BÁO CÁO KHOA HỌC: " SEQUENCE ANALYSIS OF CANINE LINE-1 ELEMENTS AND P53 GENE IN CANINE TRANSMISSIBLE VENEREAL TUMOR" DOC

Western blotCell lysates were made as described previously [12]. The celllysates or isolated exosomes were run on SDS ⁄ PAGE(4–20%) (Invitrogen) and transferred to Immobilon-P mem-branes (Millipore). Membranes were blotted with thefollowing antibodies (Santa Cruz Biotechnology, SantaCruz, CA, USA):[r]

full-length p53 using modulation of activity of the p53DNA-binding domains by oxidation of cysteine residues (topreclude binding within the p53 core domain) and/or byantibodies mapping to epitopes at t he protein C-terminus (toblock bindin g within the CTDBS). In the absence of anti-bo[r]

the most ‘reactive’ are the two apoptosis-relatedresponse elements Noxa and PUMA BS2 (four GGand two AG, or five GG and one AG, respectively).Global DNA cis-platination may shift the distributionof p53 protein molecules bound to various p53DBSstowards those less susceptible to the modification([r]

of trans-PtHMP in HL-60 cells demonstrated a signi-ficant efficiency of this new analogue to inhibit thegrowth of this human leukemia cancer cell line [6]. TheIC50values (the concentration of the compound thatafforded 50% cell killing) were comparable with thoseobtained for cisplatin. Thus, it is of i[r]

RAR–DNA binding is not due to different levels of theretinoic acid receptor induced by the treatment, as RARexpression was similar in control, vitamin A-deficiency andhypervitaminosis (Fig. 5) rats. An antibody against aprotein unrelated to vitamin A was used as a mock controland binding was not obse[r]

murine double minute 2 (MDM2). The tumor suppressorgene p53 plays a key role in regulating the cell cycle andserves as a principal mediator of growth arrest, senes-cence, and apoptosis in response to a broad array of cellu-lar damage [3]. The p21/WAF1 protein is encoded by thehuman WAF[r]

generate new blood vessels to support colonization in remote sites. The accumulation of genetic lesions may lead through an identifiable progression of altered phenotypes as is noted in colon cancer: hyperplasia →adenoma →dysplasia →carcinoma in situ →invasive carcinoma. Premalignant changes have al[r]

production in vivo, and how glucose up-regulates theexpression of NOX2 requires further investigation.It has been reported that NF-jB, p38MAPK andp53 are the key points relating to apoptosis [12]. Aninhibitor of p38MAPK was used to confirm its rolein apoptosis. The increased level of phosphorylationi[r]

phageal cancer is a multifactorial process associated with a variety of risk factors. Cumulative evidence suggests that tobacco smoking, heavy alcohol drink-ing, micronutrient deficiency, and dietary carcinogen exposure may cause the disease.[2-5] However, even in the at-risk population, only a port[r]

between HPV types 16, 18, and 33 E6 at mediating thedegradation of p53 in vivo and showed that GFP can beused as an effective epitope tag for comparing E6 levels intransfected cells.Impairment of p53 activity may not be directly propor-tional to its degradation because E6 impairs p5[r]

32595.34.Dudenhoffer,C.,Kurth,M.,Janus,F.,Deppert,W.&Wies-muller, L. (1999) Dissociation of the recombination control andthe sequence-sp ecific tra nsactivation fun ction of P53. Oncogene18, 5773–5784.35. Soubeyrand, S., Pope, L., Pakuts, B. & Hache, R.J. (2003)Threonines 2638/2[r]

rates at 38 °C, with a doubling time of about 12 h. At 32 °Cthe growth rates were slower but again approximately thesame for the first 24 h, during which both cell linescompleted at least one traverse of the cell cycle. After thistime, whereas the Pro190 cells continued to proliferate, theVal135 cell[r]

control for total p53 protein. (B) Comparison of the immunoreactivi-ty of purified murine wild-type p53 proteins with phospho-p53 (S15)antibody and PAb421 expressed in BVE or E. coli BL21-competentcells. Western blot analysis of p53 protein using PAb240 as a refer-ence con[r]

Duchenne muscular dystrophy is a degenerative and fatal disorderof muscle affecting approximately 1 in 3500 boys. Victims ofDuchenne dystrophy show early abnormalities in walking and run-ning. By the age of 5, the victim cannot run and has difficulty stand-ing, and by early adolescence, walkin[r]

69. Das, S., El-Deiry, W. S., and Somasundaram, K. (2003). Efficient growth inhibition ofHPV 16 E6-expressing cells by an adenovirus-expressing p53 homologue p73beta.Oncogene 22: 8394 – 8402.70. Boyd, J. (1996). Molecular biology in the clinicopathologic assessment of endometrialcarcinoma sub[r]

and cell–cell association also play critical roles. The changing the balance of angiogenesis inducers andcountervailing inhibitors (Hanahan and Folkman, 1996).angiogenesis-initiating signals are exemplified by vas-cular endothelial growth factor (VEGF) and acidic and One common strategy for shifting[r]

Results: Gastrointestinal tissues and peripheral blood lymphocytes ubiquitously expressed KIAA0247. 56 C RCpatients fell into two group categories according to fecal KIAA0247 mRNA expression levels. The group with higherfecal KIAA0247 (n = 22; ≥ 0.48 97) had a significantly greater five-year overall[r]

Large organizations, or large ISPs operating the DNS servers for their customers, often delegate part of the domain name space to a separate system. For example, a huge bigcompany.com might have headquarters records on the main DNS but delegate DNS chores for maintaining and housing east.bigcompany.[r]

Results: Gastrointestinal tissues and peripheral blood lymphocytes ubiquitously expressed KIAA0247. 56 C RCpatients fell into two group categories according to fecal KIAA0247 mRNA expression levels. The group with higherfecal KIAA0247 (n = 22; ≥ 0.48 97) had a significantly greater five-year overall[r]

appropriate physiologic signals. Senescent cells have been identified in patients whose premalignant lesions harbor activated oncogenes, for instance, dysplastic nevi that encode an activated form of BRAF (see below), demonstrating that induction of senescence is a protective mechanism that operates[r]