{
"id": "https://doi.org/10.6084/m9.figshare.19749200.v1",
"doi": "10.6084/M9.FIGSHARE.19749200.V1",
"url": "https://tandf.figshare.com/articles/dataset/Correlation_of_the_transcription_factors_i_IRF4_i_and_i_BACH2_i_with_the_abnormal_i_NFATC1_i_expression_in_T_cells_from_chronic_myeloid_leukemia_patients/19749200/1",
"types": {
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"schemaOrg": "Dataset",
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"creators": [
{
"name": "Zhang, Yikai",
"givenName": "Yikai",
"familyName": "Zhang"
},
{
"name": "Zeng, Xiangbo",
"givenName": "Xiangbo",
"familyName": "Zeng"
},
{
"name": "Zha, Xianfeng",
"givenName": "Xianfeng",
"familyName": "Zha"
},
{
"name": "Lai, Jing",
"givenName": "Jing",
"familyName": "Lai"
},
{
"name": "Tan, Guangxiao",
"givenName": "Guangxiao",
"familyName": "Tan"
},
{
"name": "Chen, Shaohua",
"givenName": "Shaohua",
"familyName": "Chen"
},
{
"name": "Yu, Xibao",
"givenName": "Xibao",
"familyName": "Yu"
},
{
"name": "Li, Yangqiu",
"givenName": "Yangqiu",
"familyName": "Li"
},
{
"name": "Xu, Ling",
"givenName": "Ling",
"familyName": "Xu"
}
],
"titles": [
{
"title": "Correlation of the transcription factors IRF4 and BACH2 with the abnormal NFATC1 expression in T cells from chronic myeloid leukemia patients"
}
],
"publisher": {
"name": "Taylor & Francis"
},
"container": {},
"subjects": [
{
"subject": "Cell Biology"
},
{
"subject": "Genetics"
},
{
"subject": "FOS: Biological sciences",
"schemeUri": "http://www.oecd.org/science/inno/38235147.pdf",
"subjectScheme": "Fields of Science and Technology (FOS)"
},
{
"subject": "Molecular Biology"
},
{
"subject": "Chemical Sciences not elsewhere classified"
},
{
"subject": "Immunology"
},
{
"subject": "FOS: Clinical medicine",
"schemeUri": "http://www.oecd.org/science/inno/38235147.pdf",
"subjectScheme": "Fields of Science and Technology (FOS)"
},
{
"subject": "Biological Sciences not elsewhere classified"
},
{
"subject": "Developmental Biology"
},
{
"subject": "Cancer"
},
{
"subject": "Hematology"
},
{
"subject": "Infectious Diseases"
},
{
"subject": "FOS: Health sciences",
"schemeUri": "http://www.oecd.org/science/inno/38235147.pdf",
"subjectScheme": "Fields of Science and Technology (FOS)"
},
{
"subject": "Computational Biology"
}
],
"contributors": [],
"dates": [
{
"date": "2022-05-11",
"dateType": "Created"
},
{
"date": "2024-02-19",
"dateType": "Updated"
},
{
"date": "2022",
"dateType": "Issued"
}
],
"publicationYear": 2022,
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{
"rights": "Creative Commons Attribution 4.0 International",
"rightsUri": "https://creativecommons.org/licenses/by/4.0/legalcode",
"schemeUri": "https://spdx.org/licenses/",
"rightsIdentifier": "cc-by-4.0",
"rightsIdentifierScheme": "SPDX"
}
],
"descriptions": [
{
"description": "T cell dysfunction is a common characteristic of patients with myeloid leukemia and is closely related to clinical efficacy and prognosis. In order to clarify the mechanisms leading to the T cell dysfunction, we characterized the gene expression profile of T cells from chronic myelogenous leukemia (CML) patients by microarray analysis and investigated the related regulating pathway. We employed gene expression profiling, bioinformatics and real-time quantitative reverse transcription PCR (RT-qPCR) to detect genes differentially expressed in CML patients versus healthy donors. There were 1704 genes differentially expressed between CD3+ T cells from CML patients and healthy donors, including 868 up-regulated genes and 836 down-regulated genes, which mostly related to T cell functional pathways. In particular, lower expression of NFATC1, a member of the TCR signaling pathway, was detected in CD3+ T cells from CML patients. We further found that the expression of IRF4 and BACH2, transcription factors that potentially regulate NFATC1, in CD3+ T cells from CML patients was significantly lower than that in healthy donors. We for the first time observed the altered gene expression profiles of CD3+ T cells from CML patients, and the results suggested that IRF4, BACH2 and NFATC1 may be involved in regulating T cell dysfunction in CML patients in the form of a transcriptional regulatory network. These findings may provide potential targets for tyrosine kinase inhibitors in combination with other targeted immunotherapies .",
"descriptionType": "Abstract"
}
],
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