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PMID |
Sentence |
1 |
2560858
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By WB and competitive WB assays, bovine sera that were ELISA-positive to BLV reacted with one or more of p12, p15, and p24 of BLV, and with only p24 of HTLV-I.
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2 |
2560858
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Human sera that were ELISA-positive to HTLV-I reacted with p12 and p24 of BLV, and with one or more of p12, p15, p19, and p24 of HTLV-I.
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3 |
8574147
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The majority of the clones expressed SIV p27 antigen and low levels of virus reverse transcriptase activity.
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4 |
8574147
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Western blot analysis, performed with either monoclonal or polyclonal sera, showed that a chronically infected clone (B7) produced particles which contained envelope (gp135 and gp43), gag precursors and gag proteins (p27, p16 and p8).
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5 |
9529073
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Two recombinant baculovirus-expressed P. cynomolgi MSP1 proteins, which are analogous to the 42- and 19-kDa C-terminal fragments of P. falciparum MSP1, were tested by immunizing three groups of three animals each with either p42, p19, or both together.
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6 |
9863243
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According to the protein sequence of HCV-BK and its epitope profiles which combined the hydrophilicity, accessibility, flexibility, antigenicity, charge distribution and HPLC reserve coefficient of protein using the "Goldkey" computer program, we designed and synthesized the following peptides: P1(475-495), P3(449-468), P4(658-663), P5(645-663), P6(484-489), P7(475-489), P15(655-662), P16(230-237), P17(225-237), P18(1220-1240), P19(1694-1735), P24(1230-1240), P25(1482-1493), P26(384-389), P27(2355-2389).
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7 |
10436819
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Replacement of tumour suppressor gene function using adenoviruses to transfer wild-type p53 and p16 genes can produce dramatic anti-tumour effects, both in vitro and in vivo.
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8 |
10627538
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Monospecific rabbit polyclonal antibody produced to a glutathione S-transferase-9GL fusion protein specifically immunoprecipitated a 14-kDa protein from macrophage cell cultures infected with the ASFV isolate Malawi Lil-20/1 (MAL).
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9 |
10627538
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Time course analysis and viral DNA synthesis inhibitor experiments indicated that p14 was a late viral protein.
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10 |
10699034
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The emm genes from 53 GAS isolates, collected between 1985 and 1995 from individuals with pharyngitis, impetigo, acute RF (ARF), RHD, or meningitis as well as from individuals without infections, were amplified by PCR and sequenced.
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11 |
10729731
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Three specific proteins have been detected within the embryonic coats (IGFBP3, HB-EGF, P19).
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12 |
11581178
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This study shows that immunoreactivity of the class I-specific peptide and myosin does not differ between controls and acute RF (ARF)/RHD in populations that are highly endemic for GAS, raising the possibility that the association is related to GAS exposure, not the presence of ARF/RHD.
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13 |
11836673
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Systems studied have included lysis by interleukin-2 (IL-2)-activated lymphokine-activated killer (LAK) cells, tumor necrosis factor-alpha (TNF-alpha), a p16-expressing adenovirus vector, suicide gene therapy using the herpes simplex virus-tyrosine kinase (HSV-tk) followed by ganciclovir, and immunomodulatory gene therapy with IL-2, IL-4, interferon-gamma (IFN-gamma), IFN-alpha, TNF-alpha, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-6, and IL-1beta transfected into tumors.
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14 |
11836673
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Since platelet-derived growth factor (PDGF) is thought to be an autocrine growth factor for mesothelioma STI-571 (Gleevec; Novartis, Basel, Switzerland), a highly selective inhibitor of the PDGF receptor tyrosine kinase, is being tested in a phase II trial.
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15 |
12438574
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Evidence that replication of the antitumor adenovirus ONYX-015 is not controlled by the p53 and p14(ARF) tumor suppressor genes.
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16 |
12438574
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Recent data have shown that p14(ARF), a positive regulator of p53, inhibits ONYX-015 replication in cells with a wild-type p53, a phenotype that characterizes normal cells.
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17 |
12438574
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We, however, found that ONYX-015 activates p53 in tumor cells and in normal cells and that this can occur without p14(ARF) induction.
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18 |
12438574
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We also show that ONYX-015 is not attenuated in cells with functional p53, whether or not p14(ARF) is expressed, and that where attenuation does occur, it is cell type specific.
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19 |
12438574
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Evidence that replication of the antitumor adenovirus ONYX-015 is not controlled by the p53 and p14(ARF) tumor suppressor genes.
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20 |
12438574
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Recent data have shown that p14(ARF), a positive regulator of p53, inhibits ONYX-015 replication in cells with a wild-type p53, a phenotype that characterizes normal cells.
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21 |
12438574
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We, however, found that ONYX-015 activates p53 in tumor cells and in normal cells and that this can occur without p14(ARF) induction.
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22 |
12438574
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We also show that ONYX-015 is not attenuated in cells with functional p53, whether or not p14(ARF) is expressed, and that where attenuation does occur, it is cell type specific.
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23 |
12438574
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Evidence that replication of the antitumor adenovirus ONYX-015 is not controlled by the p53 and p14(ARF) tumor suppressor genes.
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24 |
12438574
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Recent data have shown that p14(ARF), a positive regulator of p53, inhibits ONYX-015 replication in cells with a wild-type p53, a phenotype that characterizes normal cells.
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25 |
12438574
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We, however, found that ONYX-015 activates p53 in tumor cells and in normal cells and that this can occur without p14(ARF) induction.
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26 |
12438574
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We also show that ONYX-015 is not attenuated in cells with functional p53, whether or not p14(ARF) is expressed, and that where attenuation does occur, it is cell type specific.
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27 |
12438574
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Evidence that replication of the antitumor adenovirus ONYX-015 is not controlled by the p53 and p14(ARF) tumor suppressor genes.
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28 |
12438574
|
Recent data have shown that p14(ARF), a positive regulator of p53, inhibits ONYX-015 replication in cells with a wild-type p53, a phenotype that characterizes normal cells.
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29 |
12438574
|
We, however, found that ONYX-015 activates p53 in tumor cells and in normal cells and that this can occur without p14(ARF) induction.
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30 |
12438574
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We also show that ONYX-015 is not attenuated in cells with functional p53, whether or not p14(ARF) is expressed, and that where attenuation does occur, it is cell type specific.
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31 |
15050943
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The question needs to be resolved as a matter of urgency because current approaches to controlling ARF/RHD in Aboriginal communities have clearly been ineffective.
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32 |
15452215
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Some of these genes include those encoding cyclins D3, D2, B1, C, and H, cyclin-dependent kinases (cdk's) 4 and 6, the cdk inhibitors p16, p15, and p18, and other genes involved in protein degradation and DNA replication.
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33 |
15568617
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We predicted these putative aberrant translation products from the cDNA of three tumor-associated antigens (Ag): a transmembrane glycoprotein of the class I receptor tyrosine kinase erbB family HER-2, telomerase reverse transcriptase (TERT) and prostatic acid phosphatase (PAP).
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34 |
15568617
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CD8+ T cells from mice immunized with HER-2 derived protective Arf peptides specifically recognized HER-2 transfected tumor cells.
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35 |
15691231
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Genetic alterations in the tumour suppressor genes, P16/CDKN2A and neurofibromatosis 2 (NF2), are found both in human MPM and in asbestos-exposed Nf2-deficient mice.
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36 |
15721476
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Rarely, melanoma susceptibility is increased more than tenfold by heritable mutations in the cell cycle regulatory genes CDKN2A and CDK4.
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37 |
16005340
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More than a century of research, mainly in North America and Europe, has improved our understanding of ARF and RHD.
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38 |
16005340
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The most effective approach for control of ARF and RHD is secondary prophylaxis, which is best delivered as part of a coordinated control programme.
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39 |
16005340
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More than a century of research, mainly in North America and Europe, has improved our understanding of ARF and RHD.
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40 |
16005340
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The most effective approach for control of ARF and RHD is secondary prophylaxis, which is best delivered as part of a coordinated control programme.
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41 |
17055511
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We report here, for the first time, a comparison of naturally acquired antibody responses to the 42 and 19 kDa C-terminal processing products of Plasmodium vivax Merozoite Surface Protein-1 assayed by ELISA using p42 and p19 baculovirus-derived recombinant proteins, respectively.
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42 |
17288529
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The restoration of some of the mutated or deleted tumor-suppressor genes (p53, Rb, PTEN, hSNF, INK/ARF and WT) by demethylation or reacetylation of their histones has been accomplished.
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43 |
17624445
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Candidates were constructed by cloning genes encoding the MVV gag polyprotein and gag proteins p16 and p25 fused to a beta-galactosidase reporter in a plasmid backbone.
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44 |
17704944
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The mucosal IgA in the intestinal secretions of CJ1-infected birds reacted significantly with peptides P16 and P21 indicating that the specificity of the mucosal response is different from the systemic response.
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45 |
18193657
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Ongoing efforts are now addressing the epidemiology of GAS infections in developing countries so that new vaccines can be designed to prevent the infections that may trigger ARF and RHD.
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46 |
18289047
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The "methylator phenotype", with inactivation by promoter hypermethylation of numerous genes in malignant melanoma cell lines and primary tumors (p16, PTEN, RASSF1, estrogen receptor, retinoic acid receptor beta, SOCS1 and -2, MGMT etc.) offers a strong rationale for treatment approaches based on the use of DNA demethylating agents.
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47 |
19056444
|
Results showed that although the basal production of IFN-gamma and IL-6 was impaired (P<0.05) in PBMCs of neonatal foals at birth, the basal production of IL-8, IL-12(p35/p40) and IL-23(p19/p40) were either in excess of or comparable to that of older foals.
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48 |
19056444
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In response to Rhodococcus equi and CpG-ODN stimulation in vitro, PBMCs of neonatal foals showed increased (P<0.05) expression of IFN-gamma and IL-6, and preferentially increased expression of either IL-23(p19/p40) with R. equi stimulation or IL-12(p35/p40) with CpG-ODN stimulation.
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49 |
20451455
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The biology of HPV-positive oropharyngeal cancer is distinct with P53 degradation, retinoblastoma RB pathway inactivation, and P16 upregulation.
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50 |
20451455
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By contrast, tobacco-related oropharyngeal cancer is characterised by TP53 mutation and downregulation of CDKN2A (encoding P16).
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51 |
20451455
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The biology of HPV-positive oropharyngeal cancer is distinct with P53 degradation, retinoblastoma RB pathway inactivation, and P16 upregulation.
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52 |
20451455
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By contrast, tobacco-related oropharyngeal cancer is characterised by TP53 mutation and downregulation of CDKN2A (encoding P16).
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53 |
20614273
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The tumors have a distinct immunohistochemical profile characterized by strong and diffuse p16 reactivity, low or negative p53 staining and high Ki67 labeling scores.
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54 |
20943622
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HPV status is also associated with p16 expression and HPV+ tumours are less likely to harbour p53 mutations.
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55 |
21246036
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Four of these proteins, designated P8, P19, P23 and P32, had a predicted signal sequence.
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56 |
21246036
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We generated recombinant (r) P8, P19 and P23 in a Drosophila expression system for functional and immunization studies. rP8 showed anti-complement activity and rP23 demonstrated anti-coagulant activity.
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57 |
21246036
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Ixodes scapularis feeding was significantly impaired when nymphs were fed on rabbits immunized with a cocktail of rP8, rP19 and rP23, a hall mark of tick-immunity.
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58 |
21246036
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Four of these proteins, designated P8, P19, P23 and P32, had a predicted signal sequence.
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59 |
21246036
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We generated recombinant (r) P8, P19 and P23 in a Drosophila expression system for functional and immunization studies. rP8 showed anti-complement activity and rP23 demonstrated anti-coagulant activity.
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60 |
21246036
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Ixodes scapularis feeding was significantly impaired when nymphs were fed on rabbits immunized with a cocktail of rP8, rP19 and rP23, a hall mark of tick-immunity.
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61 |
22729401
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ARF and RHD are sequelae resulting from an infection of Streptococcus pyogenes.
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62 |
22729401
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Here we review and discuss the dynamic epidemiology of streptococcal infection and its associated diseases (ARF and RHD), with a focus on disease burden in temperate versus tropical regions, the tissue tropism of the organism and the efforts towards vaccine development in relation to the available animal models.
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63 |
22729401
|
ARF and RHD are sequelae resulting from an infection of Streptococcus pyogenes.
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64 |
22729401
|
Here we review and discuss the dynamic epidemiology of streptococcal infection and its associated diseases (ARF and RHD), with a focus on disease burden in temperate versus tropical regions, the tissue tropism of the organism and the efforts towards vaccine development in relation to the available animal models.
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65 |
22997239
|
Dual suppression of the cyclin-dependent kinase inhibitors CDKN2C and CDKN1A in human melanoma.
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66 |
22997239
|
To identify downstream effectors of MAPK signaling that could be used as potential additional therapeutic targets for BRAF(V600E) inhibitors, we used hTERT/CDK4R24C/p53DD-immortalized primary human melanocytes genetically modified to ectopically express BRAF ( V600E ) or NRAS ( G12D ) and observed induction of the AP-1 transcription factor family member c-Jun.
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67 |
22997239
|
Using a dominant negative approach, in vitro cell proliferation assays, western blots, and flow cytometry showed that MAPK signaling via BRAF(V600E) promotes melanoma cell proliferation at G1 through AP-1-mediated negative regulation of the INK4 family member, cyclin-dependent kinase inhibitor 2C (CDKN2C), and the CIP/KIP family member, cyclin-dependent kinase inhibitor 1A (CDKN1A).
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68 |
22997239
|
These effects were antagonized by pharmacological inhibition of CDKN2C and CDKN1A targets CDK2 and CDK4 in vitro.
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69 |
22997239
|
In contrast to BRAF ( V600E ) or NRAS ( G12D )-expressing melanocytes, melanoma cells have an inherent resistance to suppression of AP-1 activity by BRAF(V600E)- or MEK-inhibitors.
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70 |
23460736
|
The ataxia telangiectasia mutated kinase pathway regulates IL-23 expression by human dendritic cells.
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71 |
23460736
|
In this study, we show for first time, to our knowledge, that the ataxia telangiectasia mutated (ATM) pathway, involved in DNA damage sensing, acts as an IL-23 repressor.
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72 |
23460736
|
Inhibition of ATM with the highly selective antagonist KU55933 markedly increased IL-23 secretion in human monocyte-derived DC and freshly isolated myeloid DC.
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73 |
23460736
|
Priming naive CD4(+) T cells with ATM-inhibited DC increased Th17 responses over and above those obtained with mature DC.
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74 |
23460736
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Although ATM blockade increased the abundance of p19, p35, and p40 mRNA, IL-12p70 secretion was unaffected.
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75 |
23460736
|
To further examine a role for ATM in IL-23 regulation, we exposed DC to low doses of ionizing radiation.
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76 |
23460736
|
Exposure of DC to x-rays resulted in ATM phosphorylation and a corresponding depression of IL-23.
|
77 |
23460736
|
Importantly, ATM inhibition with KU55933 prevented radiation-induced ATM phosphorylation and abrogated the capacity of x-rays to suppress IL-23.
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78 |
23460736
|
To explore how ATM repressed IL-23, we examined a role for endoplasmic reticulum stress responses by measuring generation of the spliced form of X-box protein-1, a key endoplasmic reticulum stress transcription factor.
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79 |
23460736
|
Inhibition of ATM increased the abundance of X-box protein-1 mRNA, and this was followed 3 h later by increased peak p19 transcription and IL-23 release.
|
80 |
23460736
|
In summary, ATM activation or inhibition, respectively, inhibited or augmented IL-23 release.
|
81 |
23460736
|
The ataxia telangiectasia mutated kinase pathway regulates IL-23 expression by human dendritic cells.
|
82 |
23460736
|
In this study, we show for first time, to our knowledge, that the ataxia telangiectasia mutated (ATM) pathway, involved in DNA damage sensing, acts as an IL-23 repressor.
|
83 |
23460736
|
Inhibition of ATM with the highly selective antagonist KU55933 markedly increased IL-23 secretion in human monocyte-derived DC and freshly isolated myeloid DC.
|
84 |
23460736
|
Priming naive CD4(+) T cells with ATM-inhibited DC increased Th17 responses over and above those obtained with mature DC.
|
85 |
23460736
|
Although ATM blockade increased the abundance of p19, p35, and p40 mRNA, IL-12p70 secretion was unaffected.
|
86 |
23460736
|
To further examine a role for ATM in IL-23 regulation, we exposed DC to low doses of ionizing radiation.
|
87 |
23460736
|
Exposure of DC to x-rays resulted in ATM phosphorylation and a corresponding depression of IL-23.
|
88 |
23460736
|
Importantly, ATM inhibition with KU55933 prevented radiation-induced ATM phosphorylation and abrogated the capacity of x-rays to suppress IL-23.
|
89 |
23460736
|
To explore how ATM repressed IL-23, we examined a role for endoplasmic reticulum stress responses by measuring generation of the spliced form of X-box protein-1, a key endoplasmic reticulum stress transcription factor.
|
90 |
23460736
|
Inhibition of ATM increased the abundance of X-box protein-1 mRNA, and this was followed 3 h later by increased peak p19 transcription and IL-23 release.
|
91 |
23460736
|
In summary, ATM activation or inhibition, respectively, inhibited or augmented IL-23 release.
|
92 |
23687157
|
The CEL-im cell line has negative telomerase activity, and when compared with the primary passage 2 CEL cell counterpart, mRNA expression of tumor suppressor protein p53, mouse double minute 2 (Mdm2), cyclin dependent kinase (CDK) inhibitor p21 (p21(WAF)), and CDK inhibitor p16 (p16(INK4)) were downregulated in the CEL-im cell line, whereas retinoblastoma (Rb), transcription factor E2F, member 1 (E2F-1), and alternative reading frame of p16(INK4) (ARF) were upregulated.
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93 |
24254845
|
Both peptides, P13 and P16, could form amyloid fibril structures to potently enhance HIV-1 infectivity.
|
94 |
24283842
|
Employing an IL-23 p19 vaccine to block IL-23 ameliorates chronic murine colitis.
|
95 |
24337749
|
KLRG1 impairs CD4+ T cell responses via p16ink4a and p27kip1 pathways: role in hepatitis B vaccine failure in individuals with hepatitis C virus infection.
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96 |
24337749
|
In this study, we investigated the expression and function of an inhibitory receptor, killer cell lectin-like receptor subfamily G member 1 (KLRG1), in the regulation of CD4(+) T cells and HBV vaccine responses during HCV infection.
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97 |
24337749
|
We demonstrated that KLRG1 was overexpressed on CD4(+) T cells from HCV-infected, HBV vaccine nonresponders compared with HBV vaccine responders.
|
98 |
24337749
|
The capacity of CD4(+) T cells to proliferate and secrete IL-2 cytokine was inversely associated with the level of KLRG1 expression.
|
99 |
24337749
|
Importantly, blocking KLRG1 signaling resulted in a significant improvement in CD4(+) T cell proliferation and IL-2 production in HCV-infected, HBV vaccine nonresponders in response to TCR stimulation.
|
100 |
24337749
|
Moreover, blockade of KLRG1 increased the phosphorylation of Akt (Ser(473)) and decreased the expression of cell cycle inhibitors p16(ink4a) and p27(kip1), which subsequently enhanced the expression of cyclin-dependent kinase 2 and cyclin E.
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101 |
24337749
|
These results suggest that the KLRG1 pathway impairs CD4(+) T cell responses to neoantigen and induces a state of immune senescence in individuals with HCV infection, raising the possibility that blocking this negative-signaling pathway might improve HBV vaccine responses in the setting of chronic viral infection.
|
102 |
24337749
|
KLRG1 impairs CD4+ T cell responses via p16ink4a and p27kip1 pathways: role in hepatitis B vaccine failure in individuals with hepatitis C virus infection.
|
103 |
24337749
|
In this study, we investigated the expression and function of an inhibitory receptor, killer cell lectin-like receptor subfamily G member 1 (KLRG1), in the regulation of CD4(+) T cells and HBV vaccine responses during HCV infection.
|
104 |
24337749
|
We demonstrated that KLRG1 was overexpressed on CD4(+) T cells from HCV-infected, HBV vaccine nonresponders compared with HBV vaccine responders.
|
105 |
24337749
|
The capacity of CD4(+) T cells to proliferate and secrete IL-2 cytokine was inversely associated with the level of KLRG1 expression.
|
106 |
24337749
|
Importantly, blocking KLRG1 signaling resulted in a significant improvement in CD4(+) T cell proliferation and IL-2 production in HCV-infected, HBV vaccine nonresponders in response to TCR stimulation.
|
107 |
24337749
|
Moreover, blockade of KLRG1 increased the phosphorylation of Akt (Ser(473)) and decreased the expression of cell cycle inhibitors p16(ink4a) and p27(kip1), which subsequently enhanced the expression of cyclin-dependent kinase 2 and cyclin E.
|
108 |
24337749
|
These results suggest that the KLRG1 pathway impairs CD4(+) T cell responses to neoantigen and induces a state of immune senescence in individuals with HCV infection, raising the possibility that blocking this negative-signaling pathway might improve HBV vaccine responses in the setting of chronic viral infection.
|
109 |
24627691
|
Distribution of Human Papillomavirus 52 and 58 Genotypes, and Their Expression of p16 and p53 in Cervical Neoplasia.
|
110 |
24796351
|
Co-expression of a viral RNA silencing suppressor, p23 or p19, in N. benthamiana resulted in earlier accumulation and increased production (15-25%) of target protein (influenza virus hemagglutinin).
|
111 |
25124771
|
Recently, Halec et al [7] demonstrated that the molecular signature of HPV-induced carcinogenesis (presence of type-specific spliced E6*| mRNA; increased expression of p16; and decreased expression of cyclin D1, p53 and Rb) was similar in cervical cancers containing single infections with one of the eight afore-mentioned 2A or 2B carcinogens to those in cancers with single infections with group 1 carcinogens.
|
112 |
25296161
|
IL-23 p19 knockout mice exhibit minimal defects in responses to primary and secondary infection with Francisella tularensis LVS.
|
113 |
25296161
|
Thus p40 has a novel role in clearance of LVS infection that is unrelated to either IL-12 or IL-23.
|
114 |
25784737
|
We review the investigation and treatment options for ARF and RHD and, most importantly, prevention methods in an African setting.
|
115 |
25879277
|
Antigens accumulated to high levels in BdT38 and BdT19 transgenic cell lines co-expressing silencing suppressor protein P38 or P19.
|
116 |
25891492
|
However, the poorly understood immunopathology of these post-infectious diseases means that, compared to much progress in other immune-mediated diseases, we still lack useful biomarkers, new therapies or an effective vaccine in ARF and RHD.
|
117 |
25891492
|
We discuss a model for the pathogenesis of ARF and RHD in terms of current immunological concepts and the potential for application of in depth "omics" technologies to these ancient scourges.
|
118 |
25891492
|
However, the poorly understood immunopathology of these post-infectious diseases means that, compared to much progress in other immune-mediated diseases, we still lack useful biomarkers, new therapies or an effective vaccine in ARF and RHD.
|
119 |
25891492
|
We discuss a model for the pathogenesis of ARF and RHD in terms of current immunological concepts and the potential for application of in depth "omics" technologies to these ancient scourges.
|
120 |
25987900
|
Most uVIN lesions are positive at immunohistochemistry to p16(ink4a) and p14(arf), but negative to p53.
|