Gotowa bibliografia na temat „P53-regulated genes”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „P53-regulated genes”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "P53-regulated genes"
Keegan, Lunec i Neal. "p53 and p53-regulated genes in bladder cancer". BJU International 82, nr 5 (listopad 1998): 710–20. http://dx.doi.org/10.1046/j.1464-410x.1998.00822.x.
Pełny tekst źródłaXu, H., i M. R. El-Gewely. "P53 network — its downstream regulated genes". Biochemical Society Transactions 28, nr 5 (1.10.2000): A227. http://dx.doi.org/10.1042/bst028a227a.
Pełny tekst źródłaKlingler, H. Christoph. "p53 and p53 regulated genes in bladder cancer [review]". Current Opinion in Urology 9, nr 2 (marzec 1999): 172. http://dx.doi.org/10.1097/00042307-199903000-00015.
Pełny tekst źródłaRiley, Todd, Eduardo Sontag, Patricia Chen i Arnold Levine. "Transcriptional control of human p53-regulated genes". Nature Reviews Molecular Cell Biology 9, nr 5 (maj 2008): 402–12. http://dx.doi.org/10.1038/nrm2395.
Pełny tekst źródłaYu, J., L. Zhang, P. M. Hwang, C. Rago, K. W. Kinzler i B. Vogelstein. "Identification and classification of p53-regulated genes". Proceedings of the National Academy of Sciences 96, nr 25 (7.12.1999): 14517–22. http://dx.doi.org/10.1073/pnas.96.25.14517.
Pełny tekst źródłaLotem, J., H. Gal, R. Kama, N. Amariglio, G. Rechavi, E. Domany, L. Sachs i D. Givol. "Inhibition of p53-induced apoptosis without affecting expression of p53-regulated genes". Proceedings of the National Academy of Sciences 100, nr 11 (12.05.2003): 6718–23. http://dx.doi.org/10.1073/pnas.1031695100.
Pełny tekst źródłaFiordaliso, F., A. Leri, D. Cesselli, F. Limana, B. Safai, B. Nadal-Ginard, P. Anversa i J. Kajstura. "Hyperglycemia Activates p53 and p53-Regulated Genes Leading to Myocyte Cell Death". Diabetes 50, nr 10 (1.10.2001): 2363–75. http://dx.doi.org/10.2337/diabetes.50.10.2363.
Pełny tekst źródłaWang, Chao, Cui Rong Teo i Kanaga Sabapathy. "p53-Related Transcription Targets of TAp73 in Cancer Cells—Bona Fide or Distorted Reality?" International Journal of Molecular Sciences 21, nr 4 (17.02.2020): 1346. http://dx.doi.org/10.3390/ijms21041346.
Pełny tekst źródłaZhao, Renbin, Kurt Gish, Maureen Murphy, Yuxin Yin, Daniel Notterman, William H. Hoffman, Edward Tom, David H. Mack i Arnold J. Levine. "Analysis of p53-regulated gene expression patterns using oligonucleotide arrays". Genes & Development 14, nr 8 (15.04.2000): 981–93. http://dx.doi.org/10.1101/gad.14.8.981.
Pełny tekst źródłaŁasut-Szyszka, Barbara, Beata Małachowska, Agnieszka Gdowicz-Kłosok, Małgorzata Krześniak, Magdalena Głowala-Kosińska, Artur Zajkowicz i Marek Rusin. "Transcriptome Analysis of Cells Exposed to Actinomycin D and Nutlin-3a Reveals New Candidate p53-Target Genes and Indicates That CHIR-98014 Is an Important Inhibitor of p53 Activity". International Journal of Molecular Sciences 22, nr 20 (14.10.2021): 11072. http://dx.doi.org/10.3390/ijms222011072.
Pełny tekst źródłaRozprawy doktorskie na temat "P53-regulated genes"
Mpagi, Meldrick Daniel. "In Search For New p53 Regulated Genes". Wright State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=wright1227282714.
Pełny tekst źródłaBain, Peter A., i n/a. "Gene Expression Profiling of Cylindrospermopsin Toxicity". Griffith University. School of Biomolecular and Physical Sciences, 2007. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20080404.145834.
Pełny tekst źródłaBain, Peter A. "Gene Expression Profiling of Cylindrospermopsin Toxicity". Thesis, Griffith University, 2007. http://hdl.handle.net/10072/367068.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Faculty of Science, Environment, Engineering and Technology
Full Text
Walia, Vijay. "hCLCA2 IS A p53-REGULATED GENE REQUIRED FOR MESENCHYMAL TO EPITHELIAL TRANSITION IN BREAST". OpenSIUC, 2010. https://opensiuc.lib.siu.edu/dissertations/131.
Pełny tekst źródłaKrell, Jonathan. "The complex network of p53-regulated small non-coding RNAs and their gene targets in cancer". Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/28148.
Pełny tekst źródłaAlkawar, Abdulrhaman Mohammed Mohammed. "Insulin-like growth factor-1 (IGF-1) impacts p53-regulated gene products in UVB-irradiated human keratinocytes and skin epidermis". Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1588119867567084.
Pełny tekst źródłaChang, Kevin Tsun-Kai, i 張惇凱. "Identification and characterization of p53-regulated genes". Thesis, 2005. http://ndltd.ncl.edu.tw/handle/23637545337936847774.
Pełny tekst źródła國立陽明大學
生物化學研究所
93
p53 tumor suppressor is the most frequently mutated gene in human cancers. p53 must achieve its role in tumor suppression through transactivation of target genes, i.e. genes involved in cell survival or apoptosis regulation. Aiming further understanding of p53, we set out to search and to identify novel p53 downstream targets. By comparing gene expression patterns under basal or p53 activation conditions using microarray, we discovered two potential target genes, Rad and PRL-1, whitch can be up-regulated when p53 expression is induced by DNA damage or ectopically. Rad is a small G protein belonging to the RGK family, while PRL-1 is a protein tyrosine phosphatase; both are with unknown function. Rad has a p53 response element (p53RE) in the 5’ promoter region and PRL-1 has a p53RE in intron its 1. Using chromatin immunoprecipitation (ChIP) and luciferase reporter assay, we demonstrate that p53 can bind to p53REs of Rad and PRL-1 and activates their mRNA transcription under adriamycin and UV damage or p53 overexpression. p73, which has sequence hormology to p53 in the DNA binding domain, also transactivates Rad and PRL-1 through p53RE. p73 β and δ confer strongest activation among four p73 isoforms. Previous studies on Rad have revealed that Rad binds Rho-associated kinase ROCK and subsequently inhibits ROCK kinase activity upon MYPT-1 and shortens the length of neurites in neuroblastoma cells. We also show that Rad binds to ROCK I and ROCK II in vivo and repress RhoA-induced NF-κB and cyclin D1 promoter activation equally well as ROCK inhibitor Y27632 does. Rad overexpressed Cos7 shows growth suppression evidenced by colony formation assay. Our results prove that Rad and PRL-1 are p53 targets and increase mRNA levels in a p53-dependent manner. Rad protein levels also increase under p53 activation. p53 binds to promoter and intron region of Rad and PRL-1, respectively, and transactivates Rad and PRL-1 expression. Further experiments could reveal new function of p53 in regulating Rad and PRL-1 in glucose metabolism, NF-κB signaling and mechanism of controlling cell cycle reentry.
Lo, Pang-Kuo, i 駱邦國. "Cloning and Characterization of Novel p53-Regulated Genes". Thesis, 1999. http://ndltd.ncl.edu.tw/handle/61123204931547812228.
Pełny tekst źródła國立陽明大學
生物化學研究所
88
p53 is a tumor suppressor gene that functions as a guardian to maintain the integrity of the genome. It is the most frequently mutated and disrupted target in human cancers. Activation of p53 triggers cells into cell cycle arrest, apoptosis and differentiation, depending on the cell type, cellular environment and extracellular stimuli. p53 acts through direct interaction with other proteins or as a transcription factor regulating the expression of its downstream effector genes. A key approach to elucidating the biological function of p53 is to look for its direct target genes. By mRNA differential display analysis on murine IW32 erythroleukemia cells containing a temperature sensitive p53 allele (tsp53val-135) cultured at 32.5°C and 38.5°C, two novel p53-regulated genes, designated mDDA1 and mDDA3, have been identified. Induction of mDDA1 and mDDA3 occurred in all IW32 sublines expressing tsp53val-135 cultured at permissive temperature. Elevated levels of mDDA1 and mDDA3 transcripts were detected within 1 h and 2 h, respectively, after down-shifting the temperature from 38.5℃ to 32.5℃. Moreover, actinomycin D, but not cycloheximide, inhibited the p53-dependent induction of these genes, suggesting that their activation was through transcriptional regulation and did not require de novo protein synthesis. DDA1 transcript was predominantly expressed in mouse liver and human skeletal muscle, while that of DDA3 was found in multiple mouse and human tissues. Using 5''-RACE and a PCR-based genome walking method, full-length cDNAs and genomic DNAs of mDDA1 and mDDA3 were cloned. The mDDA1 cDNA encodes a putative protein of 498 amino acids containing 12 transmembrane domains. The genomic DNA of mDDA1 is 18 kb in length, consisting of six exons and five introns. Four putative p53 recognition motifs are found in intron 1; at least one of these sites was demonstrated to support the responsiveness to wild-type, but not mutant p53, in a transient transfection assay. Sequence comparison revealed that mDDA1 shares 73% and 90% identity in its nucleotide and protein sequences, respectively, to the newly identified human thiamine transporter gene (hTHTR-1). The gene structures of mDDA1 and hTHTR-1 are similar; both contain identical numbers of exon and intron, and the RNA splicing joint sites are also conserved. Therefore, mDDA1 is very likely to be the mouse homologue of the hTHTR-1. Based on these analyses, mDDA1 was hereafter named mouse THTR-1 (mTHTR-1). mTHTR-1 also shares 40% identity in its protein sequence to the reduced folate carrier-1 (RFC-1) from human and mouse. However, We have shown that mTHTR-1 exhibited very low methotrexate uptake activity when compared to that of RFC-1. The mDDA3 gene is composed of eight exons and seven introns, and a putative p53 recognition motif was found in its intron 3. Sequence analysis of the cloned mDDA3 cDNAs indicated that there were at least seven types of transcripts, differed only in their 5''-termini. Results from primer extension and RNase protection assays suggest that the 5''-heterogeneity of mDDA3 mRNAs may result from multiple transcriptional initiations as well as alternative splicing of the transcripts. Three of these mDDA3 cDNAs contain uninterrupted open reading frames; two of them encode a protein of 329 amino acids (mDDA3S) and the third, 344 amino acids (mDDA3L). Except for a 15 amino acid-extension at the N-terminus of mDDA3L, the two proteins are identical in sequence. The mDDA3 protein is rich in serine and proline; it contains one coiled-coil domain and six "PXXP" motifs capable of interacting SH3 containing proteins. Full-length human DDA3 cDNA has been obtained by homology searches of a human EST database; sequence analysis indicates that hDDA3 encodes a protein of 333 amino acids that shares 68% identity to mDDA3S. Overexpression of both mTHTR-1 and mDDA3 in H1299 non-small cell lung carcinoma cells partially suppressed colony formation. In summary, we have cloned and characterized two p53 transcriptional target genes mTHTR-1 and DDA3. Our analyses have implicated mTHTR-1 in thiamine homeostasis and suggested a role of DDA3 in the p53-mediated growth suppression. 英文摘要--------------------------------------------------------------------------------------- 3 (壹)‧緒論 1.1 細胞的生長與死亡之調控------------------------------------------------------- 5 1.2 p53 tumor suppressor ------------------------------------------------------------- 7 1.3 p53蛋白的結構與功能----------------------------------------------------------- 7 1.3.1 Transactivation domain ------------------------------------------------------- 7 1.3.2 Proline-rich domain ------------------------------------------------------------ 8 1.3.3 Central DNA-binding core domain ----------------------------------------- 8 1.3.4 C端oligomerization domain -------------------------------------------------- 9 1.3.5 C端multi-functional basic domain ------------------------------------------- 9 1.4 影響p53的上游訊息(Signals to p53) ------------------------------------------ 10 1.4.1 Translational regulation ------------------------------------------------------- 10 1.4.2 Post-translational modification ----------------------------------------------- 11 (1) Phosphorylation ----------------------------------------------------------------- 11 (2) Dephosphorylation ------------------------------------------------------------- 12 (3) Acetylation ----------------------------------------------------------------------- 12 1.4.3 Oncogenic regulation ---------------------------------------------------------- 13 1.4.4 Telomere shortening ----------------------------------------------------------- 13 1.5 p53所引發的下游訊息(Signaling out) ---------------------------------------- 14 1.5.1 p53對Cell Cycle的調控------------------------------------------------------- 14 1.5.2 p53對apoptosis的調控-------------------------------------------------------- 15 1.6 p53在維持基因體穩定所扮演的角色---------------------------------------- 18 1.7 p53 kingdom ------------------------------------------------------------------------ 19 1.7.1 The roles in DNA damaging signals ---------------------------------------- 19 1.7.2 The roles in development of embryo --------------------------------------- 20 1.7.3 Involvement in tumor suppression ------------------------------------------ 20 (貳)‧本論文研究的目的------------------------------------------------------------------ 22 (參)‧實驗材料與方法 3.1 材料------------------------------------------------------------------------------------ 23 3.1.1 化學藥品和實驗材料---------------------------------------------------------- 23 3.1.2 酵素和試劑----------------------------------------------------------------------- 23 3.1.3 質體DNA ------------------------------------------------------------------------- 24 3.1.4 cDNA ----------------------------------------------------------------------------- 24 3.1.5 細胞株---------------------------------------------------------------------------- 25 3.1.6 放射性物質---------------------------------------------------------------------- 25 3.1.7 選殖cDNA及genomic DNA的引子----------------------------------------- 25 (1) 選殖cDNA的引子--------------------------------------------------------------- 25 (2) 選殖genomic DNA的引子----------------------------------------------------- 26 3.2 方法------------------------------------------------------------------------------------ 28 3.2.1 細胞培養------------------------------------------------------------------------- 28 3.2.2 RNA的製備--------------------------------------------------------------------- 28 3.2.3 北方墨點轉漬分析(Northern blot analysis) ------------------------------ 30 3.2.4 質體製備------------------------------------------------------------------------- 32 3.2.5 DNA片段的選殖(cloning) -------------------------------------------------- 34 3.2.6 mRNA差異展現分析法(mRNA Differential Display) ----------------- 36 3.2.7 Rapid Amplification of cDNA 5''-Ends (5''RACE) ------------------------ 37 3.2.8 RNase protection assay ------------------------------------------------------- 37 3.2.9 PCR-based genome walking method --------------------------------------- 38 3.2.10 Primer extension method ---------------------------------------------------- 39 3.2.11 質體的構築--------------------------------------------------------------------- 40 3.2.12 細胞群落形成分析(Colony formation assay) --------------------------- 42 3.2.13 MTX uptake -------------------------------------------------------------------- 42 3.2.14 Luciferase assay --------------------------------------------------------------- 43 (肆)‧實驗結果與討論 4.1 p53下游基因之選殖 4.1.1 實驗結果------------------------------------------------------------------------- 45 4.1.2 討論------------------------------------------------------------------------------- 47 4.1.3 圖表------------------------------------------------------------------------------- 49 4.2 mDDA1基因之選殖與功能分析及受p53誘導之機制分析 4.2.1 實驗結果 (1) mDDA1 cDNA之選殖-------------------------------------------------------- 54 (2) mDDA1 genomic DNA之選殖---------------------------------------------- 56 (3) p53活化mDDA1表現之機制----------------------------------------------- 57 (4) mDDA1的生物功能分析---------------------------------------------------- 58 (5) mDDA1為thiamine transporter基因---------------------------------------- 59 4.2.2 討論 (1) p53誘導mTHTR-1表現之機制--------------------------------------------- 61 (2) mTHTR-1基因的生物功能角色------------------------------------------- 62 4.2.3 圖表------------------------------------------------------------------------------- 67 4.3 mDDA3基因之選殖與功能分析及受p53誘導之機制分析 4.3.1 實驗結果 (1) mDDA3 cDNA之選殖-------------------------------------------------------- 82 (2) mDDA3基因的genomic DNA之選殖------------------------------------- 83 (3) mDDA3 transcripts的5''-end heterogeneity成因之分析---------------- 83 (4) Heterogeneous mDDA3 cDNAs之分析----------------------------------- 84 (5) DDA3 transcript在老鼠和人類組織之表現分析----------------------- 85 (6) 以RNase protection和primer extension方法印證 mDDA3 mRNA的5''-end heterogeneity ------------------------------------ 85 (7) p53誘導mDDA3表現之機制----------------------------------------------- 87 (8) mDDA3的生物功能分析---------------------------------------------------- 88 (9) 人類DDA3 cDNA之選殖----------------------------------------------------- 89 4.3.2 討論------------------------------------------------------------------------------- 90 (1) Differential transcription initiation及alternative RNA splicing調控mDDA3表現之探討------------------------------------ 90 (2) mDDA3基因表現之調控---------------------------------------------------- 92 (3) mDDA3的生物功能角色---------------------------------------------------- 94 4.3.3 圖表------------------------------------------------------------------------------- 97 (伍)‧結論----------------------------------------------------------------------------------- 119 (陸)‧參考文獻----------------------------------------------------------------------------- 120 附錄 (一) 附圖------------------------------------------------------------------------------------ 139 (二) 英文論文 1. Identification of a novel mouse p53 target gene DDA3---------------------- 140 2. Transcriptional induction of a thiamine transporter gene by p53----------------------------------------------------------------------------------- 150
Huang, Hua-Ying, i 黃華盈. "The enhancer of p53 response element sequence variants in p53 family regulated genes". Thesis, 2008. http://ndltd.ncl.edu.tw/handle/32308460068627787253.
Pełny tekst źródła國防醫學院
生物及解剖學研究所
96
The p53 gene family consists of three genes, p53, p63, and p73, which encoding for sequence-specific nuclear transcription factors with high homology in their own DNA binding domain. These transcription factors could recognize the similar responsive element (RE) in their target genes. Their inactivation or aberrant expression may determine tumor progression or developmental disease. It is well-known that genes have p53 RE in promoter region can be trans-activated by p53 family members. But the regulation mechanism of the p53 RE at enhancer region is still un-clarity. The p53 REs with different core sequence, different direction, and different length are important factors for trans-activation of the p53 family members. We proposed that the regulation of p53 RE sequence variants in enhancer region is different from the promoter region. Therefore, we established an in vitro model system for analysis transcriptional regulation by different p53 REs at promoter and enhancer regions. In addition, we also analyzed the different transcriptional responses regulated by different isotypes of p53 and p63 to find out the determinant factors of these REs. Furthermore, we used the online database to search the known and predicted RE sequence be regulated by p53 family to evaluate our model. Finally, we could use this in vitro model system to search the novel genes regulated by p53 family.
Chuang, Hui-Chuan, i 莊惠娟. "Genome-wide expression profiling of p53-regulated genes in human non-small cell lung cells by cDNA microarray". Thesis, 2000. http://ndltd.ncl.edu.tw/handle/17319213262891568134.
Pełny tekst źródła國立中央大學
生命科學研究所
88
p53 is a well-studied tumor suppressor gene. In the past, many conventional methods were used to identify p53 function-associated genes. In order to identified unknown genes whose function were related with p53, colormetric cDNA microarray were used to study the genome-wide transcriptional expression pattern of genes, which are regulated by tumor suppressor gene p53 in human non small cell lung cancer cell line H1299. To chase the downstream genes of p53, the cell line H1299-p53V173L was used for experiments since it expresses wild-type p53 once the growth temperature was shifted from 37℃ to 32℃. Post temperature shift from 37℃ to 32℃, cells were harvested at the following time intervals: 0, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24 hours. The derived cDNA were labeled and hybridized to microarray membranes containing 9600 cDNA dots. The signal density of these cDNA dots were acquired with image processing for statistic analysis. Through such process, totally 144 genes were identified as p53-upregulated or p53-downregulated, and were further sequence verified. The majority of these genes are related with signal transduction, cell cycle, metabolic regulation and DNA repair. Some genes found associated with p53 in the literature were successfully identified, for instance, PCNA, ku80, APEX etc. According to the data in this thesis, p53 might control many genes expression, even though when cells were not stimulated by X-ray or hypoxia. Among those genes, the most interesting one is the MHC (major compatibility complex) class I, which plays a major role in immune response. Different alleles of MHC class I was observed significantly and consistently induced by p53. This indicates that p53 may be involved in some immune pathway to target stressed or tumor cells for elimination. The association between p53 and immune system was all the time totally ignored. With cDNA microarray technology, this association is confirmed and is worth with further investigation.
Książki na temat "P53-regulated genes"
Barlow, Jason William. Studies of p53 regulated genes in Li-Fraumeni syndrome and analysis of the effects of retinoic acid on pediatric rhabdomyosarcoma cell lines. 2003.
Znajdź pełny tekst źródłaStreszczenia konferencji na temat "P53-regulated genes"
Vinall, Ruth L., Qian Chen, George Talbott, Neil Hubbard, Clifford Tepper i Alexander Borowsky. "Abstract 2820: Use of a genetically engineered mouse model and RNA sequencing to identify genes that are aberrantly regulated by mutant p53 in prostate cells following irradiation". W Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2820.
Pełny tekst źródłaTokino, Takashi, Ryota Koyama, Masashi Idogawa i Yasushi Sasaki. "Abstract 5308: BRMS1L, a metastatic suppressor gene, is transcriptionally regulated by p53". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5308.
Pełny tekst źródłaTokino, Takashi, Ryota Koyama, Masashi Idogawa i Yasushi Sasaki. "Abstract 5308: BRMS1L, a metastatic suppressor gene, is transcriptionally regulated by p53". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-5308.
Pełny tekst źródłaKim, Reuben H., Mo K. Kang, Terresa Kim, Paul Yang, Christine Hong, Ki-Hyuk Shin i No-Hee Park. "Abstract 2256: p53 gene expression is epigenetically regulated during replicative senescence in keratinocytes". W Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2256.
Pełny tekst źródłaSuh, Seong O., Mohd Saif Zaman, Varahram Shahryari, Yi Chen, Jan Liu, Z. Laura Tabatabai, Sanjay Kakar, Guoren Deng i Rajvir Dahiya. "Abstract 2035: The levels of miR-145 are regulated by DNA methylation and p53 gene status in prostate cancer". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2035.
Pełny tekst źródła