• Asian Pacific Journal of Cancer Prevention
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• v.13 no.9
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• pp.4827-4834
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• 2012

Tumor suppressor genes have received much attention for their roles in the development of human malignancies. Gelsolin has been found to be down-regulated in several types of human cancers, including leukemias. It is, however, expressed in macrophages, which are the final differentiation derivatives for the monocytic myeloid lineage, implicating this protein in the differentiation process of such cells. In order to investigate the role of gelsolin in leukaemic cell differentiation, stable clones over-expressing ectopic gelsolin, and a control clone were established from U937 leukaemia cells. Unlike the control cells, both gelsolin-overexpressing clones displayed retarded growth, improved monocytic morphology, increased NADPH and NSE activities, and enhanced surface expression of the ${\beta}$-integrin receptor, CD11b, when compared with the parental U937 cells. Interestingly, RT-PCR and western blot analysis also revealed that gelsolin enhanced p21CIP1 mRNA and protein expression in the overexpressing clones. Moreover, transient transfection with siRNA silencing P21CIP1, but not the control siRNA, resulted in a reduction in monocytic differentiation, accompanied by an increase in proliferation. In conclusion, our work demonstrates that gelsolin, by itself, is capable of inducing monocytic differentiation in U937 leukaemia cells, most probably through p21CIP1 activation.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.150.1-150.1
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• 2003

Gelsolin, a actin binding protein, has been demonstrated to be involved in controlling cell morphology, motility, signaling, and apoptosis. It's expression is frequently downregulated in cervix cancer and several types of different human cancers indicating the role of gesolin in suppression of tumorigenicity. Apicidin, a novel histone deacetylase inhibitor, has been shown to cause growth arrest and morphological change of cancer cells, resulting from the alternation of protein expression, such as p21^${WAF1/Cip1}$ and gelsolin. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.323.1-323.1
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• 2002

Apicidin ［cyclo(N-O-methyl-l -tryptophanyl-L -isoleucinyl-D-pipecolinyl-L-2-amino-8-oxodecano y)］. a histone deacetylase inhibitor. has been shown to cause growth arrest and morphological change of cancer cells. resulting from the alternation of protein expression. such as p21WAF1/Cip1 and gelsolin. However. proteome of altered by apicidin are poorly studied. In this study. we used a functional proteornics approach to identify the proteome altered by apicidin in Hela cells at 24hr post-treatment. (omitted)

• Annals of Clinical Neurophysiology
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• v.24 no.2
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• pp.90-92
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• 2022

AGel amyloidosis is an autosomal dominantly inherited disease caused by a GSN mutation, and affected patients typically present with the clinical triad of corneal lattice dystrophy, progressive cranial neuropathy, and cutis laxa. We report a Korean family with AGel amyloidosis with predominant manifestations of facial and bulbar muscle weakness. Whole-exome sequencing revealed a common missense mutation (p.Asp214Tyr) in GSN. This case strongly suggests that AGel amyloidosis should be considered when a patient presents with progressive facial and bulbar palsies.

• Biomedical Science Letters
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• v.9 no.4
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• pp.231-240
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• 2003

Deciphering the molecular interactions of proteins forming Z-lines is pivotal for understanding the regulation of myofibril assembly, sarcomeric organization, and mechanical properties of striated muscle. The purpose of this study is to searched for potential novel ligands of the Z-line portion of nebulin. In this study interacting proteins with intra-Z-line region of nebulin were screened using a yeast two-hybrid approach. The interaction was conformed by GST pull-down assay. We identified 269 residues within villin/gelsolin homology domain of supervillin that intreacts with the serine rich region of nebulin. The specific interactions of nebulin and supervillin were confirmed in vitro by GST pull-down experiments. Our data suggest that supervillin attaches directly to the Z-line through its interaction with the serine rich domain of nebulin in skeletal muscles. This interaction may link myofibrillar Z-discs to the membrane-associated complexes, costameres.

• Journal of Periodontal and Implant Science
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• v.26 no.4
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• pp.1003-1012
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• 1996

The induction of a phenotype with preoperties may have clinical significance in the acceleration of the wound-healing process. Wound contraction involves a specialized cell known as the myofibroblast. The myofibroblasts can be identified by their intense staining of actin bundles with anti-actin antibody. Tissue-specific actin distribution is correlated with the contractile activity of the myofibroblasts and smooth muscle etc. This study was performed to determine the expression of actin filaments in the cytoplasm of cultured human gingival fibroblsts after GaAs laser(BIOSAER, Korea) irradiation. Human gingival fibroblasts were cultured from explants of normal interdental gingival tissue. The third-generation fibroblasts were used for immunohistochemical study. The cultured fibroblasts were exposed $0.53joule/cm^2$(lmW, 7 mimutes) of energy density, and then observed by immunohistochemical method using, rabbit anti0gelsolin, hen smooth muscle polyclonal antibody(Chemicon international inc.), and biotinylated goat anti-rabbit IgG(Vectastain) 24-, 36-, 48-hour after laser irradiation Following results were obtained ; 1. In nonirradiated cultures, round shaped active fibroblasts with abundant cytoplasm and prominet nucleoli were observed. 2. In 24- and 36-hour cultures after laser irradiation, spindle shaped cells with long process were observed. The intensity of stain was seen in cytoplasm of these modified fibroblasts. 3. In 48-hoour cultures after laser irradiation, stained spindle shape cell were not observed. The results suggest that the effect of the galium-arsenide laser treatment on cultured gingival fibroblasts is the rapid development of cytoplasmic actin filaments.

• Molecules and Cells
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• v.26 no.1
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• pp.93-99
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• 2008

Transcriptional silencing is regulated by promoter methylation and histone modifications such as methylation and acetylation. We constructed a Schizosaccaromyces pombe reporter strain, KCT120a, to identify modifiers of transcriptional silencing, by inserting the $ura4^+$ gene into a heterochromatic telomere region. Two compounds inhibited the activity of histone deacetylases, induced acetylation of histone H3 and caused apoptotic cell death in HeLa cells. Expression of gelsolin and $p21^{waf1/cip1}$ also increased, as it does in response to HDAC inhibitors such as TSA. Therefore, these compounds appear to be potent inhibitors of HDACs, and hence potential anti-cancer drugs. Our observations suggest that a yeast cell-based assay system for transcriptional silencing may be useful for identifying histone deacetylase inhibitors and other agents affecting chromatin remodeling.