Fathead minnow vitellogenin: Complementary DNA sequence and messenger RNA and protein expression after 17β-estradiol treatment

2000 ◽  
Vol 19 (4) ◽  
pp. 972-981 ◽  
Author(s):  
Joseph J. Korte ◽  
Michael D. Kahl ◽  
Kathleen M. Jensen ◽  
Mumtaz S. Pasha ◽  
Louise G. Parks ◽  
...  
Keyword(s):  
Protein Expression ◽  
Dna Sequence ◽  
Messenger Rna ◽  
Fathead Minnow ◽  
Estradiol Treatment ◽  
Complementary Dna ◽  
17Β Estradiol

scholarly journals Estradiol Treatment and Hormonal Fluctuations During the Estrous Cycle Modulate the Expression of Estrogen Receptors in the Auditory System and the Prepulse Inhibition of Acoustic Startle Response

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4412-4421 ◽  
Author(s):  
Konstantina Charitidi ◽  
Inna Meltser ◽  
Barbara Canlon
Keyword(s):  
Protein Expression ◽  
Estrogen Receptors ◽  
Auditory System ◽  
Prepulse Inhibition ◽  
Startle Response ◽  
Acoustic Startle ◽  
Acoustic Startle Response ◽  
Estradiol Treatment ◽  
Mrna And Protein Expression ◽  
17Β Estradiol

Estrogens' effects on hearing are documented across species, but the responsible molecular mechanisms remain unknown. The presence of estrogen receptors (ER) throughout the auditory system offers a potential pathway of direct estrogenic effects on auditory function, but little is known about how each ER's expression is regulated by the overall hormonal status of the body. In the present study, we determined the effects of ovariectomy and chronic 17β-estradiol treatment on mRNA and protein expression of ERα and ERβ in peripheral (cochlea) and central (inferior colliculus) auditory structures of mice, as well as on auditory-related behavior using the acoustic startle response (ASR), prepulse inhibition (PPI), and habituation of the startle response. 17β-Estradiol treatment down-regulated ERα but not ERβ and increased PPI and latency of the ASR. Neither the magnitude nor the habituation of ASR was affected. Furthermore, ER's mRNA and protein expression in the inner ear were analyzed throughout the estrous cycle (proestrus, estrus, metestrus, and diestrus), revealing a negative correlation of circulating estrogens with ERα expression, whereas ERβ was stable. Our findings show that ER not only are present in both the peripheral and central auditory system but also that circulating estrogen levels down-regulate ERα expression in the auditory system and affect PPI and the latency of ASR, suggesting a key role of ERα as a hormone-induced modulator of the auditory system and behavior.

scholarly journals Human beta-globin messenger RNA. III. Nucleotide sequences derived from complementary DNA.

1977 ◽  
Vol 252 (14) ◽  
pp. 5040-5053 ◽  
Author(s):  
C A Marotta ◽  
J T Wilson ◽  
B G Forget ◽  
S M Weissman
Keyword(s):  
Messenger Rna ◽  
Nucleotide Sequences ◽  
Beta Globin ◽  
Complementary Dna

scholarly journals In Vivo 17β-Estradiol Treatment Contributes to Podocyte Actin Stabilization in Female db/db Mice

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 5888-5895 ◽  
Author(s):  
Paola Catanuto ◽  
Alessia Fornoni ◽  
Simone Pereira-Simon ◽  
Fayi Wu ◽  
Kerry L. Burnstein ◽  
...  
Keyword(s):  
Actin Cytoskeleton ◽  
Transcriptional Activation ◽  
Cell Types ◽  
Proper Function ◽  
Estradiol Treatment ◽  
Diabetic Glomerulosclerosis ◽  
Podocyte Damage ◽  
Rac1 Activity ◽  
17Β Estradiol

Abstract We recently showed that 17β-estradiol (E2) treatment ameliorated type 2 diabetic glomerulosclerosis in mice in part by protecting podocyte structure and function. Progressive podocyte damage is characterized by foot process effacement, vacuolization, detachment of podocytes from the glomerular basement membrane, and apoptosis. In addition, podocytes are highly dependent on the preservation of their actin cytoskeleton to ensure proper function and survival. Because E2 administration prevented podocyte damage in our study on diabetic db/db mice and has been shown to regulate both actin cytoskeleton and apoptosis in other cell types and tissues, we investigated whether actin remodeling and apoptosis were prevented in podocytes isolated from E2-treated diabetic db/db mice. We performed G-actin/F-actin assays, Western analysis for Hsp25 expression, Ras-related C3 botulinum toxin substrate 1 (Rac1) activity, and apoptosis assays on previously characterized podocytes isolated from both in vivo-treated placebo and E2 female db/db mice. We found that in vivo E2 protects against a phenotype change in the cultured podocytes characterized by a percent increase of F-actin vs. G-actin, suppression of Hsp25 expression and transcriptional activation, increase of Rac1 activity, and decreased apoptotic intermediates. We conclude from these studies that E2 treatment protects against podocyte damage and may prevent/reduce diabetes-induced kidney disease.

scholarly journals NADH:ubiquinone oxidoreductase from bovine heart mitochondria Complementary DNA sequence of the import precursor of the 10 kDa subunit of the flavoprotein fragment

FEBS Letters ◽  
1991 ◽  
Vol 282 (1) ◽  
pp. 135-138 ◽  
Author(s):  
J.Mark Skehel ◽  
Stephanie J. Pilkington ◽  
Michael J. Runswick ◽  
Ian M. Fearnley ◽  
John E. Walker
Keyword(s):  
Dna Sequence ◽  
Heart Mitochondria ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Complementary Dna ◽  
Bovine Heart

Complementary DNA sequence of rabbit CAP18—A unique lipopolysaccharide binding protein

1991 ◽  
Vol 179 (1) ◽  
pp. 170-175 ◽  
Author(s):  
James W. Larrick ◽  
John G. Morgan ◽  
Ilona Palings ◽  
Michimasa Hirata ◽  
Michael H. Yen
Keyword(s):  
Dna Sequence ◽  
Binding Protein ◽  
Lipopolysaccharide Binding Protein ◽  
Complementary Dna ◽  
Lipopolysaccharide Binding
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