• BMB Reports
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• v.46 no.12
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• pp.617-622
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• 2013

Rac1 plays a key role in neurite outgrowth via reorganization of the actin cytoskeleton. The molecular mechanisms underlying Rac1-mediated actin dynamics in the cytosol and plasma membrane have been intensively studied, but the nuclear function of Rac1 in neurite outgrowth has not yet been addressed. Using subcellular fractionation and immunocytochemistry, we sought to explore the role of nuclear Rac1 in neurite outgrowth. bFGF, a strong agonist for neurite outgrowth in PC12 cells, stimulated the nuclear accumulation of an active form of Rac1. Rac1-PBR (Q) mutant, in which six basic residues in the polybasic region at the C-terminus were replaced by glutamine, didn't accumulate in the nucleus. In comparison with control cells, cells expressing this mutant form of Rac1 displayed a marked defect in extending neurites that was concomitant with reduced expression of MAP2 and MEK-1. These results suggest that Rac1 translocation to the nucleus functionally correlates with bFGF-induced neurite outgrowth.

• BMB Reports
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• v.53 no.4
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• pp.173-180
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• 2020

Galectin-3 is a carbohydrate-binding protein and regulates diverse functions, including cell proliferation and differentiation, mRNA splicing, apoptosis induction, immune surveillance and inflammation, cell adhesion, angiogenesis, and cancer-cell metastasis. Galectin-3 is also recommended as a diagnostic or prognostic biomarker of various diseases, including heart disease, kidney disease, and cancer. Galectin-3 exists as a cytosol, is secreted in extracellular spaces on cells, and is also detected in nuclei. It has been found that galectin-3 has different functions in cellular localization: (i) Extracellular galectin-3 mediates cell attachment and detachment. (ii) cytosolic galectin-3 regulates cell survival by blocking the intrinsic apoptotic pathway, and (iii) nuclear galectin-3 supports the ability of the transcriptional factor for target gene expression. In this review, we focused on the role of galectin-3 on translocation from cytosol to nucleus, because it happens in a way independent of carbohydrate recognition and accelerates cancer progression. We also suggested here that intracellular galecin-3 could be a potent therapeutic target in cancer therapy.

• Journal of Microbiology and Biotechnology
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• v.18 no.1
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• pp.171-175
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• 2008

Here, we report that Vibrio parahaemolyticus induces a rapid remodeling of macrophage actin and activates RhoB GTPase. Mutational analysis revealed that the effects depend on type III secretion system 1 regulated translocation of a V. parahaemolyticus effector protein, VP1686, into the macrophages. Remodeling of actin is shown to be necessary for increased bacterial uptake followed by initiation of apoptosis in macrophages. This provides evidence for functional association of the VP1686 in triggering an eat me-and-die signal to the host.

• Journal of Soil and Groundwater Environment
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• v.20 no.4
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• pp.8-14
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• 2015

Plants grown in metal-contaminated sites have to be managed and disposed of safely even in phytoremediation because heavy metals can be transferred to other organisms through the food chain, which could result in bioaccumulation in organisms of a higher trophic level. However, if the harvested plants could be used for bioenergy, the ecological risk is reduced and phytoremediation improves economic feasibility. This study researched the effects of EDDS (Ethylenediamine disuccinate) on the heavy metal uptake performance of Brassica campetris and Sorghum biocolor, both of which have potential as bioenergy plants. The results showed that EDDS could increase Pb, Cu, Ni, Cd, and Zn concentrations in the roots and shoots of both of these plants. Furthermore, EDDS reduced the metal inhibition of the S. bicolor length growth. The translocation factors (TF) of S. bicolor and B. campestris are smaller than one for all five heavy metals tested and decreased by the following order: heavy metal + EDDS > heavy metals only > uncontaminated soil. The results suggest that with regard to plant growth and metal accumulation, S. bicolor treated with EDDS is more suitable than is B. campestris for the phytoremediation of soils contaminated with multiple metal species.

• Molecules and Cells
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• v.22 no.2
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• pp.203-209
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• 2006

TBP (TATA-binding protein)-related factor 2 (TRF2) regulates transcription during a nuber of cellular processes. We previously demonstrated that it is localized in the cytoplasm and is translocated to the nucleus by DNA-damaging agents. However, the cytoplasmic localization of TRF2 is controversial. In this study, we reconfirmed its cytoplasmic localization in various ways and examined its nuclear migration. Stresses such as heat shock, redox agents, heavy metals, and osmotic shock did not affect localization whereas genotoxins such as methyl methanesulfonate (MMS), cisplatin, etoposide, and hydroxyurea caused it to migrate to the nucleus. Adriamycin, mitomycin C and ${\gamma}$-rays had no obvious effect. We determined optimal conditions for the nuclear migration. The proportions of cells with nuclei enriched for TRF2 were 25-60% and 5-10% for stressed cells and control cells, respectively. Nuclear translocation was observed after 1 h, 4 h and 12 h for cisplatin, etoposide and MMS and hydroxyurea, respectively. The association of TRF2 with the chromatin and promoter region of the proliferating cell nuclear antigen (PCNA) gene, a putative target of TRF2, was increased by MMS treatment. Thus TRF2 may be involved in genotoxin-induced transcriptional regulation.

• Journal of Periodontal and Implant Science
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• v.41 no.3
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• pp.157-163
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• 2011

Purpose: Curcumin is known to exert numerous biological effects including anti-inflammatory activity. In this study, we investigated the effects of curcumin on the production of interleukin-6 (IL-6) by murine macrophage-like RAW 264.7 cells stimulated with lipopolysaccharide (LPS) from Prevotella intermedia, a major cause of inflammatory periodontal disease, and sought to determine the underlying mechanisms of action. Methods: LPS was prepared from lyophilized P. intermedia ATCC 25611 cells by the standard hot phenol-water method. Culture supernatants were collected and assayed for IL-6. We used real-time polymerase chain reaction to detect IL-6 mRNA expression. $I{\kappa}B-{\alpha}$ degradation, nuclear translocation of NF-${\kappa}B$ subunits, and STAT1 phosphorylation were characterized via immunoblotting. DNA-binding of NF-${\kappa}B$ was also analyzed. Results: Curcumin strongly suppressed the production of IL-6 at both gene transcription and translation levels in P. intermedia LPS-activated RAW 264.7 cells. Curcumin did not inhibit the degradation of $I{\kappa}B-{\alpha}$ induced by P. intermedia LPS. Curcumin blocked NF-${\kappa}B$ signaling through the inhibition of nuclear translocation of NF-${\kappa}B$ p50 subunit. Curcumin also attenuated DNA binding activity of p50 and p65 subunits and suppressed STAT1 phosphorylation. Conclusions: Although further study is required to explore the detailed mechanism of action, curcumin may contribute to blockade of the host-destructive processes mediated by IL-6 and appears to have potential therapeutic values in the treatment of inflammatory periodontal disease.

• Asian-Australasian Journal of Animal Sciences
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• v.30 no.7
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• pp.944-949
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• 2017

Objective: Investigated the effect and mechanism of ascorbic acid on the development of porcine embryos produced by somatic cell nuclear transfer (SCNT). Methods: Porcine embryos were produced by SCNT and cultured in the presence or absence of ascorbic acid. Ten-eleven translocation 3 (TET3) in oocytes was knocked down by siRNA injection. After ascorbic acid treatment, reprogramming genes were analyzed by realtime reverse transcription-polymerase chain reaction (RT-PCR). Furthermore, relative 5-methylcytosine and 5-hydroxymethylcytosine content in pronucleus were detected by realtime PCR. Results: Ascorbic acid significantly increased the development of porcine embryos produced by SCNT. After SCNT, transcript levels of reprogramming genes, Pou5f1, Sox2, and Klf were significantly increased in blastocysts. Furthermore, ascorbic acid reduced 5-methylcytosine content in pronuclear embryos compared with the control group. Knock down of TET3 in porcine oocytes significantly prevents the demethylation of somatic cell nucleus after SCNT, even if in the presence of ascorbic acid. Conclusion: Ascorbic acid enhanced the development of porcine SCNT embryos via the increased TET3 mediated demethylation of somatic nucleus.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.16 no.2
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• pp.119-137
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• 2003

Younggaechulgam-tang has been used for treating skin diseases. In this study, I investigated the immunosuppressive effect of Younggaechul-tang in the human T cell line MOLT-4 cells. MOLT-4 cells were stimulated with the phytohemagglutinin (PHA) and phorbol 12-myristate 13-acetate (PMA) + A23187. The secretion appeared to be greater when cells were stimulated with PHA than with PMA + A23187. Younggaechulgam-tang had no affect proliferation stimulated by PHA. I showed that IL-2 secretion and expression by PHA stimulated MOLT-4 cells were inhibited by Younggaechugam-tang treatment. Maximal inhibition rate of IL-2, TNF-${\alpha}$ secretion was 80$\%$ and 30$\%$, respectively. Younggaechulgam-tang also inhibited nuclear translocation of p65 subunit of nuclear factor-kB and nuclear factor of activated T cells (NFAT). In conclusion, these results suggest that Younggaechulgam-tang may contribute to the immunosuppressive oriental drug clinically.

• Animal cells and systems
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• v.12 no.4
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• pp.211-217
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• 2008

Bax, a pro-apoptotic member of Bcl-2 family proteins, plays a central role in the mitochondria-dependent apoptosis. Apoptotic signals induce the translocation of Bax from cytosol into the mitochondria, which triggers the release of apoptogenic molecules such as cytochrome C and apoptosis-inducing factor, AIF. Bax-inhibiting peptide(BIP) is a cell permeable peptide comprised of five amino acids designed from the Bax-interaction domain of Ku70. Because BIP inhibits Bax translocation and Bax-mediated release of cytochrome C, BIP suppresses Bax-dependent apoptosis. In this study, we observed that BIP inhibited staurosporine-induced neuronal death in cultured cerebral cortex and cerebellar granule cells, but BIP failed to rescue granule cells from trophic signal deprivation-induced neuronal death, although both staurosporine-induced and trophic signal deprivation-induced neuronal death are dependent on Bax. These findings suggest that the mechanisms of the Bax activation may differ depending on the type of cell death induction, and thus BIP exhibits selective suppression of a subtype of Bax-dependent neuronal death.

• BMB Reports
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• v.29 no.6
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• pp.507-512
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• 1996

The NADPH oxidase of phagocytes catalyzes the reduction of oxygen to $O_{2}^{-}$ at the expense of NADPH The enzyme is dormant in resting neutrophils and hecomes activated on stimulation. During activation. $p47^{phox}$ (phagocyte oxidase factor), a cytosolic oxidase subunit, becomes extensively phosphorylated on a number of serines located between S303-S379. Although the biochemical role of phosphorylation is speculative, it has been suggested that phosphorylation could neutralize the strongly cationic C-terminal which may result in the change of conformation of $p47^{phox}$ and subsequent translocation of this protein and other cytosolic components to the membrane. In order to mimic the effect of phosphorylation in terms of neutralizing the positive charges, recombinant $p47^{phox}$ was treated with phenylglyoxal, which removes positive charges of arginine residues. Modification of recombinant $p47^{phox}$ resulted in the activation of oxidase in a cell-free translocation system as well as a conformational change in recombinant $p47^{phox}$ which may be responsible for the activation of the enzyme.