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Proteomic analysis of injured rat spinal cords after transplantation of human embryonic stem cells
Hye Sook Hwang,Bae Hwan Lee,Kwang Sik Kim,Kun Ho Choi,Sae Jin Oh,Kyung Jin Roh,Se Jin Hwang,Jeong Bok Lee,Hyun Soo Yun,Kye Seong Kim,Yeo Sung Yoon,Je Kyung Seong 한국실험동물학회 2007 한국실험동물학회 학술발표대회 논문집 Vol.2007 No.-
A novel splicing variant of b -TrCP1, a binding protein of b-catenin, in epithelial ovarian cancer
( Yeo-jin Lee ),( Bo-ra Lee ),( Ji Hye Kim ),( Dhan-ah Chae ),( Jin-ah Oh ),( Sooji Ham ),( Hyun-jin Choi ),( Eun-ju Lee ) 대한산부인과학회 2020 대한산부인과학회 학술대회 Vol.106 No.-
Objective: Three splicing variants of b-TrCP1, b-TrCP1-variants 1, 2, and 3, have been found in human cells. We sought to identify a novel variant, b-TrCP-variant 4, whose full-sequence has never been cloned, from ovarian cancer cells and evaluate its regulatory function on b -catenin. Methods: Normal and cancerous ovarian tissues were obtained and snap frozen in liquid nitrogen. Total RNA was isolated. Approximately 0.5-1.0 g of total RNA was reverse transcribed into cDNA using, real-time PCR. To quantitatively determine the mRNA concentration of the variants, real-time PCR was performed. Co-immunoprecipitation assay and b-galactosidase assay were done. The membrane bound proteins were developed by Western blot analysis. The expression and localization of the proteins was observed under by immunofluorescence staining and confocal microscopy. Luciferase activity was assessed using a dual-luciferase reporter assay kit. Results: A novel b-TrCP1-variant 4 harbors exon II instead of exon III of variant 1, with no change in the open reading frame. The expression of b-TrCP1-variant 4 is abundantly expressed in cancerous ovarian tissues rather than variant 1 and 2. Similar to variants 1 and 2, b-TrCP1-variant 4 directly interacts with b-catenin, one of the substrates of SCF-TrCP E3 ubiquitin ligase and down-regulates the transcriptional activity and protein expression of b-catenin with a significantly weaker effect than that by variants 1 and 2. However, the co-expression of b-TrCP1-variant 4 with variant 1 in same proportion has no effect, whereas other combinations effectively downregulate the activity of b-catenin, indicating that the heterodimer of variants 1 and 4 has no function. Conclusion: B-TrCP1-variant 4 could play a critical role in SCF-TrCP E3 ligase-mediated ubiquitination by acting as a negative regulator of -TrCP1-variant 1.
Tree Ring Growth of Clones in a Seed Orchard of A. nephrolepis during Drought Periods
Hye-Jin Lee,Sang-Jin Yoon,Seonjeong Kim,Sun-Cheon Hong,Dayoung Lee,Tae-Lim Yeo,Yoonji Hahn,Gye-Hong Cho,Yang-Gil Kim,Kwang Hyun Nam,Hyunjoong Sung,En-Bi Choi,Jun-Hui Park,Jeong-Wook Seo,Kyu-Suk Kang 한국육종학회 2023 한국육종학회 공동학술발표집 Vol.2023 No.-
YC-1 Induces S Cell Cycle Arrest and Apoptosis by Activating Checkpoint Kinases
Yeo, Eun-Jin,Ryu, Ji-Hye,Chun, Yang-Sook,Cho, Young-Suk,Jang, In-Jin,Cho, HoSung,Kim, Jinho,Kim, Myung-Suk,Park, Jong-Wan American Association for Cancer Research 2006 Cancer Research Vol.66 No.12
<P>Hypoxia-inducible factor-1alpha (HIF-1alpha) seems central to tumor growth and progression because it up-regulates genes essential for angiogenesis and the hypoxic adaptation of cancer cells, which is why HIF-1alpha inhibition is viewed as a cancer therapy strategy. Paradoxically, HIF-1alpha also leads to cell cycle arrest or the apoptosis of cancer cells. Thus, the possibility cannot be ruled out that HIF-1alpha inhibitors unlock cell cycle arrest under hypoxic conditions and prevent cell death, which would limit the anticancer effect of HIF-1alpha inhibitors. Previously, we reported on the development of YC-1 as an anticancer agent that inhibits HIF-1alpha. In the present study, we evaluated the effects of YC-1 on hypoxia-induced cell cycle arrest and cell death. It was found that YC-1 does not reverse the antiproliferative effect of hypoxia, but rather that it induces S-phase arrest and apoptosis at therapeutic concentrations that inhibit HIF-1alpha and tumor growth; however, YC-1 did not stimulate cyclic guanosine 3',5'-monophosphate production in this concentration range. It was also found that YC-1 activates the checkpoint kinase-mediated intra-S-phase checkpoint, independently of ataxia-telangiectasia mutated kinase or ataxia-telangiectasia mutated and Rad3-related kinase. These results imply that YC-1 does not promote the regrowth of hypoxic tumors because of its cell cycle arrest effect. Furthermore, YC-1 may induce the combined anticancer effects of HIF-1alpha inhibition and cell growth inhibition.</P>