Excess iodide downregulates Na+/I− symporter gene transcription through activation of PI3K/Akt pathway

2016 ◽  
Vol 426 ◽  
pp. 73-90 ◽  
Author(s):  
Caroline Serrano-Nascimento ◽  
Juan Pablo Nicola ◽  
Silvania da Silva Teixeira ◽  
Leonice Lourenço Poyares ◽  
Camilo Lellis-Santos ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Akt Pathway ◽  
Excess Iodide

Modulation of STAT3 Gene Transcription through the PI 3-Kinase/Akt Pathway: Interaction between the Transcription Factors FKHR and STAT3

2001 ◽  
Vol 29 (3) ◽  
pp. A68-A68
Author(s):  
A. Barthel ◽  
M. Kortylewski ◽  
K. -D. Krueger ◽  
H. Axer ◽  
J. Behrmann ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Gene Transcription ◽  
Akt Pathway ◽  
Pathway Interaction

Activator protein-1 is necessary for angiotensin-II stimulation of human adrenocorticotropin receptor gene transcription

2001 ◽  
Vol 268 (6) ◽  
pp. 1802-1810
Author(s):  
Danielle Naville ◽  
Estelle Bordet ◽  
Marie-Claude Berthelon ◽  
Philippe Durand ◽  
Martine Begeot
Keyword(s):  
Angiotensin Ii ◽  
Gene Transcription ◽  
Receptor Gene ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Stimulation Of

Regulation of neuronal cholecystokinin gene transcription

2001 ◽  
Vol 61 (7) ◽  
pp. 61-67 ◽  
Author(s):  
Thomas V. O. Hansen ◽  
Finn C. Nielsen
Keyword(s):  
Gene Transcription

Q-mediated late gene transcription of bacteriophage λ: RNA start point and RNase III processing sites in vivo

Virology ◽  
1988 ◽  
Vol 167 (2) ◽  
pp. 568-577 ◽  
Author(s):  
D DANIELS ◽  
M SUBBARAO ◽  
F BLATTNER ◽  
H LOZERON
Keyword(s):  
Gene Transcription ◽  
Late Gene ◽  
Bacteriophage Λ ◽  
Rnase Iii

GENE ACTIVATION IN MAMMARY CELLS

1972 ◽  
Vol 71 (2_Suppla) ◽  
pp. S346-S368 ◽  
Author(s):  
Roger W. Turkington ◽  
Nobuyuki Kadohama
Keyword(s):  
Cell Differentiation ◽  
Gene Transcription ◽  
Hormonal Regulation ◽  
Gene Activation ◽  
Milk Proteins ◽  
Mouse Mammary Gland ◽  
Nuclear Proteins ◽  
Mammary Cells ◽  
Alveolar Cells ◽  
Mammary Cell

ABSTRACT Hormonal activation of gene transcription has been studied in a model system, the mouse mammary gland in organ culture. Transcriptive activity is stimulated in mammary stem cells by insulin, and in mammary alveolar cells by prolactin and insulin. Studies on the template requirement for expression of the genes for milk proteins demonstrate that DNA methylation has an obligatory dependence upon DNA synthesis, but is otherwise independent from hormonal regulation of mammary cell differentiation. Incorporation of 5-bromo-2′deoxyuridine into DNA selectively inhibits expression of the genes for specific milk proteins. Undifferentiated mammary cells activate the synthesis of specific acidic nuclear proteins when stimulated by insulin. Several of these induced acidic nuclear proteins are undetectable in unstimulated undifferentiated cells, but appear to be characteristic components of the nuclei of differentiated cells. These results indicate that mammary cell differentiation is associated with a change in acidic nuclear proteins, and they provide evidence to support the concept that acidic nuclear proteins may be involved in the regulation of gene transcription and of mammary cell differentiation.

INHIBITION OF THYROGLOBULIN BIOSYNTHESIS AND DEGRADATION BY EXCESS IODIDE. SYNERGISM WITH LITHIUM

1976 ◽  
Vol 81 (2) ◽  
pp. 495-506 ◽  
Author(s):  
A. Radvila ◽  
R. Roost ◽  
H. Bürgi ◽  
H. Kohler ◽  
H. Studer
Keyword(s):  
Protein Synthesis ◽  
Thyroid Gland ◽  
Inhibitory Action ◽  
Inhibit Protein Synthesis ◽  
Thyrotrophic Hormone ◽  
Thyroid Glands ◽  
Pre Treatment ◽  
Excess Iodide ◽  
Kidney Liver

ABSTRACT Lithium and excess iodide inhibit the release of thyroid hormone from preformed stores. We thus tested the hypothesis that this was due to an inhibition of thyroglobulin breakdown. Rats were pre-treated with propylthiouracil (PTU) for 3 weeks in order to deplete their thyroids of thyroglobulin. While the PTU was continued, lithium chloride (0.25 mEq./100 g weight) or potassium iodide (3 mg per rat) were injected every 12 h for 3 days. Thereafter the thyroglobulin content in thyroid gland homogenates was measured. PTU pre-treatment lowered the thyroglobulin content from 4.21 to 0.22 mg/100 mg gland. Lithium caused a marked re-accumulation of thyroglobulin to 0.60 mg/100 mg within 3 days. While iodide alone had only a borderline effect, it markedly potentiated the action of lithium and a combination of the two drugs increased the thyroglobulin content to 1.04 mg/100 mg. Thyroxine was injected into similarly pre-treated animals to suppress secretion of thyrotrophic hormone. This markedly inhibited the proteolysis of thyroglobulin and 1.3 mg/100 mg gland accumulated after 3 days. Excess iodide, given in addition to thyroxine, decreased the amount of thyroglobulin accumulated to 0.75 mg/100 mg gland. To study whether this could be explained by an inhibitory action of iodide on thyroglobulin biosynthesis, thyroid glands from animals treated with excess iodide were incubated in vitro in the presence of 0.2 mm iodide for 3 h. Iodide decreased the incorporation of radioactive leucine into total thyroidal protein and into thyroglobulin by 25 and 35 % respectively. Iodide did not inhibit protein synthesis in the kidney, liver or muscle tissue. Thus, large doses of iodide selectively inhibit thyroglobulin biosynthesis.

Sign in / Sign up

Export Citation Format

Share Document