Rie Furuta

ORCID: 0000-0003-1446-0254
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About
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Research Areas
  • T-cell and Retrovirus Studies
  • Animal Disease Management and Epidemiology
  • Vector-Borne Animal Diseases
  • HIV/AIDS drug development and treatment
  • Virus-based gene therapy research
  • HIV Research and Treatment
  • Immune Cell Function and Interaction
  • Viral Infectious Diseases and Gene Expression in Insects
  • Lymphoma Diagnosis and Treatment
  • Viral Infections and Immunology Research
  • Chronic Lymphocytic Leukemia Research
  • RNA modifications and cancer
  • Autoimmune Neurological Disorders and Treatments
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Galectins and Cancer Biology
  • Glycogen Storage Diseases and Myoclonus
  • Platelet Disorders and Treatments
  • CNS Lymphoma Diagnosis and Treatment
  • Parathyroid Disorders and Treatments
  • Mast cells and histamine
  • Immunodeficiency and Autoimmune Disorders
  • Soft tissue tumor case studies
  • Vitamin K Research Studies
  • Genomic variations and chromosomal abnormalities
  • Blood Coagulation and Thrombosis Mechanisms

Wakayama Medical University
2025

Kumamoto University Hospital
2023-2024

Kyoto University
1992-2018

Kumamoto University
2017

Osaka Red Cross Hospital
2009

Thomas Jefferson University
1996

Niigata University
1991

Human T-lymphotropic virus type 1 (HTLV-1) causes the debilitating neuroinflammatory disease HTLV-1–associated myelopathy–tropical spastic paraparesis (HAM–TSP) as well adult T-cell leukemia–lymphoma (ATLL). In patients with HAM–TSP, HTLV-1 infects mainly CCR4+ T cells and induces functional changes, ultimately causing chronic spinal cord inflammation. We evaluated mogamulizumab, a humanized anti-CCR4 monoclonal antibody that targets infected cells, in HAM–TSP.

10.1056/nejmoa1704827 article EN New England Journal of Medicine 2018-02-07

Infection of T cells with human T-cell leukemia virus type-1 (HTLV-1) induces clonal proliferation and is closely associated the onset adult leukemia-lymphoma (ATL) inflammatory diseases. Although Tax expression frequently suppressed in HTLV-1-infected cells, accessory gene, HTLV-1 bZIP factor (HBZ), continuously expressed has been implicated pathogenesis. Here, we report that transduction mouse specific mutants HBZ distinguish between its RNA protein activity results differential effects on...

10.1158/0008-5472.can-15-0942 article EN Cancer Research 2015-09-18

Human T-cell leukemia virus type 1 (HTLV-1) infects mainly CD4+CCR4+ effector/memory T cells in vivo. However, it remains unknown whether HTLV-1 preferentially these or this converts infected precursor to specialized cells. Expression of viral genes vivo is critical study replication and proliferation Therefore, we first analyzed gene expression non-human primates naturally with simian (STLV-1), whose virological attributes closely resemble those HTLV-1. Although the tax transcript was...

10.1371/journal.ppat.1006722 article EN cc-by PLoS Pathogens 2017-11-29

Human T-cell leukemia virus type 1 (HTLV-1) causes adult leukemia-lymphoma (ATL) and other inflammatory diseases in infected individuals. However, a complete understanding of how HTLV-1 transforms T cells is lacking. Expression the chemokine receptor CCR4 on ATL HTLV-1-infected suggested hypothesis that may mediate features caused by HTLV-1. In this study, we show constitutively expressed bZIP factor (HBZ) encoded responsible for inducing its ability to promote proliferation migration....

10.1158/0008-5472.can-16-0361 article EN Cancer Research 2016-07-12

10.1016/j.diff.2025.100860 article EN Differentiation 2025-03-01

Rev, a major regulatory protein of human immunodeficiency virus type 1, has been demonstrated to shuttle between the nucleus and cytoplasm infected cells. The fate Rev in living cells was evaluated by pulse-chase experiments using transient expression system. Sixteen hours after chasing with unlabelled amino acids, 45% labelled still present, which clearly indicates long half-life A mutant is deficient ability migrate from degraded more slowly than wild-type protein. As well, another...

10.1128/jvi.70.2.1282-1287.1996 article EN Journal of Virology 1996-02-01

A nonfunctional mutant of human immunodeficiency virus type 1 Rev was created by deleting seven amino acid residues within the nucleolar targeting signal. This remained in cytoplasm expressed cells and strongly inhibited function interfering with nuclear/nucleolar localization coexpressed Rev. These findings suggest multimerization before migration to nucleus/nucleolus, where wild-type functions as a trans-regulator.

10.1128/jvi.66.4.2510-2513.1992 article EN Journal of Virology 1992-04-01

Applications of transdominant mutants human immunodeficiency virus type 1 (HIV-1) regulatory proteins, especially Rev mutant, have been attempted for gene therapy against AIDS, because the protein is essential viral replication. We previously reported that a mutant (dRev) lacking its nucleolar targeting signal remained out nuclei in expressed cells and strongly inhibited function Rev. To investigate effects dRev on HIV-1 replication, we established several dRev-expressing cell lines with two...

10.1128/jvi.69.3.1591-1599.1995 article EN Journal of Virology 1995-03-01

Extranodal natural killer (NK)/T-cell lymphoma (ENKTL) is a rare subtype of non-Hodgkin (NHL) with poor prognosis, particularly in relapsed or refractory patients. Thus, timely detection relapse and appropriate disease management are crucial. We present two patients ENKTL, wherein positron emission tomography-computed tomography (PET-CT) total-body coverage after induction therapy, detected newly regions the bone marrow lower leg prior to progression. Case 1: A 47-year-old woman nasal...

10.3960/jslrt.23046 article EN cc-by-nc-sa Journal of Clinical and Experimental Hematopathology 2024-01-01

<p>HBZ RNA activates survivin promoter in ILF3, p54nrb, and TLS-independent manner</p>

10.1158/0008-5472.22406643 preprint EN cc-by 2023-03-30

<p>HBZ RNA activates the survivin promoter in absence of cell cycle dependent element (CDE)/cell homology region (CHE), p53, or Sp-1 binding site</p>

10.1158/0008-5472.22406646.v1 preprint EN cc-by 2023-03-30

<p>HBZ RNA activates the survivin promoter in absence of cell cycle dependent element (CDE)/cell homology region (CHE), p53, or Sp-1 binding site</p>

10.1158/0008-5472.22406646 preprint EN cc-by 2023-03-30

<p>HBZ RNA activates survivin promoter in ILF3, p54nrb, and TLS-independent manner</p>

10.1158/0008-5472.22406643.v1 preprint EN cc-by 2023-03-30

<div>Abstract<p>Human T-cell leukemia virus type 1 (HTLV-1) causes adult leukemia-lymphoma (ATL) and other inflammatory diseases in infected individuals. However, a complete understanding of how HTLV-1 transforms T cells is lacking. Expression the chemokine receptor CCR4 on ATL HTLV-1–infected suggested hypothesis that may mediate features caused by HTLV-1. In this study, we show constitutively expressed bZIP factor (HBZ) encoded responsible for inducing its ability to promote...

10.1158/0008-5472.c.6508860.v1 preprint EN 2023-03-31
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