Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA289264 | ENA |
REPOSITORIES: ENA
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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: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) 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:Epigenetic studies of HTLV-1 bZIP factor (HBZ) over-expressed mouse
| PRJDB3760 | ENA
Project description:Genome-wide DNA-binding profile of the HTLV-1 bZIP factor
| PRJDB4048 | ENA
Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.
2019-11-12 | PXD007511 | Pride
Project description:Five percent of HTLV-1 infected subjects develops an untreatable form of cancer designated Adult T cell leukemia (ATL). The HTLV-1-encoded HBZ protein is believed to act as a viral oncogene by disarranging crucial pathways in the infected cells. Key to thisfunction is a progressive cytoplasmic-to-nuclear dislocation of HBZ and its interaction with nuclear factors whose complexity wasnot assessed until now. In this investigation we unveiled for the first time such complexity by studying the endogenous HBZinteractome in a leukemic cell line derived from an ATL patient. A high number of nuclear interactors, represented by at least 249members, were found. Among the various family of interactors, we found predominant the family involved in RNA splicing and RNAstability. A disarrangement of the splicing mechanism was demonstrated both in ATL cells and in non HTLV-1-derived leukemic cellsexpressing HBZ after genetic transfer, strongly suggesting that a major mechanism leading to HTLV-1-mediated transformationand persistence of the oncogenic state is related to this event. Our unprecedented results shed new light on the mechanisms bywhich a human retrovirus can alter the infected cell metabolism and strongly predispose and/or maintain neoplastictransformation
2022-07-27 | GSE206085 | GEO
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 | GSE94732 | GEO
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