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RISS 인기검색어
- 검색키워드
- 주제어 : Mxi1 (검색결과 3 건)
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Ko, Je Yeong,Yoo, Kyung Hyun,Song, Seon Ah,Kim, Do Yeon,Kong, Hyun Kyung,Ahn, Curie,Lee, Han Woong,Kang, Duk-Hee,Oh, Goo Taeg,Park, Jong Hoon American Society for Biochemistry and Molecular Bi 2013 JOURNAL OF BIOLOGICAL CHEMISTRY - Vol.288 No.9
<P>Cilia in ciliated cells consist of protruding structures that sense mechanical and chemical signals from the extracellular environment. Cilia are assembled with variety molecules via a process known as intraflagellar transport (IFT). What controls the length of cilia in ciliated cells is critical to understand ciliary disease such as autosomal dominant polycystic kidney disease, which involves abnormally short cilia. But this control mechanism is not well understood. Previously, multiple tubular cysts have been observed in the kidneys of max-interacting protein 1 (<I>Mxi1</I>)-deficient mice aged 6 months or more. Here, we clarified the relationship between Mxi1 inactivation and cilia disassembly. Cilia phenotypes were observed in kidneys of <I>Mxi1</I>-deficient mice using scanning electron microscopy to elucidate the effect of Mxi1 on renal cilia phenotype, and cilia disassembly was observed in <I>Mxi1</I>-deficient kidney. In addition, genes related to cilia were validated <I>in vitro</I> and <I>in vivo</I> using quantitative PCR, and <I>Ift20</I> was selected as a candidate gene in this study. The length of cilium decreased, and <I>p</I>-ERK level induced by a cilia defect increased in kidneys of <I>Mxi1</I>-deficient mice. Ciliogenesis of <I>Mxi1</I>-deficient mouse embryonic fibroblasts (MEFs) decreased, and this abnormality was restored by <I>Mxi1</I> transfection in <I>Mxi1</I>-deficient MEFs. We confirmed that ciliogenesis and <I>Ift20</I> expression were regulated by Mxi1 <I>in vitro</I>. We also determined that Mxi1 regulates <I>Ift20</I> promoter activity via Ets-1 binding to the <I>Ift20</I> promoter. These results indicate that inactivating Mxi1 induces ciliary defects in polycystic kidney.</P>
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Mxi1 influences cyst formation in three-dimensional cell culture
( Yeon Joo Yook ),( Kyung Hyun Yoo ),( Seon Ah Song ),( Min Ji Seo ),( Je Yeong Ko ),( Bo Hye Kim ),( Eun Ji Lee ),( Eunsun Chang ),( Yu Mi Woo ),( Jong Hoon Park ) 생화학분자생물학회 (구 한국생화학분자생물학회) 2012 BMB Reports Vol.45 No.3
Cyst formation is a major characteristic of ADPKD and is caused by the abnormal proliferation of epithelial cells. Renal cyst formation disrupts renal function and induces diverse complications. The mechanism of cyst formation is unclear. mIMCD-3 cells were established to develop simple epithelial cell cysts in 3-D culture. We confirmed previously that Mxi1 plays a role in cyst formation in Mxi1-deficient mice. Cysts in Mxi1 transfectanted cells were showed by collagen or mebiol gels in 3-D cell culture system. Causative genes of ADPKD were measured by q RT-PCR. Herein, Mxi1 transfectants rarely formed a simple epithelial cyst and induced cell death. Overexpression of Mxi1 resulted in a decrease in the PKD1, PKD2 and c-myc mRNA relating to the pathway of cyst formation. These data indicate that Mxi1 influences cyst formation of mIMCD-3 cells in 3-D culture and that Mxi1 may control the mechanism of renal cyst formation. [BMB reports 2012; 45(3): 189-193]
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Yoo, Kyung Hyun,Kim, Yo Na,Lee, Min Joo,Seong, Je Kyung,Park, Jong Hoon WILEY-VCH Verlag 2009 Proteomics Vol.9 No.15
<P>Autosomal dominant polycystic kidney disease is one of the most common human monogenic diseases in which extensive epithelial-lined cysts develop in kidney and other organs. Affected kidneys are not only characterized by the formation of cysts, but also by changes associated with the extracellular matrix and interstitial inflammation, which can progress to fibrosis and loss of renal function. Mxi1 protein, which is a c-myc antagonist, may be essential in controlling cellular growth and differentiation. Previously, multiple tubular cysts were observed in kidney of Mxi1-deficient mice aged 6 months and more. Presently, 2-DE and MALDI-TOF MS was employed to identify the differentially expressed proteins in the kidney. Several proteins were identified, among them, apolipoproteinA1 which is a major component of the high-density lipoprotein complex and has anti-inflammation effects, was significantly decreased in the Mxi1-deficient mouse. We confirm the development of inflammation and renal fibrosis and the expression of extracellular matrix molecules including transforming growth factor were also increased in cystic kidney. These results indicate that expression of proteins related with inflammation and renal fibrosis changes by Mxi1 inactivation in polycystic kidney.</P>
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