once Hand1-linage cells are removed from the LV, and Hand1 expression is switched off, embryonic hearts recover by
E16
.5. In contrast, conditional LV loss-of-function of both Hand1 and Hand2 results in aberrant trabeculation and thickened compact zone myocardium resulting from enhanced proliferation and a breakdown of compact zone/trabecular/ventricular septal identity. Surviving Hand1;Hand2 mutants display diminished cardiac function that is rescued by concurrent ablation of Hand-null cardiomyocytes. Collectively, we conclude that, within a mixed cardiomyocyte population, removal of defective myocardium and replacement with healthy endogenous cardiomyocytes may provide an effective strategy for cardiac repair.
...
PMID:Hand factor ablation causes defective left ventricular chamber development and compromised adult cardiac function. 2873 25
In mammals, spermatogonial stem cells (SSCs) arise from a subpopulation of prospermatogonia during neonatal testis development. Currently, molecular mechanisms directing the prospermatogonia to spermatogonial transition are not well understood. In the study, we found that reducing Sertoli cells number by Amh-cre mediated expression of diphtheria toxin (AC;
DTA
) in murine fetal testis caused defects in prospermatogonia fate decisions. Histological and immunohistochemical analyses confirmed that Sertoli cells loss occurred at embryonic day (E) 14.5. Prospermatogonia maintained mitotic arrest at
E16
.5 in control animals, in contrast, 13.4% of germ cells in AC;
DTA
testis reentered cell cycle and expressed gH2A.X and Sycp3, indicating the commitment to meiosis. After birth, the number of prospermatogonia resuming mitosis was significantly affected by Sertoli cell loss in AC;
DTA
animals. Lastly, we isolated primary Sertoli cells using a Sertoli cell specific GFP reporter line and showed dynamics of Sertoli cell transcriptomes at E12.5, E13.5,
E16
.5 and P1. By further analysis, we revealed unique gene expression patterns and potential candidate genes regulating Sertoli cell development and likely mediating interactions between Sertoli cells, prospermatogonia and other testicular cells.
...
PMID:Function and transcriptomic dynamics of Sertoli cells during prospermatogonia development in mouse testis. 3295 85