This study was conducted to visualize the lobular distribution of enhanced mRNA expression levels of heat shock proteins (HSPs) in liver samples from carbon tetra chloride (CCl4)-treated mice using hybridization (ISH). Male BALB/c mice given a single oral administration of CCl4 were euthanized 6 hours or 1 day after the administration (6 h or 1 day). Paraffin-embedded liver samples were obtained, ISH for HSPs was conducted, as well as hematoxylin-eosin staining and immunohistochemistry (IHC).
View Article and Find Full Text PDFPurpose: To elucidate whether Institute for Cancer Research (ICR) derived retinal dysfunction (IRD) 1 and IRD2 mice, spontaneous mouse models of rod-cone and rod dysfunction, respectively, develop age-related retinal degeneration.
Materials And Methods: Morphological and morphometric examinations were performed in the retinas of both mutants from 1 to 18 months of age. The rate of apoptotic cell death was determined by TUNEL techniques.
ICR-derived retinal dysfunction (IRD) 1 and IRD2 mice are new spontaneous mouse models of rod-cone and rod dysfunctions, respectively. In this study, we investigated the cause of rod dysfunction in IRD1 and IRD2 mice. Gene expression of rod phototransduction proteins was analyzed by quantitative real-time RT-PCR.
View Article and Find Full Text PDFBackground: At present, it is difficult to visualize the internalization of surface receptors induced by ubiquitination that is taken place at the plasma membrane in mammals. This problem makes it difficult to reveal molecular basis for ubiquitination-mediated internalization in mammals.
Methodology/principle Findings: In order to overcome it, we have generated T-REx-c-MIR, a novel mammalian Tet-on B cell line using a constitutively active E3 ubiquitin ligase, c-MIR, and its artificial target molecule.
The presence of post-translational regulation of MHC class II (MHC II) under physiological conditions has been demonstrated recently in dendritic cells (DCs) that potently function as antigen-presenting cells (APCs). Here, we report that MARCH-I, an E3 ubiquitin ligase, plays a pivotal role in the post-translational regulation of MHC II in B cells. MARCH-I expression was particularly high in B cells, and the forced expression of MARCH-I induced the ubiquitination of MHC II.
View Article and Find Full Text PDFA novel E3 ubiquitin ligase family that consists of viral E3 ubiquitin ligases (E3s) and their mammalian homologues was recently discovered. These novel E3s are membrane-bound molecules that share the secondary structure and catalytic domain for E3 activity. All family members have two transmembrane regions at the center and a RING-CH domain at the amino terminus.
View Article and Find Full Text PDFWe previously reported a novel E3 ubiquitin ligase (E3), designated as c-MIR, which targets B7-2 to lysosomal degradation and down-regulates the B7-2 surface expression through ubiquitination of its cytoplasmic tail. B7-2 is well known as a costimulatory molecule for Ag presentation, suggesting that the manipulation of c-MIR expression modulates immune responses in vivo. To examine this hypothesis, we generated genetically modified mice in which c-MIR was expressed under an invariant chain (Ii) promoter.
View Article and Find Full Text PDFPurpose: We developed two strains of mouse with retinal dysfunction, named the ICR-derived retinal dysfunction (IRD)1 and IRD2, from one male ICR mouse with a retinal dysfunction but a normal fundus. The purpose of this study was to describe the features of retinal dysfunction in both mutant mice.
Methods: Scotopic and photopic electroretinograms (ERGs) were recorded from IRD1 and IRD2 mice at 1 month of age to evaluate retinal function, and then the structures of the retinas in both mutant mice were observed by light microscopy at 1 and 3 months of age.
Purpose: Substantial evidence indicates that supraoligomerization of the death receptors for Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is necessary for efficient activation of the apoptotic pathway. Bivalent IgG antibodies can induce the efficient apoptosis by mimicking the natural ligands but only after these antibodies are further oligomerized by cross-linking. In this study, we generated a novel agonist antibody to TRAIL receptor 2 (TRAIL-R2) capable of inducing apoptosis without cross-linking and elucidated its mode of action and efficacy.
View Article and Find Full Text PDFFibroblast growth factors (FGFs)/fibroblast growth factor receptor-3 signaling interferes with endochondral bone growth. However, the exact mechanisms by which FGFs inhibit endochondral ossification remain to be elucidated. In the present study, we utilized immunohistochemical techniques to clarify the effects of FGF-2 on the proximal tibial growth plate cartilage, when injected systemically into growing rats.
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