Notch signalling is critical for the development of the nervous system. In the zebrafish mind-bomb mutants, disruption of E3 ubiquitin ligase activity inhibits Notch signalling. In these utant embryos, precocious development of primary neurons leading to depletion of neural progenitor cells results in a neurogenic phenotype characterized by defects in neural patterning and brain development. Cyclin-dependent kinase 5 (Cdk5), a predominant neuronal kinase, is involved in a variety of essential functions of the nervous system. Most recently, mammalian studies on Notch and Cdk5 regulating each other’s function have been emerging. The status of Cdk5 in the mindbomb mutant embryos with excessive primary neurons is not known. In situ hybridization of the zebrafish mindbomb mutant embryos uncovered a robust upregulation in Cdk5 expression but with a reduced Cdk5 activity. The implications of these findings in both the mammalian system and zebrafish are discussed in this mini-review to provide a glimpse into the relationship between Notch and Cdk5 that may explain certain neurodevelopmental defects associated with either mutations in ubiquitin ligase or altered expression of Cdk5. and Corresponding author: Jyotshna Kanungo
Cardiac fibroblast-myofibroblast transformation (CMT) is a critical event in the initiation of myocardial fibrosis. Notch signaling has been shown to regulate myofibroblast transformation from other kinds of cells. However, whether Notch signaling is also involved in CMT remains unclear. In the present study, expressions of Notch receptors in cardiac fibroblasts (CFs) were examined, effects of Notch signaling inhibi tor N-[N-(3,5-difluorophenacetyl)- l-alanyl]-S-phenylglycine t-butyl ester (DAPT) and transforming growth factor-β1 (TGF-β1) on CMT were determined by increasing alpha-smooth muscle actin (α-SMA) expression and collagen synthesis, and Notch signaling was examined by analyzing expressions of Notch receptors. The results showed that: (1) Notch receptor 1, 2, 3 and 4 were all expressed in CFs; (2) DAPT promoted CMT in a time -dependent manner; (3) During the period of CMT induced by TGF-β1, expressions of Notch receptor 1, 3 and 4 in CFs were down-regulated, whereas there was no change for Notch receptor 2. Moreover, the downtrends of Notch 1, 3 and 4 were corresponding to the trend growth of α-SMA expression and collagen synthesis. These results suggested that inhibiting of Notch signaling might promote CMT. The down-regulations of Notch receptor 1, 3 and 4 induced by TGF-β1 may facilitate CMT. In conclusion, inhibition of Notch signaling might be a novel mech anism of CMT in myocardial fibrosis., Y.-H. Fan ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
In this note, we point out that Theorem 3.1 as well as Theorem 3.5 in G. D. Çaylı and F. Karaçal (Kybernetika 53 (2017), 394-417) contains a superfluous condition. We have also generalized them by using closure (interior, resp.) operators.
The paper discusses basics of calculus of backward fractional differences and sums. We state their definitions, basic properties and consider a special two-term linear fractional difference equation. We construct a family of functions to obtain its solution.
In this note we study fields $F$ with the property that the simple transcendental extension $F(u)$ of $F$ is isomorphic to some subfield of $F$ but not isomorphic to $F$. Such a field provides one type of solution of the Schröder-Bernstein problem for fields.
We study the stability of average optimal control of general discrete-time Markov processes. Under certain ergodicity and Lipschitz conditions the stability index is bounded by a constant times the Prokhorov distance between distributions of random vectors determinating the "original and the perturbated" control processes.