Iyoko Katoh

TL;DR: In p53-deficient cells, p51A induced growth-suppression and apoptosis, and up-regulated p21waf-1 through p53 regulatory elements, and expression of p5I mRNA was found in a limited number of tissues, including skeletal muscle, placenta, mammary glands, prostate, trachea, thymus, salivary gland, uterus, heart and lung.

TL;DR: In this article, a protease was purified from Moloney murine leukemia virus (Mo-MuLV) and a sequence was determined and aligned with the amino acid sequence deduced from the DNA sequence by other workers, and the map order of the gag-pol gene was proposed to be 5'-p15-p12-p30p10-protease-reverse transcriptase-endonuclease-3'.

TL;DR: P51A induces differentiation under genotoxic circumstances and there may be cellular factors that control p51A protein stability and transactivating ability, which suggest the possibility that p53-accumulated cells underwent apoptosis without exhibiting the feature of erythroid differentiation.

TL;DR: Results indicate that the cellular signaling cascades activated by pro-inflammatory cytokines and environmental stresses are also activated as a result of lytic infection with SV, and may contribute to the delayed onset of apoptosis in the host cells and the facilitation of viral replication.

TL;DR: Results indicate a homotypic interaction dependent on the presumed oligomerization domain of the p51 proteins, which may function in biological processes apart from p53.