Results 1 to 10 of about 60,065 (147)

HBZ and its roles in HTLV-1 oncogenesis

open access: yesFrontiers in Microbiology, 2012
Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL). The minus strand of HTLV-1 provirus encodes a bZIP protein donated as HTLV-1 bZIP factor (HBZ).
Tiejun Zhao
exaly   +3 more sources

Splicing-dependent restriction of the HBZ gene by Tax underlies biphasic HTLV-1 infection. [PDF]

open access: yesPLoS Pathogens
HTLV-1 is an oncovirus that encodes a transactivator Tax and a regulatory gene 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 ...
Yi Liang   +12 more
doaj   +2 more sources

Stability of the HTLV-1 Antisense-Derived Protein, HBZ, Is Regulated by the E3 Ubiquitin-Protein Ligase, UBR5

open access: yesFrontiers in Microbiology, 2018
Human T-cell leukemia virus type 1 (HTLV-1) encodes a protein derived from the antisense strand of the proviral genome designated HBZ (HTLV-1 basic leucine zipper factor). HBZ is the only viral gene consistently expressed in infected patients and adult T-
Jacob Al-Saleem   +2 more
exaly   +3 more sources

The Role of HBZ in HTLV-1-Induced Oncogenesis

open access: yesViruses, 2016
Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL) and chronic inflammatory diseases. HTLV-1 bZIP factor (HBZ) is transcribed as an antisense transcript of the HTLV-1 provirus.
Tiejun Zhao
exaly   +3 more sources

HTLV-1 HBZ Protein Resides Exclusively in the Cytoplasm of Infected Cells in Asymptomatic Carriers and HAM/TSP Patients

open access: yesFrontiers in Microbiology, 2019
Human T cell lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) in a subset of infected subjects.
Claudine Piqué   +2 more
exaly   +3 more sources

HTLV-1 Tax and HBZ cooperatively promote leukemogenesis through miR-155-mediated PTEN suppression and PI3K-Akt activation [PDF]

open access: yesJournal of Virology
Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATLL), but the full scope of its oncogenic mechanisms remains elusive.
Xiaoru Xin   +5 more
doaj   +2 more sources

Role of HTLV-1 Tax and HBZ in the Pathogenesis of HAM/TSP

open access: yesFrontiers in Microbiology, 2017
Human T cell lymphotropic virus type 1 (HTLV-1) infection can lead to development of adult T cell leukemia/lymphoma (ATL) or HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) in a subset of infected subjects.
Yoshimi Enose-Akahata, Steven Jacobson
exaly   +3 more sources

HTLV-1 Hbz protein, but not hbz mRNA secondary structure, is critical for viral persistence and disease development.

open access: yesPLoS Pathogens, 2023
Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic cause of adult T-cell leukemia/lymphoma (ATL) and encodes a viral oncoprotein (Hbz) that is consistently expressed in asymptomatic carriers and ATL patients, suggesting its importance in the ...
Victoria Maksimova   +8 more
doaj   +1 more source

The endogenous HBZ interactome in ATL leukemic cells reveals an unprecedented complexity of host interacting partners involved in RNA splicing

open access: yesFrontiers in Immunology, 2022
Adult T-cell leukemia/lymphoma (ATL) is a T-cell lymphoproliferative neoplasm caused by the human T-cell leukemia virus type 1 (HTLV-1). Two viral proteins, Tax-1 and HBZ play important roles in HTLV-1 infectivity and in HTLV-1-associated pathologies by ...
Mariam Shallak   +10 more
doaj   +1 more source

TAX and HBZ: hFc Ɣ 1 proteins as targets for passive immunotherapy [PDF]

open access: yesIranian Journal of Basic Medical Sciences, 2022
Objective(s): Human T leukemia virus type one (HTLV-1) causes two life-threatening diseases in around five percent of infected subjects, a T cell malignancy and a neurodegenerative disease.
Mohammad Akbarin   +6 more
doaj   +1 more source

Home - About - Disclaimer - Privacy