# |
PMID |
Sentence |
1 |
12045092
|
Recombination is initiated by the lymphoid-specific RAG1 and RAG2 proteins, which cooperate to make double-strand breaks at specific recognition sequences (recombination signal sequences, RSSs).
|
2 |
12045092
|
Broken ends are then processed and joined with the help of several factors also involved in repair of radiation-damaged DNA, including the DNA-dependent protein kinase (DNA-PK) and the Ku, Artemis, DNA ligase IV, and Xrcc4 proteins, and possibly histone H2AX and the Mre11/Rad50/Nbs1 complex.
|
3 |
16166097
|
The transcription factor PDX-1 plays a crucial role during pancreatic development and in the function of insulin-producing beta cells.
|
4 |
16166097
|
These proteins, Ku70 and Ku80, are regulatory subunits of DNA-dependent protein kinase (DNA-PK).
|
5 |
16166097
|
We determined that the interaction between PDX-1 and Ku70 or Ku80 is dependent on the homeodomain of PDX-1.
|
6 |
16166097
|
Most interestingly, we demonstrated in vitro that the DNA-PK phosphorylates PDX-1 on threonine 11.
|
7 |
16166097
|
However, in response to radiation, which activates DNA-PK, a second form of the PDX-1 protein appears rapidly.
|
8 |
16166097
|
In correlation with this degradation, we observed a subsequent reduction in the activation of the insulin promoter and a decrease in PDX-1-mediated gene expression, i.e. glut2 and glucokinase.
|
9 |
16166097
|
Our study demonstrates that radiation, through the activation of DNA-PK, may regulate PDX-1 protein expression.
|
10 |
16166097
|
The transcription factor PDX-1 plays a crucial role during pancreatic development and in the function of insulin-producing beta cells.
|
11 |
16166097
|
These proteins, Ku70 and Ku80, are regulatory subunits of DNA-dependent protein kinase (DNA-PK).
|
12 |
16166097
|
We determined that the interaction between PDX-1 and Ku70 or Ku80 is dependent on the homeodomain of PDX-1.
|
13 |
16166097
|
Most interestingly, we demonstrated in vitro that the DNA-PK phosphorylates PDX-1 on threonine 11.
|
14 |
16166097
|
However, in response to radiation, which activates DNA-PK, a second form of the PDX-1 protein appears rapidly.
|
15 |
16166097
|
In correlation with this degradation, we observed a subsequent reduction in the activation of the insulin promoter and a decrease in PDX-1-mediated gene expression, i.e. glut2 and glucokinase.
|
16 |
16166097
|
Our study demonstrates that radiation, through the activation of DNA-PK, may regulate PDX-1 protein expression.
|
17 |
16166097
|
The transcription factor PDX-1 plays a crucial role during pancreatic development and in the function of insulin-producing beta cells.
|
18 |
16166097
|
These proteins, Ku70 and Ku80, are regulatory subunits of DNA-dependent protein kinase (DNA-PK).
|
19 |
16166097
|
We determined that the interaction between PDX-1 and Ku70 or Ku80 is dependent on the homeodomain of PDX-1.
|
20 |
16166097
|
Most interestingly, we demonstrated in vitro that the DNA-PK phosphorylates PDX-1 on threonine 11.
|
21 |
16166097
|
However, in response to radiation, which activates DNA-PK, a second form of the PDX-1 protein appears rapidly.
|
22 |
16166097
|
In correlation with this degradation, we observed a subsequent reduction in the activation of the insulin promoter and a decrease in PDX-1-mediated gene expression, i.e. glut2 and glucokinase.
|
23 |
16166097
|
Our study demonstrates that radiation, through the activation of DNA-PK, may regulate PDX-1 protein expression.
|
24 |
16166097
|
The transcription factor PDX-1 plays a crucial role during pancreatic development and in the function of insulin-producing beta cells.
|
25 |
16166097
|
These proteins, Ku70 and Ku80, are regulatory subunits of DNA-dependent protein kinase (DNA-PK).
|
26 |
16166097
|
We determined that the interaction between PDX-1 and Ku70 or Ku80 is dependent on the homeodomain of PDX-1.
|
27 |
16166097
|
Most interestingly, we demonstrated in vitro that the DNA-PK phosphorylates PDX-1 on threonine 11.
|
28 |
16166097
|
However, in response to radiation, which activates DNA-PK, a second form of the PDX-1 protein appears rapidly.
|
29 |
16166097
|
In correlation with this degradation, we observed a subsequent reduction in the activation of the insulin promoter and a decrease in PDX-1-mediated gene expression, i.e. glut2 and glucokinase.
|
30 |
16166097
|
Our study demonstrates that radiation, through the activation of DNA-PK, may regulate PDX-1 protein expression.
|
31 |
16504547
|
Down-regulation of PARP-1, but not of Ku80 or DNA-PKcs', results in higher gene targeting efficiency.
|
32 |
16504547
|
To test this hypothesis, we examined gene targeting frequencies (TF) in DNA-PK(cs), Ku80 and poly(ADP-ribose) polymerase (PARP-1) nullizygous cells.
|
33 |
16504547
|
We observed a 3-fold TF increase in PARP-1 knockout embryonic stem (ES) cells, which is consistent with the predicted role of PARP-1 as a switch between HR and NHEJ.
|
34 |
16504547
|
To a lesser extent, such effect could be reproduced upon chemical inhibition of PARP-1.
|
35 |
16504547
|
Down-regulation of PARP-1, but not of Ku80 or DNA-PKcs', results in higher gene targeting efficiency.
|
36 |
16504547
|
To test this hypothesis, we examined gene targeting frequencies (TF) in DNA-PK(cs), Ku80 and poly(ADP-ribose) polymerase (PARP-1) nullizygous cells.
|
37 |
16504547
|
We observed a 3-fold TF increase in PARP-1 knockout embryonic stem (ES) cells, which is consistent with the predicted role of PARP-1 as a switch between HR and NHEJ.
|
38 |
16504547
|
To a lesser extent, such effect could be reproduced upon chemical inhibition of PARP-1.
|
39 |
16982777
|
We unexpectedly found that the corepressor silencing mediator for retinoid and thyroid hormone receptor (SMRT) associates with the DNA-PK repair complex.
|
40 |
16982777
|
The SMRT/histone deacetylase 3 complex is required for the transcriptional repressive property of the Ku70 subunit of the repair complex.
|
41 |
23747725
|
The first strain, C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg, carries the diphtheria toxin receptor (hDTR) driven by the human insulin gene promoter, while the other strain, C57BL/6-ins2(BAC)-TRECK-Tg, expresses hDTR cDNA under the control of the mouse insulin II gene promoter.
|
42 |
23747725
|
With regard to the C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg strain, only one of three Tg strains exhibited proper expression of hDTR in pancreatic β cells.
|
43 |
23747725
|
Using the C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg model, we tried to perform regenerative therapeutic approaches: allogeneic transplantation of pancreatic islet cells from C57BL/6 and xenogeneic transplantation of CD34(+) human umbilical cord blood cells.
|
44 |
23747725
|
Both approaches successfully rescued C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg mice from hyperglycemia caused by DT administration.
|
45 |
23747725
|
The first strain, C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg, carries the diphtheria toxin receptor (hDTR) driven by the human insulin gene promoter, while the other strain, C57BL/6-ins2(BAC)-TRECK-Tg, expresses hDTR cDNA under the control of the mouse insulin II gene promoter.
|
46 |
23747725
|
With regard to the C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg strain, only one of three Tg strains exhibited proper expression of hDTR in pancreatic β cells.
|
47 |
23747725
|
Using the C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg model, we tried to perform regenerative therapeutic approaches: allogeneic transplantation of pancreatic islet cells from C57BL/6 and xenogeneic transplantation of CD34(+) human umbilical cord blood cells.
|
48 |
23747725
|
Both approaches successfully rescued C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg mice from hyperglycemia caused by DT administration.
|
49 |
23747725
|
The first strain, C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg, carries the diphtheria toxin receptor (hDTR) driven by the human insulin gene promoter, while the other strain, C57BL/6-ins2(BAC)-TRECK-Tg, expresses hDTR cDNA under the control of the mouse insulin II gene promoter.
|
50 |
23747725
|
With regard to the C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg strain, only one of three Tg strains exhibited proper expression of hDTR in pancreatic β cells.
|
51 |
23747725
|
Using the C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg model, we tried to perform regenerative therapeutic approaches: allogeneic transplantation of pancreatic islet cells from C57BL/6 and xenogeneic transplantation of CD34(+) human umbilical cord blood cells.
|
52 |
23747725
|
Both approaches successfully rescued C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg mice from hyperglycemia caused by DT administration.
|
53 |
23747725
|
The first strain, C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg, carries the diphtheria toxin receptor (hDTR) driven by the human insulin gene promoter, while the other strain, C57BL/6-ins2(BAC)-TRECK-Tg, expresses hDTR cDNA under the control of the mouse insulin II gene promoter.
|
54 |
23747725
|
With regard to the C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg strain, only one of three Tg strains exhibited proper expression of hDTR in pancreatic β cells.
|
55 |
23747725
|
Using the C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg model, we tried to perform regenerative therapeutic approaches: allogeneic transplantation of pancreatic islet cells from C57BL/6 and xenogeneic transplantation of CD34(+) human umbilical cord blood cells.
|
56 |
23747725
|
Both approaches successfully rescued C.B-17/Icr-Prkdc(scid)/Prkdc(scid)-INS-TRECK-Tg mice from hyperglycemia caused by DT administration.
|