- (アデノウイルスE1Aと結合するCREB転写因子)E1A結合性p300タンパク質、E1A結合p300タンパク質
WordNet
- having partial rights and privileges or subordinate status; "an associate member"; "an associate professor"
- a person who joins with others in some activity or endeavor; "he had to consult his associate before continuing"
- a person with subordinate membership in a society, institution, or commercial enterprise; "associates in the law firm bill at a lower rate than do partners"
- any event that usually accompanies or is closely connected with another; "first was the lightning and then its thunderous associate"
- make a logical or causal connection; "I cannot connect these two pieces of evidence in my mind"; "colligate these facts"; "I cannot relate these events at all" (同)tie_in, relate, link, colligate, link up, connect
- any of a large group of nitrogenous organic compounds that are essential constituents of living cells; consist of polymers of amino acids; essential in the diet of animals for growth and for repair of tissues; can be obtained from meat and eggs and milk and legumes; "a diet high in protein"
- the 5th letter of the Roman alphabet (同)e
PrepTutorEJDIC
- 〈人〉'を'(…の)『仲間に加える』,(…に)連合させる《+『名』〈人〉+『with』+『名』》 / (…と)…'を'結びつけて考える(起こす)《+『名』+『with』+『名』》 / (…と)『仲間になる』,交際する《+『with』+『名』》 / (…と)合体する,提携する《+『with』+『名』》 / 『仲間』,『同僚』;組合員 / 準会員 / 付属物;連想されるもの / 連合した;仲間の,同僚の / 補助の,準…
- 蛋白(たんばく)質
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- 1. 肥大型心筋症の遺伝学 genetics of hypertrophic cardiomyopathy
- 2. ライソゾーム膜蛋白質2欠損症（糖原病IIb型、ダノン病） lysosome associated membrane protein 2 deficiency glycogen storage disease iib danon disease
- 3. 1型糖尿病の病因 pathogenesis of type 1 diabetes mellitus
- 4. パーキンソン病の病因および発症機序 etiology and pathogenesis of parkinson disease
- 5. 糸球体の免疫障害の機序 mechanisms of immune injury of the glomerulus
English Journal
- Carbamylated erythropoietin promotes neurite outgrowth and neuronal spine formation in association with CBP/p300.
- Choi M1, Ko SY2, Lee IY2, Wang SE2, Lee SH2, Oh DH3, Kim YS4, Son H5.Author information 1Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, 17 Haengdang-dong, Sungdong-gu, Seoul 133-791, Republic of Korea.2Graduate School of Biomedical Science and Engineering, Hanyang University, 17 Haengdang-dong, Sungdong-gu, Seoul 133-791, Republic of Korea.3Department of Psychiatry, College of Medicine and Institute of Mental Health, Hanyang University, 17 Haengdang-dong, Sungdong-gu, Seoul 133-791, Republic of Korea.4Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, 17 Haengdang-dong, Sungdong-gu, Seoul 133-791, Republic of Korea; Graduate School of Biomedical Science and Engineering, Hanyang University, 17 Haengdang-dong, Sungdong-gu, Seoul 133-791, Republic of Korea.5Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University, 17 Haengdang-dong, Sungdong-gu, Seoul 133-791, Republic of Korea; Graduate School of Biomedical Science and Engineering, Hanyang University, 17 Haengdang-dong, Sungdong-gu, Seoul 133-791, Republic of Korea. Electronic address: hyeonson@hanyang.ac.kr.AbstractBoth erythropoietin (EPO) and carbamylated EPO (cEPO) have been shown to increase the length of neurites and spine density in neurons. However, the molecular mechanism underlying the EPO- and cEPO-induced neuronal differentiation has yet to be investigated. To address this issue, we investigated epigenetic modifications that regulate gene expression in neurons. Neurons treated with EPO or cEPO display an upregulation of E1A-binding protein (p300) and p300-mediated p53 acetylation, possibly increasing the transactivation activity of p53 on growth-associated protein 43 (GAP43). Treatment of cells with cEPO markedly increases spine formation and potentiates p300-mediated transactivation of PSD95, Shank2 and 3 compared to EPO. These results demonstrate that cEPO controls neuronal differentiation via acetylation of transcription factors and subsequent transactivation of target genes. These findings have important medical implications because cEPO is of interest in the development of therapeutic agents against neuropsychiatric disorders.
- Biochemical and biophysical research communications.Biochem Biophys Res Commun.2014 Mar 4. pii: S0006-291X(14)00328-3. doi: 10.1016/j.bbrc.2014.02.066. [Epub ahead of print]
- Both erythropoietin (EPO) and carbamylated EPO (cEPO) have been shown to increase the length of neurites and spine density in neurons. However, the molecular mechanism underlying the EPO- and cEPO-induced neuronal differentiation has yet to be investigated. To address this issue, we investigated epi
- PMID 24607903
- Landscape of genomic alterations in cervical carcinomas.
- Ojesina AI1, Lichtenstein L2, Freeman SS3, Pedamallu CS4, Imaz-Rosshandler I5, Pugh TJ4, Cherniack AD3, Ambrogio L3, Cibulskis K3, Bertelsen B6, Romero-Cordoba S5, Treviño V7, Vazquez-Santillan K5, Guadarrama AS5, Wright AA8, Rosenberg MW3, Duke F9, Kaplan B4, Wang R10, Nickerson E3, Walline HM11, Lawrence MS3, Stewart C3, Carter SL3, McKenna A3, Rodriguez-Sanchez IP12, Espinosa-Castilla M5, Woie K13, Bjorge L14, Wik E14, Halle MK14, Hoivik EA14, Krakstad C14, Gabiño NB5, Gómez-Macías GS12, Valdez-Chapa LD12, Garza-Rodríguez ML12, Maytorena G15, Vazquez J15, Rodea C15, Cravioto A15, Cortes ML3, Greulich H16, Crum CP17, Neuberg DS18, Hidalgo-Miranda A5, Escareno CR19, Akslen LA20, Carey TE21, Vintermyr OK20, Gabriel SB3, Barrera-Saldaña HA12, Melendez-Zajgla J5, Getz G22, Salvesen HB23, Meyerson M24.Author information 11] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA [3].21] The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA [2].3The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA.41] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA.5Instituto Nacional de Medicina Genomica, Mexico City 14610, Mexico.6Department of Pathology, Haukeland University Hospital, N5021 Bergen, Norway.7Tecnológico de Monterrey, Monterrey 64849, Mexico.81] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.9Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA.101] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Thoracic Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.11Cancer Biology Program, Program in the Biomedical Sciences, Rackham Graduate School, University of Michigan, Ann Arbor, Michigan 48109, USA.12Facultad de Medicina y Hospital Universitario 'Dr. José Eluterio González' de la Universidad Autónoma de Nuevo León, Monterrey, Nuevo León 64460, México.13Department of Obstetrics and Gynecology, Haukeland University Hospital, N5021 Bergen, Norway.141] Department of Obstetrics and Gynecology, Haukeland University Hospital, N5021 Bergen, Norway [2] Department of Clinical Science, Centre for Cancer Biomarkers, University of Bergen, N5020 Bergen, Norway.15Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.161] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA [3] Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.17Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.18Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA.191] Instituto Nacional de Medicina Genomica, Mexico City 14610, Mexico [2] Claremont Graduate University, Claremont, California 91711, USA.201] Department of Pathology, Haukeland University Hospital, N5021 Bergen, Norway [2] Centre for Cancer Biomarkers, Department of Clinical Medicine, University of Bergen, N5020 Bergen, Norway.21Head and Neck Oncology Program and Department of Otolaryngology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 38109, USA.221] The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA [2] Massachusetts General Hospital Cancer Center and Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.231] Department of Obstetrics and Gynecology, Haukeland University Hospital, N5021 Bergen, Norway [2] Department of Clinical Science, Centre for Cancer Biomarkers, University of Bergen, N5020 Bergen, Norway [3].241] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] The Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA [3] Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA [4].AbstractCervical cancer is responsible for 10-15% of cancer-related deaths in women worldwide. The aetiological role of infection with high-risk human papilloma viruses (HPVs) in cervical carcinomas is well established. Previous studies have also implicated somatic mutations in PIK3CA, PTEN, TP53, STK11 and KRAS as well as several copy-number alterations in the pathogenesis of cervical carcinomas. Here we report whole-exome sequencing analysis of 115 cervical carcinoma-normal paired samples, transcriptome sequencing of 79 cases and whole-genome sequencing of 14 tumour-normal pairs. Previously unknown somatic mutations in 79 primary squamous cell carcinomas include recurrent E322K substitutions in the MAPK1 gene (8%), inactivating mutations in the HLA-B gene (9%), and mutations in EP300 (16%), FBXW7 (15%), NFE2L2 (4%), TP53 (5%) and ERBB2 (6%). We also observe somatic ELF3 (13%) and CBFB (8%) mutations in 24 adenocarcinomas. Squamous cell carcinomas have higher frequencies of somatic nucleotide substitutions occurring at cytosines preceded by thymines (Tp*C sites) than adenocarcinomas. Gene expression levels at HPV integration sites were statistically significantly higher in tumours with HPV integration compared with expression of the same genes in tumours without viral integration at the same site. These data demonstrate several recurrent genomic alterations in cervical carcinomas that suggest new strategies to combat this disease.
- Nature.Nature.2014 Feb 20;506(7488):371-5. doi: 10.1038/nature12881. Epub 2013 Dec 25.
- Cervical cancer is responsible for 10-15% of cancer-related deaths in women worldwide. The aetiological role of infection with high-risk human papilloma viruses (HPVs) in cervical carcinomas is well established. Previous studies have also implicated somatic mutations in PIK3CA, PTEN, TP53, STK11 and
- PMID 24390348
- PML4 facilitates erythroid differentiation by enhancing the transcriptional activity of GATA-1.
- Wu J1, Zhou LQ, Yu W, Zhao ZG, Xie XM, Wang WT, Xiong J, Li M, Xue Z, Wang X, Zhang P, Mao BB, Hao DL, Lv X, Liu DP.Author information 1State Key Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, and.AbstractPromyelocytic leukemia protein (PML) has been implicated as a participant in multiple cellular processes including senescence, apoptosis, proliferation, and differentiation. Studies of PML function in hematopoietic differentiation previously focused principally on its myeloid activities and also indicated that PML is involved in erythroid colony formation. However, the exact role that PML plays in erythropoiesis is essentially unknown. In this report, we found that PML4, a specific PML isoform expressed in erythroid cells, promotes endogenous erythroid genes expression in K562 and primary human erythroid cells. We show that the PML4 effect is GATA binding protein 1 (GATA-1) dependent using GATA-1 knockout/rescued G1E/G1E-ER4 cells. PML4, but not other detected PML isoforms, directly interacts with GATA-1 and can recruit it into PML nuclear bodies. Furthermore, PML4 facilitates GATA-1 trans-activation activity in an interaction-dependent manner. Finally, we present evidence that PML4 enhances GATA-1 occupancy within the globin gene cluster and stimulates cooperation between GATA-1 and its coactivator p300. These results demonstrate that PML4 is an important regulator of GATA-1 and participates in erythroid differention by enhancing GATA-1 trans-activation activity.
- Blood.Blood.2014 Jan 9;123(2):261-70. doi: 10.1182/blood-2013-02-483289. Epub 2013 Nov 19.
- Promyelocytic leukemia protein (PML) has been implicated as a participant in multiple cellular processes including senescence, apoptosis, proliferation, and differentiation. Studies of PML function in hematopoietic differentiation previously focused principally on its myeloid activities and also ind
- PMID 24255919
Japanese Journal
- Selection of the best target site for ribozyme-mediated cleavage within a fusion gene for adenovirus E1A-associated 300 kDa protein (p300) and luciferase
- KAWASAKI H.
- Nucleic Acids Res. 24, 3010-3016, 1996
- NAID 80009137267
- Involvement of the cell-cycle inhibitor Cip1/WAF1 and the E1A-associated p300 protein in terminal differentiation
- MISSERO C
- Proc. Natl. Acad. Sci. USA 92, 5451-5455, 1995
- NAID 80008367940
- Adenovirus E1A associated protein P300 as a functional homologue of the transcriptional co-activator CBP
- LUNDBLAD J. R.
- Nature 374, 85-88, 1995
- NAID 80008144343
Related Links
- ChemicalBook あなたのためにE1A-associated p300 proteinの化学的性質を提供し て、融点、価格、蒸気圧、沸点、毒性、比重、沸点、密度、分子式、分子量、物理的な 性質、毒性 税関のコードなどの情報、同時にあなたは更にE1A-associated p300 ...
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| リンク元 | 「E1A結合p300タンパク質」「E1A結合性p300タンパク質」 |
| 関連記事 | 「associate」「associated」「E」「E1」 |
「E1A結合p300タンパク質」
「E1A結合性p300タンパク質」
「associate」
- vt.
- 結合する、連合させる。連想によって結びつける。(人を)仲間/友達などとしての関係に置く。(化)会合させる
- vi.
- 仲間/友人などとして交際する(with)。一つにまとめる、連合する
- n.
- 仕事仲間、提携者、同僚。友人、朋友。準会員。従業員、社員
- 密接な蒸す偽付きのある物、付随する物、つきもの。準国家
- 連想によって心に浮かぶ言葉/思い、連想物
- adj.
- 仲間の、同僚の。製紙機械員に次ぐ資格の
- 付随する、連想される
- 関
- accompany、association、associative、attach、bearing、bind、binding、bond、bonding、coassemble、colleague、combine、conjoin、conjugate、conjugation、conjunction、connect、connection、correlate、correlation、couple、dock、engage、engagement、federation、implication、join、joint、ligate、link、linkage、peer、pertinent、reference、relate、relation、relationship、relative、relevance、relevant、symphysial、union
「associated」
- adj.
- 随伴の、随伴性の
「E」