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RISS 인기검색어
- 검색키워드
- 저자 : Byun Mi Ran (검색결과 39 건)
- 무료
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- 유료
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Phorbaketal A stimulates osteoblast differentiation through TAZ mediated Runx2 activation
Byun, Mi Ran,Kim, A Rum,Hwang, Jun-Ha,Sung, Mi Kyung,Lee, Yeon Kyung,Hwang, Buyng Su,Rho, Jung-Rae,Hwang, Eun Sook,Hong, Jeong-Ho Elsevier 2012 FEBS letters Vol.586 No.8
<P><B>Highlights</B></P><P>► Phorbaketal A stimulates osteogenesis. ► Phorbaketal A increases TAZ-mediated osteoblast marker gene expression. ► ERK is an important kinase for phorbaketal A induced osteogenic differentiation. ► Phorbaketal A is suggested as a potential compound for stimulating bone formation.</P> <P><B>Abstract</B></P><P>Osteoporosis arises from an imbalance between osteoblastic bone formation and osteoclastic bone resorption. In this study, we screened molecules from marine natural products that stimulate osteoblast differentiation. We found that phorbaketal A significantly stimulates osteoblast differentiation in mesenchymal cells. Increased interaction of TAZ and Runx2 stimulated phorbaketal A-induced expression of osteoblastic marker genes. The activation of ERK was important for the stimulation of differentiation because an inhibitor of ERK blocked phorbaketal A-induced osteogenic differentiation. Taken together, the results showed that phorbaketal A stimulates TAZ-mediated osteoblast differentiation through the activation of ERK.</P><P><B>Structured summary of protein interactions</B></P><P><B>TAZ</B> physically interacts with <B>RUNX2</B> by pull down (View interaction)</P>
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Byun, Mi Ran,Kim, Cheol Hyun,Lee, Ho Sub,Choi, Jin Woo,Lee, Sang Kwan Elsevier 2019 Phytochemistry Vol.164 No.-
<P><B>Abstract</B></P> <P>Repositioning of plant extracts and chemical drugs can accelerate drug development. However, its success rate may depend on what the clue is for the repositioning. Recently, repositioning based on correction of unwarranted gene expression pattern has suggested the possibility of new drug development. Here, we designed a similar method for the repositioning of nutraceutical ginseng (<I>Panax ginseng</I> C.A.Mey.), which is one of the most validated natural therapeutic products for various diseases. We analyzed ginseng-induced gene expression profiles using the connectivity map algorithm, which is a database that connects diseases, chemical drugs, and gene expression. Ginseng was predicted to show the same effects as those of topoisomerase I inhibitors. In a subsequent <I>in vitro</I> assay, ginseng extract unwound coiled or supercoiled DNA, an effect comparable to that of the topoisomerase I inhibitor, camptothecin. Furthermore, ginseng extract induced synthetic lethality with suppression of the Werner syndrome gene. The collected data implicate ginseng as a candidate antitumor agent owing to its topoisomerase I inhibitory activity and further validate the usefulness of differentially expressed gene similarity-based repurposing of other natural products.</P> <P><B>Highlights</B></P> <P> <UL> <LI> A functional similarity between natural extracts and already known drugs was analyzed based on gene expression patterns. </LI> <LI> Target of natural products can be predicted by such an analysis. </LI> <LI> <I>Panax ginseng</I>extract intervenes topoisomerase I activity as effectively as the professional inhibitors like camptothecin. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>- Gene expression patterns between ginseng and other chemical drugs was compared. - The analysis revealed inhibitory effect of ginseng against topoisomerase I activity.</P> <P>[DISPLAY OMISSION]</P>
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Byun, Mi Ran,Sung, Mi Kyung,Kim, A Rum,Lee, Cham Han,Jang, Eun Jung,Jeong, Mi Gyeong,Noh, Minsoo,Hwang, Eun Sook,Hong, Jeong-Ho American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.14
<P>Osteoporosis is a degenerative bone disease characterized by low bone mass and is caused by an imbalance between osteoblastic bone formation and osteoclastic bone resorption. It is known that the bioactive compounds present in green tea increase osteogenic activity and decrease the risk of fracture by improving bone mineral density. However, the detailed mechanism underlying these beneficial effects has yet to be elucidated. In this study, we investigated the osteogenic effect of (−)-epicatechin gallate (ECG), a major bioactive compound found in green tea. We found that ECG effectively stimulates osteoblast differentiation, indicated by the increased expression of osteoblastic marker genes. Up-regulation of osteoblast marker genes is mediated by increased expression and interaction of the transcriptional coactivator with PDZ-binding motif (TAZ) and Runt-related transcription factor 2 (RUNX2). ECG facilitates nuclear localization of TAZ through PP1A. PP1A is essential for osteoblast differentiation because inhibition of PP1A activity was shown to suppress ECG-mediated osteogenic differentiation. Taken together, the results showed that ECG stimulates osteoblast differentiation through the activation of TAZ and RUNX2, revealing a novel mechanism for green tea-stimulated osteoblast differentiation.</P>
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SRC activates TAZ for intestinal tumorigenesis and regeneration
Byun, Mi Ran,Hwang, Jun-Ha,Kim, A Rum,Kim, Kyung Min,Park, Jung Il,Oh, Ho Taek,Hwang, Eun Sook,Hong, Jeong-Ho Elsevier 2017 Cancer letters Vol.410 No.-
<P><B>Abstract</B></P> <P>Proto-oncogene tyrosine-protein kinase Src (cSRC) is involved in colorectal cancer (CRC) development and damage-induced intestinal regeneration, although the cellular mechanisms involved are poorly understood. Here, we report that transcriptional coactivator with PDZ binding domain (TAZ) is activated by cSRC, regulating CRC cell proliferation and tumor formation, where cSRC overexpression increases TAZ expression in CRC cells. In contrast, knockdown of <I>cSRC</I> decreases TAZ expression. Additionally, direct phosphorylation of TAZ at Tyr316 by cSRC stimulates nuclear localization and facilitates transcriptional enhancer factor TEF-3 (TEAD4)-mediated transcription. However, a TAZ phosphorylation mutant significantly decreased cell proliferation, wound healing, colony forming, and tumor formation. In a CRC mouse model, <I>Apc</I> <SUP> <I>Min/+</I> </SUP>, activated SRC expression was associated with increased TAZ expression in polyps and TAZ depletion decreased polyp formation. Moreover, intestinal TAZ knockout mice had intestinal regeneration defects following γ-irradiation. Finally, significant correspondence between SRC activation and TAZ overexpression was observed in CRC patients. These results suggest that TAZ is a critical factor for SRC-mediated intestinal tumor formation and regeneration.</P> <P><B>Highlights</B></P> <P> <UL> <LI> TAZ is activated by cSRC in colorectal cell proliferation and tumor formation. </LI> <LI> cSRC phosphorylates TAZ at Tyr316 and stimulates nuclear localization of TAZ and facilitates TEAD4-mediated transcription. </LI> <LI> In <I>Apc</I> <SUP> <I>Min/+</I> </SUP>mouse, TAZ depletion decreases polyp formation. </LI> <LI> Intestinal specific TAZ knockout mice have intestinal regeneration defects following γ-irradiation. </LI> <LI> Correspondence between SRC activation and TAZ overexpression is observed in CRC patients. </LI> </UL> </P>
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Clioquinol induces autophagy in cultured astrocytes and neurons by acting as a zinc ionophore
Park, Mi-Ha,Lee, Sook-Jeong,Byun, Hyae-ran,Kim, Yunha,Oh, Young J.,Koh, Jae-Young,Hwang, Jung Jin Elsevier 2011 Neurobiology of disease Vol.42 No.3
<P><B>Abstract</B></P><P>Recent studies have demonstrated that clioquinol, an antibiotic with an anti-amyloid effect, acts as a zinc ionophore under physiological conditions. Because increases in labile zinc may induce autophagy, we examined whether clioquinol induces autophagy in cultured astrocytes in a zinc-dependent manner.</P><P>Within 1h of exposure to 0.1–10μM clioquinol, the levels of microtubule-associated protein 1 light chain 3 (LC3)-II, a marker of autophagy, began to increase in astrocytes. Confocal live-cell imaging of GFP-LC3-transfected astrocytes showed the formation of LC3(+) autophagic vacuoles (AVs), providing a further indication that clioquinol induced autophagy. Addition of 3-methyladenine or small-interfering RNA against autophagy-related gene 6 (ATG6/Beclin-1) blocked clioquinol-induced increases in LC3-II. FluoZin-3 fluorescence microscopy showed that, like the zinc ionophore pyrithione, clioquinol increased intracellular zinc levels in the cytosol and AVs in an extracellular zinc-dependent manner. Zinc chelation with N,N,N′,N′-tetrakis-(2-pyridylmethyl) ethylenediamine (TPEN) reduced, and addition of zinc increased the levels of LC3-II and LC3(+) puncta, indicating that zinc influx plays a key role therein. Moreover, astrocytes and SH-SY5Y cells expressing mutant huntingtin (mHttQ74) accumulated less aggregates when treated with clioquinol, and this effect was reversed by TPEN. These results indicate that clioquinol-induced autophagy is likely to be physiologically functional.</P><P>The present study demonstrates that clioquinol induces autophagy in a zinc-dependent manner and contributes to clearance of aggregated proteins in astrocytes and neurons. Hence, in addition to its metal-chelating effect in and around amyloid beta (Aβ) plaques, clioquinol may contribute to the reduction of Aβ loads by activating autophagy by increasing or normalizing intracellular zinc levels in brain cells.</P> <P><B>Research Highlights</B></P><P>► Clioquinol acts as a zinc ionophore and introduces zinc into autophagic vacuoles. ► Clioquinol induces autophagy in astrocytic cultures in a zinc-dependent manner. ► Autophagy induced by clioquinol reduces accumulation of huntingtin aggregates. ► Excessive clioquinol induces autophagic cell death especially in neurons. ► In conclusion, adequate doses of clioquinol may have beneficial actions in the Alzheimer's Diseases brains.</P>
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Son, A-Ran,Kim, Min-Seuk,Jo, Hae,Byun, Hae-Mi,Shin, Dong-Min The Korean Society of Pharmacology 2012 The Korean Journal of Physiology & Pharmacology Vol.16 No.1
The receptor activator of NF-${\kappa}B$ ligand (RANKL) signal is an activator of tumor necrosis factor receptor-associated factor 6 (TRAF6), which leads to the activation of NF-${\kappa}B$ and other signal transduction pathways essential for osteoclastogenesis, such as $Ca^{2+}$ signaling. However, the intracellular levels of inositol 1,4,5-trisphosphate ($IP_3$) and $IP_3$-mediated cellular function of RANKL during osteoclastogenesis are not known. In the present study, we determined the levels of $IP_3$ and evaluated $IP_3$-mediated osteoclast differentiation and osteoclast activity by RANKL treatment of mouse leukemic macrophage cells (RAW 264.7) and mouse bone marrow-derived monocyte/macrophage precursor cells (BMMs). During osteoclastogenesis, the expression levels of $Ca^{2+}$ signaling proteins such as $IP_3$ receptors ($IP_3Rs$), plasma membrane $Ca^{2+}$ ATPase, and sarco/endoplasmic reticulum $Ca^{2+}$ ATPase type2 did not change by RANKL treatment for up to 6 days in both cell types. At 24 h after RANKL treatment, a higher steady-state level of $IP_3$ was observed in RAW264.7 cells transfected with green fluorescent protein (GFP)-tagged pleckstrin homology (PH) domains of phospholipase C (PLC) ${\delta}$, a probe specifically detecting intracellular $IP_3$ levels. In BMMs, the inhibition of PLC with U73122 [a specific inhibitor of phospholipase C (PLC)[ and of $IP_3Rs$ with 2-aminoethoxydiphenyl borate (2APB; a non-specific inhibitor of $IP_3Rs$) inhibited the generation of RANKL-induced multinucleated cells and decreased the bone-resorption rate in dentin slice, respectively. These results suggest that intracellular $IP_3$ levels and the $IP_3$-mediated signaling pathway play an important role in RANKL-induced osteoclastogenesis.
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기초간호자연과학의 병태생리학, 병원미생물, 약물의 기전과 효과 내용별 필요도에 대한 연구
최명애,변영순,서영숙,황애란,김희승,홍해숙,박미정,최스미,이경숙,서화숙,신기수 대한기초간호자연과학회 2000 Journal of korean biological nursing science Vol.2 No.1
The purpose of this study was to define the content of the requisite knowledge of pathophysiology, clinical microbiology, and mechanisms and effects of drugs needed for clinical knowledge for nursing practice. Contents of knowledge on pathological physiology, clinical microbiology, and mechanisms and effects of drugs were constructed from syllabus of basic nursing subjects in 4 colleges of nursing, and textbooks. The degree of need of 72 items was measured with a 4 point scale. The subjects of this study were college-graduated 136 nurses from seven university hospitals in Seoul and three in Chonnam Province, Kyungbook Province, and Inchon. They have been working at internal medicine ward, surgical ward, intensive care unit, obstetrics and gynecology ward, pediatrics ward, opthalmology ward, ear, nose, and throat ward, emergency room, rehabilitation ward, cancer ward, and hospice ward. The results were as follows : 1. The highest scored items of the knowledge of pathophysiology, clinical microbiology, and mechanisms and effects of drugs necessary for nursing practice were side effects of drugs, anticoagulants, mechanisms of drugs, antihypertensive drugs, tolerance and addiction of drugs, interactions among drugs, hospital infection in the order of importance. The lowest scored item was structure of microrganisms. 2. The highest order of need according to unit was repair in tissue injury unit, definition·etiology·classification of inflammation in inflammation unit, trasplantation and immunologic response in alterations in immunity unit, thrombus and thrombosis in disorders of cardiovascular function unit, gene disorders in genetic disorders unit, hospital infection in infection unit, virus in microrganisms unit, side reactions of drugs in introduction unit, anticonvulsants in drugs for central nervous system unit, local anesthesia in anesthesia unit, anticoagulants in drugs for cardiovascular system unit, anti-inflammatory drugs in antibiotics unit, anti-ulcer drugs in drugs for digestive system unit, and bronchodilators in drugs for respiratory system unit. 3. The common content of the knowledge of pathophysiology, clinical microbiology, and mechanisms and effects of drugs needed for all clinical areas in nursing were side effects of drugs, anticoagulants, interactions among drugs, and hospital infection. However, the degree of need of each pathological physiology, clinical microbiology, and mechanisms and effects of drugs was different depending on clinical areas. 4. Significant differences in the knowledge of pathophysiology, clinical microbiology, and mechanisms and effects of drugs necessary for nursing practice such as tissue changes due to injurious stimuli, degenerative changes of tissue, alterations in metabolism of carbohydrates, ischemia, hyperemia and congestion, hospital infection, structure of microorganism, classification of microorganism, bacteria, virus, antidepressants, antipsychotic drugs, antiemetic drugs, antiparkinsonism drugs, antianxiety drugs, antibiotics, tuberculostatics, antiviral drugs, antifungal drugs, parasiticides, antiulcer drugs, antidiarrheais, and anti constipation drugs were shown according to the work area. 5. Significant differences in the knowledge of pathophysiology, clinical microbiology, and mechanisms and effects of drugs necessary for nursing practice such as transplantation and immunologic response, alterations in the metabolism of uric acid, structure of microorganism, classification of microorganism, immunosuppresants, drugs for congestive heart failure were demonstrated according to the duration of work. Based on these findings, all the 72 items constructed by Korean Academic Society of Basic Nursing Science should be included as contents of the knowledge of pathophysiology, clinical microbiology. and mechanisms and effects of drugs
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