scholarly journals Up-regulation of spermidine/spermine N1-acetyltransferase (SSAT) expression is a part of proliferative but not anabolic response of mouse kidney.

2002 ◽  
Vol 49 (4) ◽  
pp. 969-977 ◽  
Author(s):  
Magdalena Dudkowska ◽  
Agnieszka Stachurska ◽  
Barbara Grzelakowska-Sztabert ◽  
Małgorzata Manteuffel-Cymborowska
Keyword(s):  
Transcriptional Regulation ◽  
Expression Pattern ◽  
Proliferative Response ◽  
Experimental Models ◽  
Mouse Kidney ◽  
Polyamine Biosynthesis ◽  
Adenosylmethionine Decarboxylase ◽  
Differential Expression Pattern ◽  
Post Transcriptional Regulation ◽  
Ssat Activity

A differential expression pattern of spermidine/spermine N(1)-acetyltransferase (SSAT), the enzyme critical to proper homeostasis of cellular polyamines, is reported in mouse kidney undergoing hyperplasia and hypertrophy. We have shown that SSAT activity and SSAT mRNA are significantly induced by antifolate CB 3717 and folate that evoke a drug-injury-dependent hyperplasia. In contrast, SSAT activity is down-regulated in the testosterone-induced hypertrophic kidney, while SSAT mRNA is positively controlled by this androgen. Catecholamine depletion evoked by reserpine drastically decreases the folate-induced activity of S-adenosylmethionine decarboxylase (AdoMetDC), which limits polyamine biosynthesis, but has no effect on SSAT activity augmented by CB 3717. Our results document that the increased SSAT expression solely accompanies the proliferative response of mouse kidney, and suggest the importance of post-transcriptional regulation to the control of SSAT activity in both hyperplastic and hypertrophic experimental models.

scholarly journals Post-transcriptional regulation of the content of spermidine/spermine N1-acetyltransferase by N1N12-bis(ethyl)spermine

1995 ◽  
Vol 305 (2) ◽  
pp. 451-458 ◽  
Author(s):  
L Parry ◽  
R Balaña Fouce ◽  
A E Pegg
Keyword(s):  
Transcriptional Regulation ◽  
Half Life ◽  
Mammalian Cells ◽  
Significant Proportion ◽  
Untranslated Regions ◽  
Translation Regulation ◽  
Polyamine Analogues ◽  
Post Transcriptional Regulation ◽  
Rate Limiting ◽  
Ssat Activity

Spermidine/spermine N1-acetyltransferase (SSAT) is the rate-limiting enzyme for the degradation and excretion of polyamines in mammalian cells, and its activity is known to be increased enormously on exposure to polyamines and polyamine analogues. The mechanism by which such an analogue, BESM [N1N12-bis(ethyl)spermine], increases the content of SSAT was investigated by transfecting COS-7 cells with plasmids containing SSAT cDNA in the pEUK expression vector. Despite a large increase in mRNA production, there was only a very small increase in SSAT activity in the transfected cells. When BESM was added at 36 h after transfection, there was a large and very rapid increase in SSAT protein amounting to 380-fold in 12 h without any increase in the mRNA. SSAT protein turned over very rapidly, with a half-life of about 20 min. In the presence of BESM, this turnover was greatly reduced, and the half-life increased to more than 13 h. However, this increase was not sufficient to account for all of the increase in SSAT protein, suggesting that there is also regulation of the translation of the mRNA by BESM. Further evidence for such translation regulation was obtained by studying the polysomal distribution of the SSAT mRNA. In the absence of BESM, most of the mRNA was present in fractions which sedimented more slowly than the monoribosome peak. In BESM-treated cells, a significant proportion of the SSAT mRNA was moved into the small-polysome region of the gradient. The expression of SSAT and the effects of BESM on the polysomal distribution of SSAT mRNA were not affected by the 5′- or 3′-untranslated regions of the mRNA, since constructs which lacked all of these regions gave similar results to constructs containing the entire mRNA sequence. These results show that the increased transcription of the SSAT gene that occurs in the presence of polyamine analogues such as BESM is not sufficient for SSAT expression and that post-transcriptional regulation is critical for the control of SSAT content.

Differential expression pattern of protein ARVCF in nephron segments of human and mouse kidney

2008 ◽  
Vol 130 (5) ◽  
pp. 943-956 ◽  
Author(s):  
Britta Walter ◽  
Tanja Schlechter ◽  
Michaela Hergt ◽  
Irina Berger ◽  
Ilse Hofmann
Keyword(s):  
Differential Expression ◽  
Expression Pattern ◽  
Mouse Kidney ◽  
Nephron Segments ◽  
Differential Expression Pattern ◽  
Human And Mouse

scholarly journals Wnt/β-catenin signaling and p68 conjointly regulate CHIP in colorectal cancer

2021 ◽  
Author(s):  
Satadeepa Kal ◽  
Shrabastee Chakraborty ◽  
Subhajit Karmakar ◽  
Mrinal K Ghosh
Keyword(s):  
Colorectal Cancer ◽  
Transcriptional Regulation ◽  
Cancer Cells ◽  
Expression Pattern ◽  
Transcriptional Activation ◽  
Nuclear Translocation ◽  
Wnt Signaling Pathway ◽  
Differential Expression Pattern ◽  
Colorectal Cancer Cells ◽  
Canonical Wnt

The differential expression pattern of Carboxy terminus of Hsc70 Interacting Protein (CHIP, alias STIP1 Homology and U box Containing Protein 1 or STUB1) in cancers is associated with ubiquitination mediated degradation of its client proteins. Emerging evidences suggest its abundant expression of CHIP in colorectal cancer compared to normal tissues, but the mechanistic detail of this augmented expression pattern is unclear. The signature driver of canonical Wnt pathway, β catenin, and its co-activator RNA helicase p68, are also overexpressed in colorectal cancer. In this study, we describe a novel mechanism of Wnt/ β catenin and p68 mediated transcriptional activation of CHIP gene leading to enhanced proliferation of colorectal cancer cells. Wnt3A treatment and pharmacological activation of canonical Wnt signaling pathway resulted in increased nuclear translocation of β catenin and elevated expression of CHIP. Likewise, overexpression and knockdown of β catenin and p68 upregulated and downregulated CHIP expression, respectively, at both mRNA and protein levels. After cloning CHIP promoter, the increased and decreased promoter activities of CHIP induced by overexpression and knockdown of either β catenin or p68 further confirmed transcriptional regulation of CHIP gene by Wnt/ β catenin signaling cascade. p68 along with β catenin were found to occupy Transcription Factor 4 (TCF4) binding sites on endogenous CHIP promoter and regulate its transcription. Finally, enhanced cellular propagation and migration of colorectal cancer cells induced by Wnt/ β catenin p68 CHIP axis established the significance of this pathway in oncogenesis. To the best of our knowledge, this is the first report elucidating the mechanistic details of transcriptional regulation of CHIP (STUB1) gene expression.

43-OR: Post-transcriptional Regulation of Slc16a1 mRNA Is Essential for Maintaining Normal ß-Cell Function

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 43-OR
Author(s):  
DINA MOSTAFA ◽  
AKINORI TAKAHASHI ◽  
TADASHI YAMAMOTO
Keyword(s):  
Transcriptional Regulation ◽  
Cell Function ◽  
Post Transcriptional Regulation
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