N-myc遺伝子
- 関
- c-myc gene、c-myc proto-oncogene、myc gene、myc oncogene
WordNet
- (genetics) a segment of DNA that is involved in producing a polypeptide chain; it can include regions preceding and following the coding DNA as well as introns between the exons; it is considered a unit of heredity; "genes were formerly called factors" (同)cistron, factor
- the 14th letter of the Roman alphabet (同)n
- informal term for information; "give me the gen on your new line of computers"
PrepTutorEJDIC
- 遺伝子
- nitrogenの化学記号
- 『私の』 / 《親しみをこめた呼び掛けに用いて》 / 《驚きを表して》おや,まあ
- neodymiumの化学記号
UpToDate Contents
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English Journal
- Mature miR-183, negatively regulated by transcription factor GATA3, promotes 3T3-L1 adipogenesis through inhibition of the canonical Wnt/β-catenin signaling pathway by targeting LRP6.
- Chen C1, Xiang H2, Peng YL3, Peng J4, Jiang SW5.Author information 1Key Laboratory of Swine Genetics and Breeding of Agricultural Ministry and Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, PR China; Hunan Institute of Animal & Veterinary Science, Changsha 410131, PR China.2Key Laboratory of Swine Genetics and Breeding of Agricultural Ministry and Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, PR China.3Hunan Institute of Animal & Veterinary Science, Changsha 410131, PR China.4Department of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, PR China. Electronic address: pjhzau@163.com.5Key Laboratory of Swine Genetics and Breeding of Agricultural Ministry and Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, PR China. Electronic address: jswhzau@163.com.AbstractDifferentiation of preadipocytes into adipocytes and the formation of the subsequent adipose tissue are critical for mammalian growth and development. The molecular mechanism relating to preadipocyte differentiation and adipogenesis from the perspective of miRNAs is not yet completely understood. Here we investigated whether miR-183 functioned in the differentiation process. Both gain-of-function and loss-of-function assays demonstrated that miR-183 positively regulated 3T3-L1 differentiation by enhancing the expression of adipogenic marker genes such as CCAAT/enhancer binding protein α (C/EBPα), peroxisome proliferator-activated receptor γ (PPARγ), adiponectin and fatty acid synthase (FAS), as well as the triglyceride content and accumulation of lipid droplets. Meanwhile, low-density lipoprotein receptor-related protein 6 (LRP6) was known to impair the canonical Wnt/β-catenin signaling pathway and thereafter reduce c-myc and nuclear β-catenin protein. We showed that the inhibition of LRP6 by siRNA promoted 3T3-L1 adipogenic differentiation and adipogenesis. Further analysis showed that mouse miR-183 gene had its own transcription unit containing CpG islands, transcription start site (TSS), coding sequence (CDS) and polyA signal within the flanking sequences 2500nt upstream and downstream of mouse miR-183 in genome. The core promoter of miR-183 gene was identified and transcription factor GATA3 (GATA binding protein 3) significantly inhibited the expression of mature miR-183 by binding to its core promoter in vivo, as indicated by thechromatin immunoprecipitation (ChIP) assay. These results suggest that miR-183, though negatively regulated by transcription factor GATA3, enhances 3T3-L1 preadipocyte differentiation and adipogenesis through the inhibition of the canonical Wnt/β-catenin signaling pathway by targeting LRP6.
- Cellular signalling.Cell Signal.2014 Jun;26(6):1155-65. doi: 10.1016/j.cellsig.2014.02.003. Epub 2014 Feb 18.
- Differentiation of preadipocytes into adipocytes and the formation of the subsequent adipose tissue are critical for mammalian growth and development. The molecular mechanism relating to preadipocyte differentiation and adipogenesis from the perspective of miRNAs is not yet completely understood. He
- PMID 24556500
- Complex IGH rearrangements in multiple myeloma: Frequent detection discrepancies among three different probe sets.
- Kim GY1, Gabrea A, Demchenko YN, Bergsagel L, Roschke AV, Kuehl WM.Author information 1Genetics Branch, National Cancer Institute, Bethesda, MD.AbstractPrimary IGH translocations involving seven recurrent partner loci and oncogenes are present in about 40% of multiple myeloma tumors. Secondary IGH rearrangements, which occur in a smaller fraction of tumors, usually are complex structures, including insertions or translocations that can involve three chromosomes, and often with involvement of MYC. The main approach to detect IGH rearrangements is interphase-but sometimes metaphase-FISH strategies that use a telomeric variable region probe and a centromeric constant region/ Eα enhancer or 3' flanking probe to detect a separation of these two probes, or a fusion of these probes with probes located at nonrandom partner sites in the genome. We analyzed 18 myeloma cell lines for detection discrepancies among Vysis, Cytocell, and in-house IGH probe sets that hybridize with differing sequences in the IGH locus. There were no detection discrepancies for the three telomeric IGH probes, or for unrearranged IGH loci or primary IGH translocations using the centromeric IGH probes. However, the majority of complex IGH rearrangements had detection discrepancies among the three centromeric IGH probes. © 2014 Wiley Periodicals, Inc.
- Genes, chromosomes & cancer.Genes Chromosomes Cancer.2014 Jun;53(6):467-74. doi: 10.1002/gcc.22158. Epub 2014 Mar 3.
- Primary IGH translocations involving seven recurrent partner loci and oncogenes are present in about 40% of multiple myeloma tumors. Secondary IGH rearrangements, which occur in a smaller fraction of tumors, usually are complex structures, including insertions or translocations that can involve thre
- PMID 24585545
- Destruxin B inhibits hepatocellular carcinoma cell growth through modulation of the Wnt/β-catenin signaling pathway and epithelial-mesenchymal transition.
- Huynh TT1, Rao YK2, Lee WH3, Chen HA4, Le TD5, Tzeng DT6, Wang LS7, Wu AT8, Lin YF9, Tzeng YM10, Yeh CT11.Author information 1Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan; Department of Neurosurgery, University of Medicine and Pharmacy, Ho Chi Minh City, Viet Nam.2Institute of Biochemical Sciences and Technology, Chaoyang University of Technology, Taichung, Taiwan.3Department of Pathology, Taipei Medical University-Shuang Ho Hospital, Taipei, Taiwan.4Departments of Surgery, Taipei Medical University-Shuang Ho Hospital, Taipei, Taiwan.5Department of Hepatitis, Cho Ray Hospital, Ho Chi Minh City, Viet Nam.6Institute of Genomics and Bioinformatics, National Chung Hsing University, Taichung, Taiwan.7Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan; Division of Thoracic Surgery, Department of Surgery, Taipei Medical University-Shuang Ho Hospital, Taipei, Taiwan.8The Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.9Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan.10Institute of Biochemical Sciences and Technology, Chaoyang University of Technology, Taichung, Taiwan. Electronic address: ymtzeng@cyut.edu.tw.11Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan; Departments of Surgery, Taipei Medical University-Shuang Ho Hospital, Taipei, Taiwan; Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan. Electronic address: ctyeh@tmu.edu.tw.AbstractThe aberrant activation of Wnt/β-catenin signaling plays an important role in the carcinogenesis and progression of hepatocellular carcinoma (HCC). Therefore, the Wnt/β-catenin signaling molecules are attractive candidates for the development of targeted therapies for this disease. The present study showed that destruxin B (DB) inhibits the proliferation and induces the apoptosis of HCC cells by decreasing the protein expression of anti-apoptotic Bcl-2 and Bcl-xL and increasing the expression of the proapoptotic protein Bax. More importantly, DB also attenuates Wnt-signaling in HCC cells by downregulating β-catenin, Tcf4, and β-catenin/Tcf4 transcriptional activity, which results in the decreased expression of β-catenin target genes, such as cyclin D1, c-myc, and survivin. Furthermore, DB affects the migratory and invasive abilities of Sk-Hep1 cells through the suppression of markers of the epithelial-mesenchymal transition (EMT). A synergistic anti-proliferative and migratory effect was achieved using the combination of DB and sorafenib in Sk-Hep1 cells. In conclusion, DB acts as a novel Wnt/β-catenin inhibitor and reduces the aggressiveness and invasive potential of HCC by altering the cells' EMT status and mobility. DB in combination with sorafenib may be considered for future clinical use for the management of metastatic HCC.
- Toxicology in vitro : an international journal published in association with BIBRA.Toxicol In Vitro.2014 Jun;28(4):552-61. doi: 10.1016/j.tiv.2014.01.002. Epub 2014 Jan 13.
- The aberrant activation of Wnt/β-catenin signaling plays an important role in the carcinogenesis and progression of hepatocellular carcinoma (HCC). Therefore, the Wnt/β-catenin signaling molecules are attractive candidates for the development of targeted therapies for this disease. The present stu
- PMID 24434019
Japanese Journal
- Unexpected Intraparenchymal Hematoma Caused by Brain Metastasis in a Patient With Neuroblastoma : Case Report
- OKURA Hidehiro,YATOMI Kenji,SAITO Youhei,KASUGA Chinatsu,ISHII Hisato,KARAGIOZOV Kostadin,MIYAJIMA Masakazu,ARAI Hajime
- Neurologia medico-chirurgica = 神経外科 51(11), 784-788, 2011-11-15
- … The related factors in this patient with abdominal neuroblastoma included elevated serum lactate dehydrogenase, N-myc gene amplification, and coexisting orbital metastasis, which all occurred within 22 months from initial diagnosis. …
- NAID 10030030426
- The effect of Ndrg2 expression on astroglial activation
- Takeichi Toshiaki,Takarada-Iemata Mika,Hashida Koji,Sudo Hirofumi,Okuda Tomohiko,Kokame Koichi,Hatano Taku,Takanashi Masashi,Funabe Sayaka,Hattori Nobutaka,Kitamura Osamu,Kitao Yasuko,Hori Osamu
- Neurochemistry International 59(1), 21-27, 2011-08-00
- … N-myc downstream-regulated gene 2 (Ndrg2) is a differentiation- and stress-associated molecule predominantly expressed in astrocytes in the central nervous system (CNS). … In cultured astrocytes, gene silencing of Ndrg2 significantly enhanced the numbers of 5-bromo-2′-deoxy-uridine (BrdU)-incorporated and proliferating cell nuclear antigen (PCNA)-positive cells, and reduced the length of cell processes and the amount of F-actin. …
- NAID 120003221535
Related Links
- Complete information for MYC gene (protein-coding), v-myc avian myelocytomatosis viral oncogene homolog, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium ... ...
- This gene is a member of the N-myc downregulated gene family which belongs to the alpha/beta hydrolase superfamily. The protein encoded by this gene is a cytoplasmic protein involved in stress responses, hormone ...
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;関:c-myc gene
- 関
- c-myc gene、c-myc proto-oncogene、myc gene、N-myc gene
[★]
c-myc遺伝子
- 関
- c-myc proto-oncogene、myc gene、myc oncogene、N-myc gene
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myc遺伝子
- 関
- c-myc gene、c-myc proto-oncogene、myc oncogene、N-myc gene
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- 英
- N-myc gene
- 関
- c-myc遺伝子、myc遺伝子、c-myc癌原遺伝子
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- 関
- number of experiment、sample size
- pの前の[n]はmと記載する。synptom→symptom
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- 関
- muscle, muscular, muscularis, musculus
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myc遺伝子
- 関
- c-myc gene、c-myc proto-oncogene、myc oncogene、N-myc gene
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[★]
ネオジム neodymium