Mus musculus
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR031536.fastq.gz | Fastqsanger.gz | |||
| DRR031537.fastq.gz | Fastqsanger.gz | |||
| DRR031538.fastq.gz | Fastqsanger.gz | |||
| DRR031539.fastq.gz | Fastqsanger.gz | |||
| DRR031540.fastq.gz | Fastqsanger.gz |
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Project description:Human T-cell leukemia virus type 1 (HTLV-1) encodes HTLV-1 bZIP factor (HBZ), which is thought to be crucial for neoplastic and inflammatory diseases caused by HTLV-1. So, we analyzed the transcriptional profile of HBZ expressing cells and how HBZ affect the expression of apoptosis-related genes. We used microarrays to detail the effect of HTLV-1 bZIP factor (HBZ), which is encoded in the minus strand of HTLV-1 genome on gene expression. Especially how HBZ affect the expression of apoptosis-related genes.
2013-06-18 | GSE48029 | GEO
Project description:Human T-cell leukemia virus type 1 (HTLV-1) encodes HTLV-1 bZIP factor (HBZ), which is thought to be crucial for neoplastic and inflammatory diseases caused by HTLV-1. So, we analyzed the transcriptional profile of HBZ expressing cells and how HBZ affect the expression of apoptosis-related genes. We used microarrays to detail the effect of HTLV-1 bZIP factor (HBZ), which is encoded in the minus strand of HTLV-1 genome on gene expression. Especially how HBZ affect the expression of apoptosis-related genes. Jurkat cells stably expressing HBZ were stimulated with or without PMA and ionomycin for 9hours. Then RNA extraction and hybridization on Affymetrix microarrays were performed.
2013-06-18 | E-GEOD-48029 | biostudies-arrayexpress
Project description:Human T-cell leukemia virus type 1 (HTLV-1) bZIP factor (HBZ) which is encoded in the minus strand of HTLV-1 provirus, possesses dual function as protein, and also as RNA. To know the effect of HBZ RNA and protein in primary T-cells, we introduced HBZ, or its mutant TTG (exclude protein activity), or SM (exclude RNA activity) with retrovirus vector into CD4 positive murine T cells, and analysed the transcriptome profiling. We found that HBZ RNA altered cell cycle progression, cell survival related genes, while HBZ protein altered immunology related genes. This microarray results demonstrated that HBZ RNA and protein possess distinct functions in primary cells.
2016-04-01 | GSE70649 | GEO
Project description:Human T-cell leukemia virus type 1 (HTLV-1) bZIP factor (HBZ) which is encoded in the minus strand of HTLV-1 provirus, possesses dual function as protein, and also as RNA. To know the effect of HBZ RNA and protein in primary T-cells, we introduced HBZ, or its mutant TTG (exclude protein activity), or SM (exclude RNA activity) with retrovirus vector into CD4 positive murine T cells, and analysed the transcriptome profiling. We found that HBZ RNA altered cell cycle progression, cell survival related genes, while HBZ protein altered immunology related genes. This microarray results demonstrated that HBZ RNA and protein possess distinct functions in primary cells. CD4 positive cells were enriched from murine splenocyte, and cultured with irradiated antigen presenting cells (APC). HBZ, or its mutant were introduced with retroviral vector. Forty eight hours after introduction, cells were washed and cultured with recombinant human IL-2. Further 48 hours after culture, virus infected cells were sorted and analysed by agilent microarray.
2016-04-01 | E-GEOD-70649 | biostudies-arrayexpress
Project description:The effect of HTLV-1 bZIP factor (HBZ) RNA and protein in mouse CD4 T cells
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Project description:Effect of HTLV-1 bZIP factor(HBZ) on microRNA expression profile.
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Project description:HTLV-1 is an oncovirus that encodes a transactivator Tax and a latent oncogene HBZ. HTLV-1 early or infectious replication depends on Tax; during HTLV-1 late infection, HBZ plays a crucial role in driving the proliferation of infected cells and maintaining viral persistence. The biphasic replication pattern of HTLV-1 dictated by Tax and HBZ represents a result of viral host adaptation, but how HTLV-1 coordinates Tax and HBZ expression to facilitate early and late infection remains elusive. Here we reveal that HBZ RNA splicing exhibits distinct patterns in Tax+ and Tax- HTLV-1 infected cells. We demonstrate that Tax interacts with the host spliceosome and inhibits HBZ splicing by competitively binding splicing factors including WDR83 and GPATCH1. As a result, Tax confers a natural constraint on HBZ, counterbalancing its anti-replication effect at HTLV-1 early infection, while unleashing HBZ to drive HTLV-1 mitotic propagation during late infection. The splicing-dependent restriction of HBZ by Tax thus represents a critical interplay central to HTLV-1 persistence.
2025-06-19 | PXD065208 |
Project description:Genome-wide DNA-binding profile of the HTLV-1 bZIP factor
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Project description:Adult T-cell Leukemia/Lymphoma (ATLL) is a frequently incurable disease associated with the human lymphotropic virus type I (HTLV-I). The transcription factor HBZ is the only virally encoded gene that is expressed in all ATLL cases, but it is unclear why it may be essential in ATLL and how it might be targeted therapeutically. Here we performed RNA interference screening of ATLL lines and discovered that their proliferation depends on the transcription factors BATF3 and IRF4, which regulate the identity of normal immune cells. These factors, which are highly expressed in ATLL, cooperatively bind and transactivate genes that distinguish ATLL from other T cell malignancies, including BATF3 itself. HBZ binds to an ATLL-specific BATF3 super-enhancer and thereby regulates the expression of BATF3 and its downstream targets, including the oncogene MYC. The BET protein inhibitor JQ1 collapsed the transcriptional network directed by HBZ and BATF3, and was consequently toxic for ATLL lines and patient samples in vitro, and blocked growth of ATLL xenografts. Our study demonstrates that the HTLV-I virus exploits a regulatory module that can potentially be attacked therapeutically with BET protein inhibitors.
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Project description:Adult T-cell Leukemia/Lymphoma (ATLL) is a frequently incurable disease associated with the human lymphotropic virus type I (HTLV-I). The transcription factor HBZ is the only virally encoded gene that is expressed in all ATLL cases, but it is unclear why it may be essential in ATLL and how it might be targeted therapeutically. Here we performed RNA interference screening of ATLL lines and discovered that their proliferation depends on the transcription factors BATF3 and IRF4, which regulate the identity of normal immune cells. These factors, which are highly expressed in ATLL, cooperatively bind and transactivate genes that distinguish ATLL from other T cell malignancies, including BATF3 itself. HBZ binds to an ATLL-specific BATF3 super-enhancer and thereby regulates the expression of BATF3 and its downstream targets, including the oncogene MYC. The BET protein inhibitor JQ1 collapsed the transcriptional network directed by HBZ and BATF3, and was consequently toxic for ATLL lines and patient samples in vitro, and blocked growth of ATLL xenografts. Our study demonstrates that the HTLV-I virus exploits a regulatory module that can potentially be attacked therapeutically with BET protein inhibitors.
2018-07-10 | GSE94409 | GEO