Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA291437 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2133990_1.fastq.gz | Fastqsanger.gz | |||
| SRR2133990_2.fastq.gz | Fastqsanger.gz | |||
| SRR2133991_1.fastq.gz | Fastqsanger.gz | |||
| SRR2133991_2.fastq.gz | Fastqsanger.gz | |||
| SRR2133992_1.fastq.gz | Fastqsanger.gz |
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Project description:Insults to cellular health cause p53 protein accumulation and loss of p53 function leads to tumorigenesis. Thus, p53 has to be tightly controlled. Here we report that the BTB/POZ domain transcription factor PATZ1 (MAZR), previously known for its transcriptional suppressor functions in T lymphocytes, is a crucial regulator of p53. The novel inhibitory role of PATZ1 on the p53 protein marks it as a proto-oncogene. PATZ1 deficient cells have reduced proliferative capacity which we assess by RNASeq and real time cell growth rate analysis. PATZ1 modifies the expression of p53 target genes associated with cell proliferation gene ontology terms. Moreover, PATZ1 regulates several genes involved in cellular adhesion and morphogenesis. Significantly, treatment with the DNA damage inducing drug doxorubicin results in the loss of the PATZ1 transcription factor, as p53 accumulates. We find that PATZ1 binds to p53 and inhibits p53 dependent transcription activation. We examine the mechanism of this functional inhibitory interaction and demonstrate that PATZ1 excludes p53 from DNA binding. This study documents PATZ1 as a novel player in the p53 pathway. RNA-seq was used to define differentially expressed genes in wild-type and PATZ1-/- MEFs. Each sample was represented in triplicate.
2015-03-27 | E-GEOD-65864 | biostudies-arrayexpress
Project description:PATZ1 is a DNA damage responsive transcription factor that inhibits p53 function
| PRJNA275243 | ENA
Project description:Insults to cellular health cause p53 protein accumulation and loss of p53 function leads to tumorigenesis. Thus, p53 has to be tightly controlled. Here we report that the BTB/POZ domain transcription factor PATZ1 (MAZR), previously known for its transcriptional suppressor functions in T lymphocytes, is a crucial regulator of p53. The novel inhibitory role of PATZ1 on the p53 protein marks it as a proto-oncogene. PATZ1 deficient cells have reduced proliferative capacity which we assess by RNASeq and real time cell growth rate analysis. PATZ1 modifies the expression of p53 target genes associated with cell proliferation gene ontology terms. Moreover, PATZ1 regulates several genes involved in cellular adhesion and morphogenesis. Significantly, treatment with the DNA damage inducing drug doxorubicin results in the loss of the PATZ1 transcription factor, as p53 accumulates. We find that PATZ1 binds to p53 and inhibits p53 dependent transcription activation. We examine the mechanism of this functional inhibitory interaction and demonstrate that PATZ1 excludes p53 from DNA binding. This study documents PATZ1 as a novel player in the p53 pathway.
2017-07-29 | GSE71529 | GEO
Project description:Insults to cellular health cause p53 protein accumulation and loss of p53 function leads to tumorigenesis. Thus, p53 has to be tightly controlled. Here we report that the BTB/POZ domain transcription factor PATZ1 (MAZR), previously known for its transcriptional suppressor functions in T lymphocytes, is a crucial regulator of p53. The novel inhibitory role of PATZ1 on the p53 protein marks it as a proto-oncogene. PATZ1 deficient cells have reduced proliferative capacity which we assess by RNASeq and real time cell growth rate analysis. PATZ1 modifies the expression of p53 target genes associated with cell proliferation gene ontology terms. Moreover, PATZ1 regulates several genes involved in cellular adhesion and morphogenesis. Significantly, treatment with the DNA damage inducing drug doxorubicin results in the loss of the PATZ1 transcription factor, as p53 accumulates. We find that PATZ1 binds to p53 and inhibits p53 dependent transcription activation. We examine the mechanism of this functional inhibitory interaction and demonstrate that PATZ1 excludes p53 from DNA binding. This study documents PATZ1 as a novel player in the p53 pathway.
2015-03-27 | GSE65864 | GEO
Project description:Long noncoding RNAs (lncRNAs) are prevalent genes with frequently exquisite regulation but mostly unknown functions. Here we demonstrate a role of lncRNAs in guiding signal transduction. DNA damage activates transcription of DINO (Damage Induced NOncoding) via p53. DINO knockdown blocks DNA damage-induced gene expression and cell cycle arrest. Conversely, enforced expression of DINO activates damage signaling without DNA damage. DINO binds p53 and selectively promotes SET7 methylation of p53 at lysine 372 over other substrates, which stabilizes p53 in an auto-amplification loop. Our results suggest that inducible lncRNA can achieve catalysis-like effects to rewire cellular signaling networks. RNA was isolated from human fetal lung fibroblasts, HCT116 p53+/+, or HCT116 p53-/- cells treated with doxorubicin or sham for 26 hours. Human fetal lung fibroblasts were transfected with siRNAs targeting DINO or non-targeting control and subsequently treated with doxorubicin for 26 hours.
2012-11-20 | E-GEOD-42368 | biostudies-arrayexpress
Project description:miR-seq to find miRs that are induced by DNA damage and whose induction requires ABL kinase activity Use p53-inactive HEK293T cells. Use doxorubicin to induce DNA damage. Use imatinib co-treatment to inhibit ABL kinase activity
2015-07-01 | E-GEOD-59028 | biostudies-arrayexpress
Project description:The goal of this experiment was to determine the role of the lncRNA DINO in the DNA damage response in regulating transcription factor occupancy of human fibroblasts. DINO, an inducible long noncoding in respose to DNA damage, is required for cell cycle arrest and induction of several p53 regulated genes. We hypothesized that ATACseq in DINO-depleted cells may uncover a role for DINO in transcription factor recruitment to p53 responsive genes following DNA damage.
2016-09-26 | GSE76417 | GEO
Project description:Liver cancer is the third most common cause of cancer death in the world. POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1) is a transcription factor associated with various cancers. However, the role of PATZ1 in cancer progression remains controversial. Here we report that PATZ1 regulates cell proliferation by directly regulating CDKN1B (p27) in hepatocellular carcinoma HepG2 cells. PATZ1 level was found to be ectopically expressed in hepatocellular carcinoma cells compared to normal primary human hepatocytes, thus affirming its relevance in liver cancer. Our gene expression microarray and PATZ1 ChIP-seq analysis further revealed strong enrichment in gene ontology terms related to cellular proliferation. Importantly, siRNA-mediated PATZ1 knockdown in HepG2 cells led to an increased rate of colony formation, elevated Ki-67 expression and greater S phase entry. Furthermore, the increased cancer cell proliferation was accompanied with suppressed expression of the cyclin-dependent kinase inhibitor CDKN1B. Consistently, PATZ1 binds to the genomic loci flanking the transcriptional start site of CDKN1B and positively regulates its promoter activity. Additionally, we found that PATZ1 associates with p53 and the absence of p53 abrogated the PATZ1-mediated regulation of CDKN1B expression. In conclusion, our study provides novel mechanistic insights into the role of PATZ1 in liver cancer progression, thereby providing a promising therapeutic intervention to alleviate tumor burden in liver cancer.
2020-12-31 | GSE113859 | GEO
Project description:Liver cancer is the third most common cause of cancer death in the world. POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1) is a transcription factor associated with various cancers. However, the role of PATZ1 in cancer progression remains controversial. Here we report that PATZ1 regulates cell proliferation by directly regulating CDKN1B (p27) in hepatocellular carcinoma HepG2 cells. PATZ1 level was found to be ectopically expressed in hepatocellular carcinoma cells compared to normal primary human hepatocytes, thus affirming its relevance in liver cancer. Our gene expression microarray and PATZ1 ChIP-seq analysis further revealed strong enrichment in gene ontology terms related to cellular proliferation. Importantly, siRNA-mediated PATZ1 knockdown in HepG2 cells led to an increased rate of colony formation, elevated Ki-67 expression and greater S phase entry. Furthermore, the increased cancer cell proliferation was accompanied with suppressed expression of the cyclin-dependent kinase inhibitor CDKN1B. Consistently, PATZ1 binds to the genomic loci flanking the transcriptional start site of CDKN1B and positively regulates its promoter activity. Additionally, we found that PATZ1 associates with p53 and the absence of p53 abrogated the PATZ1-mediated regulation of CDKN1B expression. In conclusion, our study provides novel mechanistic insights into the role of PATZ1 in liver cancer progression, thereby providing a promising therapeutic intervention to alleviate tumor burden in liver cancer.
2020-12-31 | GSE114030 | GEO