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PMID |
Sentence |
1 |
7822811
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Here we 1) map the fine specificity of these T cells, 2) delineate a homologous peptide sequence near the N-terminus of p69, and 3) demonstrate T cell recognition of this p69 sequence (T cell epitope p69, Tep69) by patient T cells.
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2 |
7822811
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Whereas BSA triggers T cell proliferation, recombinant p69 and a synthetic Tep69 peptide induce early stages of T cell activation (IL-2R transcription) but insufficient IL-2 production and thus anergy.
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3 |
9032395
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The Rep proteins of adeno-associated virus type 2 (AAV) are known to bind to Rep recognition sequences (RRSs) in the AAV inverted terminal repeats (ITRs), the AAV p5 promoter, and the preferred AAV integration site in human chromosome 19, called AAVS1.
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4 |
9032395
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We used the 16-mer core sequences of the RRSs in the AAV ITRs and AAVS1 separately as query sequences and identified 18 new RRSs in or flanking the genes coding for the following: tyrosine kinase activator protein 1 (TKA-1); colony stimulating factor-1; insulin-like growth factor binding protein 2 (IGFBP-2); histone H2B.1; basement membrane heparan sulfate proteoglycan, also known as perlecan; the AF-9 gene product, which is involved in the chromosomal translocation t (9:11)(p22:q23); the betaB subunit of the hormone known as inhibin; interleukin-2 enhancer binding factor; an endoplasmic reticulum-Golgi intermediate compartment resident protein called p63; a global transcription activator (hSNF2L); the beta-actin repair domain; a retinoic acid-inducible factor, also known as midkine; a breast tumor autoantigen; a growth-arrest- and DNA-damage-inducible protein called gadd45; the cyclin-dependent kinase inhibitor called KIP2, which inhibits several G1 cyclin-cyclin-dependent kinase complexes; and the hereditary breast and ovarian cancer gene (BRCA1).
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5 |
16831876
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Glyoxalase II, a detoxifying enzyme of glycolysis byproduct methylglyoxal and a target of p63 and p73, is a pro-survival factor of the p53 family.
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6 |
16831876
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The p53 family proteins are transcription factors and have both common and distinct functions. p53 is a classic tumor suppressor, whereas p63 and p73 have fundamental functions in development.
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7 |
16831876
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To gain an insight into the functional diversities among the p53 family, target genes specifically regulated by p63 and p73 were examined.
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8 |
16831876
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Here, we found that the GLX2 gene, which encodes glyoxalase II enzyme, is up-regulated by p63 and p73.
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9 |
16831876
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Accordingly, a specific responsive element was found in intron 1 of the GLX2 gene, which can be activated and bound by p63 and p73.
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10 |
16831876
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Interestingly, a deficiency in GLX2 also enhances the susceptibility of a cell to DNA damage-induced apoptosis in a p53-dependent manner.
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11 |
16831876
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Given that methylglyoxal is frequently generated under both physiological and pathological conditions, we postulate that GLX2 serves as a pro-survival factor of the p53 family and plays a critical role in the normal development and in the pathogenesis of various human diseases, including cancer, diabetes, and neurodegenerative diseases.
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12 |
16831876
|
Glyoxalase II, a detoxifying enzyme of glycolysis byproduct methylglyoxal and a target of p63 and p73, is a pro-survival factor of the p53 family.
|
13 |
16831876
|
The p53 family proteins are transcription factors and have both common and distinct functions. p53 is a classic tumor suppressor, whereas p63 and p73 have fundamental functions in development.
|
14 |
16831876
|
To gain an insight into the functional diversities among the p53 family, target genes specifically regulated by p63 and p73 were examined.
|
15 |
16831876
|
Here, we found that the GLX2 gene, which encodes glyoxalase II enzyme, is up-regulated by p63 and p73.
|
16 |
16831876
|
Accordingly, a specific responsive element was found in intron 1 of the GLX2 gene, which can be activated and bound by p63 and p73.
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17 |
16831876
|
Interestingly, a deficiency in GLX2 also enhances the susceptibility of a cell to DNA damage-induced apoptosis in a p53-dependent manner.
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18 |
16831876
|
Given that methylglyoxal is frequently generated under both physiological and pathological conditions, we postulate that GLX2 serves as a pro-survival factor of the p53 family and plays a critical role in the normal development and in the pathogenesis of various human diseases, including cancer, diabetes, and neurodegenerative diseases.
|
19 |
16831876
|
Glyoxalase II, a detoxifying enzyme of glycolysis byproduct methylglyoxal and a target of p63 and p73, is a pro-survival factor of the p53 family.
|
20 |
16831876
|
The p53 family proteins are transcription factors and have both common and distinct functions. p53 is a classic tumor suppressor, whereas p63 and p73 have fundamental functions in development.
|
21 |
16831876
|
To gain an insight into the functional diversities among the p53 family, target genes specifically regulated by p63 and p73 were examined.
|
22 |
16831876
|
Here, we found that the GLX2 gene, which encodes glyoxalase II enzyme, is up-regulated by p63 and p73.
|
23 |
16831876
|
Accordingly, a specific responsive element was found in intron 1 of the GLX2 gene, which can be activated and bound by p63 and p73.
|
24 |
16831876
|
Interestingly, a deficiency in GLX2 also enhances the susceptibility of a cell to DNA damage-induced apoptosis in a p53-dependent manner.
|
25 |
16831876
|
Given that methylglyoxal is frequently generated under both physiological and pathological conditions, we postulate that GLX2 serves as a pro-survival factor of the p53 family and plays a critical role in the normal development and in the pathogenesis of various human diseases, including cancer, diabetes, and neurodegenerative diseases.
|
26 |
16831876
|
Glyoxalase II, a detoxifying enzyme of glycolysis byproduct methylglyoxal and a target of p63 and p73, is a pro-survival factor of the p53 family.
|
27 |
16831876
|
The p53 family proteins are transcription factors and have both common and distinct functions. p53 is a classic tumor suppressor, whereas p63 and p73 have fundamental functions in development.
|
28 |
16831876
|
To gain an insight into the functional diversities among the p53 family, target genes specifically regulated by p63 and p73 were examined.
|
29 |
16831876
|
Here, we found that the GLX2 gene, which encodes glyoxalase II enzyme, is up-regulated by p63 and p73.
|
30 |
16831876
|
Accordingly, a specific responsive element was found in intron 1 of the GLX2 gene, which can be activated and bound by p63 and p73.
|
31 |
16831876
|
Interestingly, a deficiency in GLX2 also enhances the susceptibility of a cell to DNA damage-induced apoptosis in a p53-dependent manner.
|
32 |
16831876
|
Given that methylglyoxal is frequently generated under both physiological and pathological conditions, we postulate that GLX2 serves as a pro-survival factor of the p53 family and plays a critical role in the normal development and in the pathogenesis of various human diseases, including cancer, diabetes, and neurodegenerative diseases.
|
33 |
16831876
|
Glyoxalase II, a detoxifying enzyme of glycolysis byproduct methylglyoxal and a target of p63 and p73, is a pro-survival factor of the p53 family.
|
34 |
16831876
|
The p53 family proteins are transcription factors and have both common and distinct functions. p53 is a classic tumor suppressor, whereas p63 and p73 have fundamental functions in development.
|
35 |
16831876
|
To gain an insight into the functional diversities among the p53 family, target genes specifically regulated by p63 and p73 were examined.
|
36 |
16831876
|
Here, we found that the GLX2 gene, which encodes glyoxalase II enzyme, is up-regulated by p63 and p73.
|
37 |
16831876
|
Accordingly, a specific responsive element was found in intron 1 of the GLX2 gene, which can be activated and bound by p63 and p73.
|
38 |
16831876
|
Interestingly, a deficiency in GLX2 also enhances the susceptibility of a cell to DNA damage-induced apoptosis in a p53-dependent manner.
|
39 |
16831876
|
Given that methylglyoxal is frequently generated under both physiological and pathological conditions, we postulate that GLX2 serves as a pro-survival factor of the p53 family and plays a critical role in the normal development and in the pathogenesis of various human diseases, including cancer, diabetes, and neurodegenerative diseases.
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40 |
20041964
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Immunocytochemical methods for the localization of cell proliferation antigen (PCNA), androgen receptor (AR) and p63 protein were carried out, and apoptotic cells were identified by TUNEL essay.
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41 |
20041964
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Insulin treatment was effective in preventing testosterone decrease, p63-positive cell increase and apoptotic rates, but did not interfere in cell proliferation.
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42 |
20041964
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Immunocytochemical methods for the localization of cell proliferation antigen (PCNA), androgen receptor (AR) and p63 protein were carried out, and apoptotic cells were identified by TUNEL essay.
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43 |
20041964
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Insulin treatment was effective in preventing testosterone decrease, p63-positive cell increase and apoptotic rates, but did not interfere in cell proliferation.
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44 |
22076171
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Immunohistochemical results of the tumor were as follows: α-methylacyl-coenzyme A rasemase (AMACR) +++, vimentin +++, cytokeratin (CK) 18 +++, CD10 +++, S-100 protein +, MUC1 ++, MUC2 ++, MUC5AC ++, MUC6 ++, panCK Cam5.2 +, CK7 +, CK8 +, CK14 +, CK19 +, CK20 +, p53 +, HepPar1 +, CD68 +, platelet-derived growth factor-α (PDGFRA) +, PanCK AE1/3 -, PanCK WSS -, PanCK MNF115 -, CK 35BE12 -, CK5/6 -, EMA -, desmin -, smooth muscle antigen -, α-fetoprotein -, CEA -, estrogen receptor -, progesterone receptor -, HER2 -, p63 -, and KIT -.
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45 |
22076171
|
These results suggest that OPRCC can express colloidal iron, low molecular weight CKs, S100 protein, MUC1, MUC2, MUC5AC, MUC6, p53, PDGFRA, and HepPar1.
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46 |
23729543
|
Mutations in SLC29A3 lead to pigmentary hypertrichosis and non-autoimmune insulin-dependent diabetes mellitus (PHID) and H syndromes, familial Rosai-Dorfman disease, and histiocytosis-lymphadenopathy plus syndrome.
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47 |
23729543
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PHID syndrome is a novel monogenic autoinflammatory syndrome (AIS) associated with severe elevation of serum amyloid.
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48 |
23729543
|
In contrast to other AIS, blockade of interleukin-1 and tumor necrosis-α was ineffective.
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49 |
23729543
|
Mutations in SLC29A3 lead to pigmentary hypertrichosis and non-autoimmune insulin-dependent diabetes mellitus (PHID) and H syndromes, familial Rosai-Dorfman disease, and histiocytosis-lymphadenopathy plus syndrome.
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50 |
23729543
|
PHID syndrome is a novel monogenic autoinflammatory syndrome (AIS) associated with severe elevation of serum amyloid.
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51 |
23729543
|
In contrast to other AIS, blockade of interleukin-1 and tumor necrosis-α was ineffective.
|