Isolation of 10 differentially expressed cDNAs in p53-induced apoptosis: activation of the vertebrate homologue of the drosophila seven in absentia gene.

Amson, Robert; Nemani, Mona; Roperch, Jean-Pierre; Israeli, David; Bougueleret, Lydie; Gall, Isabelle Le; Medhioub, Monia; Linares-Cruz, Gustavo; Lethrosne, Florence; Pasturaud, Patricia; Piouffre, Laurence; Prieur, Sylvie; Susini, Laurent; Alvaro, Véronique; Millasseau, P; Guidicelli, Catherine; Bui, Hung; Massart, Catherine; Cazes, Lucien; Dufour, Fabienne; Bruzzoni‐Giovanelli, Heriberto; Owadi, H Ouman; Hennion, C; Charpak, Georges; Telerman, Adam

doi:10.1073/pnas.93.9.3953

Cited by 153 publications

(120 citation statements)

References 33 publications

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“…It is noteworthy that we found signi®cantly more divergence in the abundance of many SAGE tags when comparing REF-Phe132 versus 388C REF-Val135 than when comparing REFVal135 328C versus 388C. The former comparisons have been used previously for the identi®cation of potential p53-regulated genes by di erential display (Amson et al, 1996). Regardless, it is interesting that each of the known genes showing biased expression within REF-Phe132 cells has been linked to cellular growth regulation (Ambartsumian et al, 1995;Arai et al, 1996;Chambers, 1995;Guo et al, 1995;Perillo et al, 1995;Wright et al, 1996;Oates et al, 1996).…”

Section: Phe132mentioning

confidence: 66%

SAGE transcript profiles for p53-dependent growth regulation

et al. 1997

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Serial analysis of gene expression (SAGE) allows for a quantitative, representative, and comprehensive pro®le of gene expression. We have utilized SAGE technology to contrast the di erential gene expression pro®le in rat embryo ®broblast cells producing temperature-sensitive p53 tumor suppressor protein at permissive or nonpermissive temperatures. Analysis of *15 000 genes revealed that the expression of 14 genes (P50.001, 50.03% abundance) was dependent on functional p53 protein, whereas the expression of three genes was signi®cantly higher in cells producing non-functional p53 protein. Those genes whose expression was increased by functional p53 include RAS, U6 snRNA, cyclin G, EGR-1, and several novel genes. The expression of actin, tubulin, and HSP70 genes was elevated at the nonpermissive temperature for p53 function. Interestingly, the expression of several genes was dependent on a nontemperature-sensitive mutant p53 suggesting altered transcription pro®les dependent on speci®c p53 mutant proteins. These results demonstrate the utility of SAGE for rapidly and reproducibly evaluating global transcriptional responses within di erent cell populations.

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Section: Phe132mentioning

confidence: 66%

SAGE transcript profiles for p53-dependent growth regulation

et al. 1997

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“…Tumor suppressor-activated pathway 6 (TSAP6) was initially discovered because differentially regulated following p53 activation 1 and was later shown to be strongly activated in tumor suppression and reversion, which is why we named it TSAP6, in contrast with other transcripts which are inhibited in their expression (TSIPs). 1,2 Its promoter contains a functional p53-responsive element.…”

mentioning

confidence: 99%

“…1,2 Its promoter contains a functional p53-responsive element. 3 TSAP6 is part of a family of oxydoreductases with six transmembrane domains 4 and was recently identified as a ferrireductase (Steap3).…”

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confidence: 99%

Exosome secretion, including the DNA damage-induced p53-dependent secretory pathway, is severely compromised in TSAP6/Steap3-null mice

et al. 2008

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TSAP6 (tumor suppressor-activated pathway 6), also known as Steap3, is a direct p53 transcriptional target gene. It regulates protein secretion, for example translationally controlled tumor protein (TCTP), which is implicated in tumor reversion. In keeping with the latter, we show herein that TSAP6 is a glycosylated protein present in the trans-Golgi network, endosomal-vesicular compartment and cytoplasmic membrane. To further investigate the physiological function of TSAP6, we have generated TSAP6-deficient mice. These mice exhibit microcytic anemia with abnormal reticulocyte maturation and deficient transferrin receptor downregulation, a process known to be dependent on exosomal secretion. Moreover, we provide direct evidence that exosome production is severely compromised in TSAP6-null cells. Finally, we show that the DNA damage-induced p53-dependent nonclassical exosomal secretory pathway is abrogated in TSAP6-null cells. Given the fact that exosomes are used as cell-free vaccines against cancer and that they could be involved in the biogenesis and spread of human immunodeficiency virus, it is important to understand their regulation. The results presented here provide the first genetic demonstration that exosome formation is a tightly controlled biological process dependent of TSAP6.

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“…Signi®cant advances have been made recently toward the identi®cation of potential p53 e ector genes. For example, through the method of di erential display, Amson et al (1996) have isolated ten cDNA fragments activated by p53 in myeloid leukemia cells. In addition, Polyak et al (1997) utilizing the SAGE approach (Velculescu et al, 1995), found a total of 14 mRNAs that are markedly increased in levels upon ectopic p53 expression.…”

Section: Introductionmentioning

confidence: 99%

Identification of a novel mouse p53 target gene DDA3

Lo¹,

Chen²,

Lo³

et al. 1999

Oncogene

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We have identi®ed a novel p53 regulated gene designated DDA3 through di erential mRNA display on IW32 erythroleukemia cells containing a temperature sensitive p53 allele, tsp53val-135. DDA3 mRNA induction could be observed in all sublines expressing tsp53val-135 cultured at permissive temperature as well as in NIH3T3 cells undergoing DNA damage. Upregulation of DDA3 could be detected within 2 h after down-shifting the temperature to 32.58C; upon shifting back to 38.58C, DDA3 mRNA rapidly degraded with a half-life of less than 2 h. Actinomycin D, but not cycloheximide, inhibited the p53 dependent DDA3 induction, suggesting that the activation is through transcriptional regulation and does not require de novo protein synthesis. DDA3 was expressed in multiple mouse tissues including brain, spleen, lung, kidney and testis. Full-length DDA3 cDNA was cloned and it contained an open reading frame predicted to encode a proline rich protein of 329 amino acids. Overexpression of DDA3 in H1299 lung carcinoma cells suppressed colony formation. These results suggest that DDA3 is a p53-regulated gene that might participate in the p53-mediated growth suppression.

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Isolation of 10 differentially expressed cDNAs in p53-induced apoptosis: activation of the vertebrate homologue of the drosophila seven in absentia gene.

Cited by 153 publications

References 33 publications

SAGE transcript profiles for p53-dependent growth regulation

SAGE transcript profiles for p53-dependent growth regulation

Exosome secretion, including the DNA damage-induced p53-dependent secretory pathway, is severely compromised in TSAP6/Steap3-null mice

Identification of a novel mouse p53 target gene DDA3

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