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Zależna od ubikwityny degradacja białek Nagroda Nobla z chemii w 2004 roku

100%

Grzelakowska-Sztabert B.

Kosmos

2005

tom 54

nr 2-3

133-148

In the article Nobel laureates in chemistry for 2004 - Irvine Rose, Avram Hershko and Aron Ciechanover - and their achievements in elucidating the ubiquitin-mediated protein degradation are presented and the function of ubiquitin in this process is shortly reviewed. Moreover, ubiquitin ligases involved in the ubiquitylation of the main cell cycle regulators as well as the mechanisms regulated by their activities are described. Examples of the abnormalities of functioning of the ubiquitin/proteasome system in various diseases and possibilities of pharmacological intervension in its action are also presented.

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

51%

Dudkowska M. , Stachurska A. , Grzelakowska-Sztabert B. , Manteuffel-Cymborowska M.

Acta Biochimica Polonica

2002

tom 49

nr 4

969-977

A differential expression pattern of spermidine/spermine N1-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.

Androgen receptor and c-Myc transcription factors as putative partners in the in vivo cross-talk between androgen receptor-mediated and c-Met-mediated signalling pathways

51%

Dudkowska M. , Jaworski T. , Grzelakowska-Sztabert B. , Manteuffel-Cymborowska M.

Acta Biochimica Polonica

2007

tom 54

nr 2

253-259

Cross-talk between two signal transduction pathways leads to a negative regulation of androgen-induced ornithine decarboxylase (ODC) gene expression in the mouse kidney. One pathway is triggered by testosterone via the intracellular androgen receptor, AR, and the other is induced by antifolate CB 3717 or folate via hepatocyte growth factor and its cell membrane receptor c-Met. Here we report the studies of the expression of AR and c-Myc transcription factors involved in ODC transactivation. Administration of CB 3717 or folate decreased the expression of AR. In contrast, testosterone did not modify AR mRNA content but augmented the AR protein. Furthermore, we demonstrate that administration of folate, but not testosterone, increases c-Myc transcript and protein level. We also document that activation of both examined pathways does not decrease the testosterone-induced AR protein level, but markedly increases c-Myc protein which is nearly 2-fold up-regulated compared to its level evoked solely by testosterone. We suspect that this pronounced increase of c-Myc protein might have functional consequences mirrored by down-regulated expression of AR target genes, among them ODC.

A quinazoline antifolate as inhibitor of folate metabolism in mouse L-cells

44%

Sikora E. , Grzelakowska-Sztabert B.

Acta Biochimica Polonica

1983

tom 30

nr 2

193-201