Assessment system of artillery firing tasks of antiaircraft units

W pracy opisano przeznaczenie, budowę i zasadę działania opracowywanego systemu określania odległości przelotu pocisku względem ruchomej tarczy powietrznej, ze szczególnym uwzględnieniem fizycznych uwarunkowań możliwości detekcji zaburzeń ośrodka wywołanych ruchem pocisku z prędkością naddźwiękową. Przedstawiono wybrane wyniki badań laboratoryjnych i poligonowych urządzenia.The purpose, construction and operation of the developed system for determining the projectile miss distance with respect to movement air shield are described in this paper, with particular emphasis on the physical conditions of the possibility of medium disturbances detection caused by a projectile motion with a supersonic speeds. Selected results of laboratory and firing field tests of device are presented

Non–SCF-type F-box protein Roy1/Ymr258c interacts with a Rab5-like GTPase Ypt52 and inhibits Ypt52 function

Non–SCF-type F-box protein Roy1 interacts with the Rab5-like small GTPase Ypt52. Skp1 is indispensable for the interaction of Roy1 and Ypt52. Roy1 binds to GDP and the nucleotide-free form of Ypt52 and inhibits the formation of GTP-bound, active Ypt52. Roy1 negatively modulates cell viability and intracellular transport by suppressing Ypt52

Notch-induced Asb2 expression promotes protein ubiquitination by forming non-canonical E3 ligase complexes

Notch signaling controls multiple developmental processes, thus demanding versatile functions. We have previously shown that this may be partly achieved by accelerating ubiquitin-mediated degradation of important regulators of differentiation. However, the underlying mechanism was unknown. We now find that Notch signaling transcriptionally activates the gene encoding ankyrin-repeat SOCS box-containing protein 2 (Asb2). Asb2 promotes the ubiquitination of Notch targets such as E2A and Janus kinase (Jak) 2, and a dominant-negative (DN) mutant of Asb2 blocks Notch-induced degradation of these proteins. Asb2 likely binds Jak2 directly but associates with E2A through Skp2. We next provide evidence to suggest that Asb2 bridges the formation of non-canonical cullin-based complexes through interaction with not only ElonginB/C and Cullin (Cul) 5, but also the F-box-containing protein, Skp2, which is known to associate with Skp1 and Cul1. Consistently, ablating the function of Cul1 or Cul5 using DN mutants or siRNAs protected both E2A and Jak2 from Asb2-mediated or Notch-induced degradation. By shifting monomeric E3 ligase complexes to dimeric forms through activation of Asb2 transcription, Notch could effectively control the turnover of a variety of substrates and it exerts diverse effects on cell proliferation and differentiation