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195501“…RESULTS: Phosphospecific antibodies, mutational analysis, and in vitro kinase assays demonstrated that Brk specifically mediated STAT5b phosphorylation at the activating tyrosine, Y699. …”
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195502“…BACKGROUND: Drosophila has six receptor protein tyrosine phosphatases (RPTPs), five of which are expressed primarily in neurons. Mutations in all five affect axon guidance, either alone or in combination. …”
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195503“…During Vif-negative HIV-1 replication, A3G is incorporated into HIV-1 particles, induces mutations in reverse transcribed viral DNA and inhibits reverse transcription. …”
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195504“…Two human colon cancer cell lines were used (WIDR and SW620 both p53 mutated). LOHP plus FA were applied for 2 h, just before a 48 h FU exposure. …”
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195505por Mirjolet, J-F, Barberi-Heyob, M, Didelot, C, Peyrat, J-P, Abecassis, J, Millon, R, Merlin, J-L“…In relation with p53 functionality, but independently of p53 mutational status, after exposure to 5-FU equitoxic concentration, all cell lines were able to arrest in G1. …”
Publicado 2000
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195506“…BACKGROUND: Numerous papers have addressed the association of mutations and polymorphisms of susceptibility genes with autoimmune inflammatory disorders. …”
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195507“…BACKGROUND: Several studies have demonstrated that synthetic lethal genetic interactions between gene mutations provide an indication of functional redundancy between molecular complexes and pathways. …”
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195508“…When the three amino acids Q138, P139 and D140 were all mutated to glycine, binding of F1-40 to the recombinant BoNT/A light chain peptide was abolished. …”
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195509por Colley, Beverly S, Cavallin, Melissa A, Biju, KC, Marks, David R, Fadool, Debra A“…To examine the possibility that the Src homology 2 (SH2) domains of Grb10 were directly binding to basally phosphorylated tyrosines in Kv1.3, we utilized point mutations to substitute multiple tyrosine residues with phenylalanine. …”
Publicado 2009
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195510por Lee, Nancy, Woodrum, Chelsey L, Nobil, Alison M, Rauktys, Aubrey E, Messina, Michael P, Dabora, Sandra L“…BACKGROUND: Tuberous sclerosis complex (TSC) is an autosomal dominant tumor suppressor syndrome, characterized by hamartomatous growths in the brain, skin, kidneys, lungs, and heart, which lead to significant morbidity. TSC is caused by mutations in the TSC1 or TSC2 genes, whose products, hamartin and tuberin, form a tumor suppressor complex that regulates the PI3K/Akt/mTOR pathway. …”
Publicado 2009
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195511“…Many researchers have evaluated life-history traits of C. elegans in investigations covering quite different aspects such as ecotoxicology, inbreeding depression and heterosis, dietary restriction/supplement, mutations, and ageing. Such traits include juvenile growth rates, age at sexual maturity, adult body size, age-specific fecundity/mortality, total reproduction, mean and maximum lifespan, and intrinsic population growth rates. …”
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195512por Daher, João Paulo L, Ying, Mingyao, Banerjee, Rebecca, McDonald, Rebecca S, Hahn, Myriam Dumas, Yang, Lichuan, Flint Beal, M, Thomas, Bobby, Dawson, Valina L, Dawson, Ted M, Moore, Darren J“…BACKGROUND: Missense mutations and multiplications of the α-synuclein gene cause autosomal dominant familial Parkinson's disease (PD). α-Synuclein protein is also a major component of Lewy bodies, the hallmark pathological inclusions of PD. …”
Publicado 2009
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195513por Bruni, Roberto, Costantino, Angela, Tritarelli, Elena, Marcantonio, Cinzia, Ciccozzi, Massimo, Rapicetta, Maria, El Sawaf, Gamal, Giuliani, Alessandro, Ciccaglione, Anna Rita“…RQA greatly strengthened the reliability of the hypothesis by the scoring of a lot of cross-recurrences between FP and CT peptides hydrophobicity patterning largely outnumbering chance expectations and pointing to putative interaction sites. Intriguingly, mutations in the CT region of E1, reducing the fusion process in vitro, strongly reduced the amount of cross-recurrence further supporting interaction between this region and FP. …”
Publicado 2009
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195514por Van Poucke, Mario, Melkebeek, Vesna, Erkens, Tim, Van Zeveren, Alex, Cox, Eric, Peelman, Luc J“…Two silent and 2 missense (both S → L at position 360 and 633) mutations were found, but none was associated with the F4ab/ac receptor phenotype. …”
Publicado 2009
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195515por Möckelmann, Nikolaus, von Schönfels, Witigo, Buch, Stephan, von Kampen, Oliver, Sipos, Bence, Egberts, Jan Hendrik, Rosenstiel, Philip, Franke, Andre, Brosch, Mario, Hinz, Sebastian, Röder, Christian, Kalthoff, Holger, Fölsch, Ulrich R, Krawczak, Michael, Schreiber, Stefan, Bröring, Clemens Dieter, Tepel, Jürgen, Schafmayer, Clemens, Hampe, Jochen“…Subgroup analyses for N = 143 patients with early manifestation of CRC (≤50 age at diagnosis) were performed for all CARD loci and subgroup analyses for diverse age strata were carried out for CARD15 mutations R702W, G908R and L1007fs. In addition, all SNPs were tested for association with disease presentation and family history of CRC. …”
Publicado 2009
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195516por Fan, Catherine, He, Lizhi, Kapoor, Anil, Rybak, Adrian P, De Melo, Jason, Cutz, Jean-Claude, Tang, Damu“…BACKGROUND: PTEN is the second most mutated tumor suppressor gene other than p53. It suppresses tumorigenesis by dephosphorylating phosphatidylinositol (3,4,5)-triphosphate (PIP3) to phosphatidylinositol (4,5)-biphosphate (PIP2), thereby directly inhibiting phosphatidylinositol 3 kinase (PI3K)-mediated tumorigenic activities. …”
Publicado 2009
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195517por Palacios, Gustavo, Hornig, Mady, Cisterna, Daniel, Savji, Nazir, Bussetti, Ana Valeria, Kapoor, Vishal, Hui, Jeffrey, Tokarz, Rafal, Briese, Thomas, Baumeister, Elsa, Lipkin, W. Ian“…Virus genomic sequencing of 26 Argentinian samples representing both severe and mild disease indicated no evidence of reassortment, mutations associated with resistance to antiviral drugs, or genetic drift that might contribute to virulence. …”
Publicado 2009
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195518“…Analysis of potential novel MHCII binding peptides resulting from fusion of hDM to C6 MH3B1 and the two mutations in hDM, and of the structure of hDM compared to the wild-type enzyme suggests that hDM-C6 MH3B1 should exhibit minimal immunogenicity in humans. …”
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195519por Li, Nanfang, Wang, Hongmei, Yang, Jin, Zhou, Ling, Hong, Jing, Guo, Yanying, Luo, Wenli, Chang, Jianhang“…RESULTS: By systemically screening variations of NEDD4L, we did not identify any functional mutations in NEDD4L. A new common variation (296921-296923delTTG), which is not found in the NCBI database, was identified. …”
Publicado 2009
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195520“…Results in this paper suggest that several genes are important in the regulation of androstenone level in boars and warrant further evaluation of the above mentioned candidate genes, including analyses in different breeds, identification of causal mutations and possible gene interactions.…”
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