In Vivo Notch Signaling Blockade Induces Abnormal Spermatogenesis in the Mouse
نویسندگان
چکیده
منابع مشابه
In Vivo Notch Signaling Blockade Induces Abnormal Spermatogenesis in the Mouse
In a previous study we identified active Notch signaling in key cellular events occurring at adult spermatogenesis. In this study, we evaluated the function of Notch signaling in spermatogenesis through the effects of in vivo Notch blockade. Adult CD1 male mice were either submitted to a long term DAPT (?-secretase inhibitor) or vehicle treatment. Treatment duration was designed to attain one h...
متن کاملAbnormal cerebellar signaling induces dystonia in mice.
Dystonia is a relatively common neurological syndrome characterized by twisting movements or sustained abnormal postures. Although the basal ganglia have been implicated in the expression of dystonia, recent evidence suggests that abnormal cerebellar function is also involved. In these studies, a novel mouse model was developed to study the role of the cerebellum in dystonia. Microinjection of ...
متن کاملphylogeography and genetic diversity of the lesser mouse- eared bat (myotis blythii) in iran
in current study, 63 samples of bat populations collected from differ regions were used for evaluating the geographic variations. twenty cranial and dental characters for traditional morphometric and landmarks method on the ventral, dorsal skull and mandible for geometry morphometric studies were used. statistical analyses of traditional morphometric and geometry morphometric data indicated low...
Activation of Notch1 signaling in cardiogenic mesoderm induces abnormal heart morphogenesis in mouse.
Notch signaling is implicated in many developmental processes. In our current study, we have employed a transgenic strategy to investigate the role of Notch signaling during cardiac development in the mouse. Cre recombinase-mediated Notch1 (NICD1) activation in the mesodermal cell lineage leads to abnormal heart morphogenesis, which is characterized by deformities of the ventricles and atrioven...
متن کاملNotch signaling maintains Leydig progenitor cells in the mouse testis.
During testis development, fetal Leydig cells increase their population from a pool of progenitor cells rather than from proliferation of a differentiated cell population. However, the mechanism that regulates Leydig stem cell self-renewal and differentiation is unknown. Here, we show that blocking Notch signaling, by inhibiting gamma-secretase activity or deleting the downstream target gene Ha...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: PLoS ONE
سال: 2014
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0113365