Human LANP/ANP (26-55), prepro ELISA Kit

pp32 (ANP32A) is a nuclear phosphoprotein expressed as a nomnutated form in self-renewing cell populations and neoplastic cells. Mechanistically, PP32 may regulate pathways important in the process of differentiation as part of separate complexes inhibiting histone acetylation and regulating immediate-early and cytokine mRNA stability. Prostatic adenocarcinomas express pp32 in a differentiation related manner-well-differentiated tumors express lower levels of PP32 than poorly differentiated tumors. In benign prostate, PP32 is expressed in basal cells but not in terminally differentiated glandular cells. Based on these observations, we hypothesized that reduction of pp32 expression might be an important differentiation signal. We used antisense pp32 and RNAi transfection to study the effects of reduced pp32 expression in the TSU-Pr1 carcinoma cell line. pp32 reduction induced Tsu-Pr1 cells to differentiate into neuronal-like cells with associated inhibition of growth. Reduction of pp32 and consequent differentiation were accompanied by a marked reduction in expression of SET, which complexes with PP32, by a marked change in acetylation status of histone 114, and by further differential expression of genes in differentiation pathways. Thus, reduction of PP32 in the undifferentiated TSU-Pr1 neoplastic cell line induces differentiation and thus may be an element of a differentiation control pathway in both normal and neoplastic cells.

In this study, to clarify the protective mechanism of a peptide from shrimp anti-lipopolysaccharide (LPS) factor (SALF) against endotoxin shock, we evaluated the effects of the SALF and LPS on the production and release of tumor necrosis factor (TNF)-alpha in vitro using the RAW264.7 murine macrophage cell line. Stimulation by LPS induced the production of inflammatory cytokines, and the SALF was able to modulate TNF-alpha production in LPS-stimulated RAW264.7 cells. Microarray studies revealed a transcriptional profile which was assessed in the presence or absence of the SALF by a quantitative real-time polymerase chain reaction. Pretreatment with the SALF significantly downregulated the expression of nuclear factor (NF)-kappa B in the presence of LPS. In contrast, pretreatment with the SALF significantly elevated the expressions of Anp32a, CLU, and SLPI, which are considered to be immune-related genes in the presence of LPS. Inhibitor studies suggested that the SALF's modulation of LPS-induced TNF-alpha production involved a complex mechanism with mitogen-activated protein kinase kinase, calcium, and protein kinase C. The data from this study, which imply that the SALF can suppress TNF-alpha production, suggest a role for the SALF in the defense mechanism which can potentially be applied to mammals for endotoxin treatment. (C) 2010 Elsevier Inc. All rights reserved.