Publications by authors named "Amanda W Rushing"

The complex retrovirus, human T-cell leukemia virus type 1 (HTLV-1), primarily infects CD4+ T-cells in vivo. Infectious spread within this cell population requires direct contact between virally-infected and target cells. The HTLV-1 accessory protein, HBZ, was recently shown to enhance HTLV-1 infection by activating intracellular adhesion molecule 1 (ICAM-1) expression, which promotes binding of infected cells to target cells and facilitates formation of a virological synapse.

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Adult T-cell leukemia and lymphoma (ATLL) is an intractable T-cell neoplasia caused by a retrovirus, namely human T-cell leukemia virus type 1 (HTLV-1). Patients suffering from ATLL present a poor prognosis and have a dearth of treatment options. In contrast to the sporadic expression of viral transactivator protein Tax present at the 5' promoter region long terminal repeats (LTR), HTLV-1 bZIP gene (HBZ) is encoded by 3'LTR (the antisense promoter) and maintains its constant expression in ATLL cells and patients.

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Adult T-cell Leukemia (ATL) is a lymphoproliferative disease of CD4+ T-cells infected with Human T-cell Leukemia Virus type I (HTLV-1). With the exception of allogeneic hematopoietic stem cell transplantation, there are no effective treatments to cure ATL, and ATL cells often acquire resistance to conventional chemotherapeutic agents. Accumulating evidence shows that development and maintenance of ATL requires key contributions from the viral protein, HTLV-1 basic leucine zipper factor (HBZ).

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Adult T-cell leukemia (ATL) is a fatal malignancy of CD4 T cells infected with human T-cell leukemia virus type 1 (HTLV-1). ATL cells often exhibit random gross chromosomal rearrangements that are associated with the induction and improper repair of double-stranded DNA breaks (DSBs). The viral oncoprotein Tax has been reported to impair DSB repair but has not been shown to be consistently expressed throughout all phases of infection.

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Article Synopsis
  • Adult T-cell leukemia (ATL) is a serious cancer linked to the HTLV-1 virus, which inactivates the tumor suppressor protein p53 primarily through the viral protein Tax and another protein called HBZ.
  • The study found that HBZ repressed p53 activity by inhibiting two histone acetyltransferases (HATs), p300/CBP and HBO1, leading to reduced p53 acetylation and impaired transcription of target genes like p21/CDKN1A and GADD45A.
  • This mechanism helps explain how p53 is less active in ATL cells, particularly in cases where Tax is not present due to changes in the HTLV-1 provirus, affecting many patient samples
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