# |
PMID |
Sentence |
1 |
12167488
|
Synergistic effect of dimethyl sulfoxide on glucagon-like peptide 1 (GLP-1)-stimulated insulin secretion and gene transcription in INS-1 cells: characterization and implications.
|
2 |
12167488
|
GLP-1 enhances both insulin secretion and insulin gene expression in a glucose-dependent manner via activation of its putative G-protein-coupled receptor on pancreatic beta-cells.
|
3 |
12167488
|
Analysis of intracellular signaling components revealed that DMSO did not elevate cAMP levels, protein kinase A activity, or phosphorylated levels of CRE-binding protein (CREB), CRE-modulator (CREM), and activating transcription factor-1 (ATF-1).
|
4 |
12167488
|
These data suggest that GLP-1 induces insulin gene transcription in a CREB, CREM, and ATF-1-independent manner in beta-cells.
|
5 |
23568554
|
The transcription factor cAMP responsive element-binding protein (CREB) and activating transcription factors (ATFs) are downstream components of the insulin/IGF cascade, playing crucial roles in maintaining cell viability and embryo survival.
|
6 |
23568554
|
One of the CREB target genes is adiponectin, which acts synergistically with insulin.
|
7 |
23568554
|
We have studied the CREB-ATF-adiponectin network in rabbit preimplantation development in vivo and in vitro.
|
8 |
23568554
|
From the blastocyst stage onwards, CREB and ATF1, ATF3, and ATF4 are present with increasing expression for CREB, ATF1, and ATF3 during gastrulation and with a dominant expression in the embryoblast (EB).
|
9 |
23568554
|
In vitro stimulation with insulin and IGF-I reduced CREB and ATF1 transcripts by approximately 50%, whereas CREB phosphorylation was increased.
|
10 |
23568554
|
Activation of CREB was accompanied by subsequent reduction in adiponectin and adiponectin receptor (adipoR)1 expression.
|
11 |
23568554
|
Analysis of embryonic adipoRs showed an increased expression of adipoR1 and no changes in adipoR2 transcription.
|
12 |
23568554
|
We conclude that the transcription factors CREB and ATFs vitally participate in embryo-maternal cross talk before implantation in a cell lineage-specific manner.
|
13 |
23568554
|
Embryonic CREB/ATFs act as insulin/IGF sensors.
|
14 |
23568554
|
Lack of insulin is compensated by a CREB-mediated adiponectin expression, which may maintain glucose uptake in blastocysts grown in diabetic mothers.
|
15 |
23568554
|
The transcription factor cAMP responsive element-binding protein (CREB) and activating transcription factors (ATFs) are downstream components of the insulin/IGF cascade, playing crucial roles in maintaining cell viability and embryo survival.
|
16 |
23568554
|
One of the CREB target genes is adiponectin, which acts synergistically with insulin.
|
17 |
23568554
|
We have studied the CREB-ATF-adiponectin network in rabbit preimplantation development in vivo and in vitro.
|
18 |
23568554
|
From the blastocyst stage onwards, CREB and ATF1, ATF3, and ATF4 are present with increasing expression for CREB, ATF1, and ATF3 during gastrulation and with a dominant expression in the embryoblast (EB).
|
19 |
23568554
|
In vitro stimulation with insulin and IGF-I reduced CREB and ATF1 transcripts by approximately 50%, whereas CREB phosphorylation was increased.
|
20 |
23568554
|
Activation of CREB was accompanied by subsequent reduction in adiponectin and adiponectin receptor (adipoR)1 expression.
|
21 |
23568554
|
Analysis of embryonic adipoRs showed an increased expression of adipoR1 and no changes in adipoR2 transcription.
|
22 |
23568554
|
We conclude that the transcription factors CREB and ATFs vitally participate in embryo-maternal cross talk before implantation in a cell lineage-specific manner.
|
23 |
23568554
|
Embryonic CREB/ATFs act as insulin/IGF sensors.
|
24 |
23568554
|
Lack of insulin is compensated by a CREB-mediated adiponectin expression, which may maintain glucose uptake in blastocysts grown in diabetic mothers.
|
25 |
23571712
|
GLP-1(28-36) improves β-cell mass and glucose disposal in streptozotocin-induced diabetic mice and activates cAMP/PKA/β-catenin signaling in β-cells in vitro.
|
26 |
23571712
|
An in vitro investigation revealed that GLP-1(28-36)amide stimulates β-catenin (β-cat) Ser(675) phosphorylation in both the clonal INS-1 cell line and rat primary pancreatic islet cells.
|
27 |
23571712
|
GLP-1(28-36)amide was also shown to increase cellular cAMP levels, PKA enzymatic activity, and cAMP response element-binding protein (CREB) and cyclic AMP-dependent transcription factor-1 (ATF-1) phosphorylation.
|
28 |
23571712
|
Furthermore, GLP-1(28-36)amide treatment enhanced islet insulin secretion and increased the growth of INS-1 cells, which was associated with increased cyclin D1 expression.
|
29 |
23571712
|
Finally, PKA inhibition attenuated the effect of GLP-1(28-36)amide on β-cat Ser(675) phosphorylation and cyclin D1 expression in the INS-1 cell line.
|
30 |
23571712
|
Our observations suggest that GLP-1(28-36)amide may exert its effect through the PKA/β-catenin signaling pathway.
|