-
Je něco špatně v tomto záznamu ?
The cell type-specific effect of TAp73 isoforms on the cell cycle and apoptosis
J Holcakova, P Ceskova, R Hrstka, P Muller, L Dubska, PJ Coates, E Palecek, B Vojtesek
Jazyk angličtina Země Polsko
NLK
BioMedCentral
od 2006-03-01
BioMedCentral Open Access
od 2006
PubMed Central
od 2006
Europe PubMed Central
od 2006
ProQuest Central
od 2006-03-01 do 2014-12-31
Health & Medicine (ProQuest)
od 2006-03-01 do 2014-12-31
ROAD: Directory of Open Access Scholarly Resources
od 2006
Springer Nature OA/Free Journals
od 2006-03-01
- MeSH
- aktivace transkripce MeSH
- alternativní sestřih MeSH
- apoptóza fyziologie MeSH
- buněčné linie MeSH
- buněčný cyklus fyziologie MeSH
- DNA vazebné proteiny genetika metabolismus MeSH
- financování organizované MeSH
- genetická transkripce MeSH
- jaderné proteiny genetika metabolismus MeSH
- lidé MeSH
- nádorové supresorové proteiny metabolismus MeSH
- nádorový supresorový protein p53 genetika metabolismus MeSH
- protein - isoformy genetika metabolismus MeSH
- sekvenční analýza hybridizací s uspořádaným souborem oligonukleotidů MeSH
- signální transdukce fyziologie MeSH
- stanovení celkové genové exprese MeSH
- trans-aktivátory genetika metabolismus MeSH
- vazba proteinů MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
p73, a member of the p53 family, exhibits activities similar to those of p53, including the ability to induce growth arrest and apoptosis. p73 influences chemotherapeutic responses in human cancer patients, in association with p53. Alternative splicing of the TP73 gene produces many p73 C- and N-terminal isoforms, which vary in their transcriptional activity towards p53-responsive promoters. In this paper, we show that the C-terminal spliced isoforms of the p73 protein differ in their DNA-binding capacity, but this is not an accurate predictor of transcriptional activity. In different p53-null cell lines, p73beta induces either mitochondrial-associated or death receptor-mediated apoptosis, and these differences are reflected in different gene expression profiles. In addition, p73 induces cell cycle arrest and p21(WAF1) expression in H1299 cells, but not in Saos-2. This data shows that TAp73 isoforms act differently depending on the tumour cell background, and have important implications for p73-mediated therapeutic responses in individual human cancer patients.
- 000
- 03286naa 2200577 a 4500
- 001
- bmc11004927
- 003
- CZ-PrNML
- 005
- 20121203105233.0
- 008
- 110310s2008 pl e eng||
- 009
- AR
- 040 __
- $a ABA008 $b cze $c ABA008 $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a pl
- 100 1_
- $a Holčáková, Jitka $7 xx0125776
- 245 14
- $a The cell type-specific effect of TAp73 isoforms on the cell cycle and apoptosis / $c J Holcakova, P Ceskova, R Hrstka, P Muller, L Dubska, PJ Coates, E Palecek, B Vojtesek
- 314 __
- $a Department of Oncological and Experimental Pathology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.
- 520 9_
- $a p73, a member of the p53 family, exhibits activities similar to those of p53, including the ability to induce growth arrest and apoptosis. p73 influences chemotherapeutic responses in human cancer patients, in association with p53. Alternative splicing of the TP73 gene produces many p73 C- and N-terminal isoforms, which vary in their transcriptional activity towards p53-responsive promoters. In this paper, we show that the C-terminal spliced isoforms of the p73 protein differ in their DNA-binding capacity, but this is not an accurate predictor of transcriptional activity. In different p53-null cell lines, p73beta induces either mitochondrial-associated or death receptor-mediated apoptosis, and these differences are reflected in different gene expression profiles. In addition, p73 induces cell cycle arrest and p21(WAF1) expression in H1299 cells, but not in Saos-2. This data shows that TAp73 isoforms act differently depending on the tumour cell background, and have important implications for p73-mediated therapeutic responses in individual human cancer patients.
- 650 _2
- $a alternativní sestřih $7 D017398
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a apoptóza $x fyziologie $7 D017209
- 650 _2
- $a buněčný cyklus $x fyziologie $7 D002453
- 650 _2
- $a buněčné linie $7 D002460
- 650 _2
- $a DNA vazebné proteiny $x genetika $x metabolismus $7 D004268
- 650 _2
- $a stanovení celkové genové exprese $7 D020869
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a jaderné proteiny $x genetika $x metabolismus $7 D009687
- 650 _2
- $a sekvenční analýza hybridizací s uspořádaným souborem oligonukleotidů $7 D020411
- 650 _2
- $a vazba proteinů $7 D011485
- 650 _2
- $a protein - isoformy $x genetika $x metabolismus $7 D020033
- 650 _2
- $a signální transdukce $x fyziologie $7 D015398
- 650 _2
- $a trans-aktivátory $x genetika $x metabolismus $7 D015534
- 650 _2
- $a genetická transkripce $7 D014158
- 650 _2
- $a aktivace transkripce $7 D015533
- 650 _2
- $a nádorový supresorový protein p53 $x genetika $x metabolismus $7 D016159
- 650 _2
- $a nádorové supresorové proteiny $x metabolismus $7 D025521
- 650 _2
- $a financování organizované $7 D005381
- 700 1_
- $a Češková, Pavla $7 xx0148511
- 700 1_
- $a Hrstka, Roman $7 xx0077297
- 700 1_
- $a Müller, Petr $7 xx0036920
- 700 1_
- $a Zdražilová Dubská, Lenka $7 xx0080373
- 700 1_
- $a Coates, Philip J.
- 700 1_
- $a Paleček, Emil, $d 1930-2018 $7 jk01091562
- 700 1_
- $a Vojtěšek, Bořivoj, $d 1960- $7 xx0001694
- 773 0_
- $t Cellular & Molecular Biology Letters $w MED00008291 $g Roč. 13, č. 3 (2008), s. 404-420
- 910 __
- $a ABA008 $b x $y 1
- 990 __
- $a 20110414093818 $b ABA008
- 991 __
- $a 20121203105305 $b ABA008
- 999 __
- $a ok $b bmc $g 832843 $s 696967
- BAS __
- $a 3
- BMC __
- $a 2008 $b 13 $c 3 $d 404-420 $m Cellular and Molecular Biology Letters $n Cell. Mol. Biol. Lett. $x MED00008291
- LZP __
- $a 2011-4B/vtme