479 results match your criteria Human T-Cell Lymphotrophic Viruses

HTLV-1 activates YAP via NF-κB/p65 to promote oncogenesis.

Proc Natl Acad Sci U S A 2022 03;119(9)

Laboratory of Virus Control, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan;

Adult T-cell leukemia/lymphoma (ATL) is an aggressive malignancy caused by human T-cell leukemia virus type 1 (HTLV-1) infection. HTLV-1 exerts its oncogenic functions by interacting with signaling pathways involved in cell proliferation and transformation. Dysregulation of the Hippo/YAP pathway is associated with multiple cancers, including virus-induced malignancies. Read More

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HTLV-1 infection promotes excessive T cell activation and transformation into adult T cell leukemia/lymphoma.

J Clin Invest 2021 12;131(24)

Division of Genomics and Transcriptomics, Joint Research Center for Human Retrovirus Infection.

Human T cell leukemia virus type 1 (HTLV-1) mainly infects CD4+ T cells and induces chronic, persistent infection in infected individuals, with some developing adult T cell leukemia/lymphoma (ATL). HTLV-1 alters cellular differentiation, activation, and survival; however, it is unknown whether and how these changes contribute to the malignant transformation of infected cells. In this study, we used single-cell RNA-sequencing and T cell receptor-sequencing to investigate the differentiation and HTLV-1-mediated transformation of T cells. Read More

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December 2021

Feedback Loop Regulation between Pim Kinases and Tax Keeps Human T-Cell Leukemia Virus Type 1 Viral Replication in Check.

J Virol 2022 02 24;96(3):e0196021. Epub 2021 Nov 24.

Department of Pathology and Laboratory Medicine, University of Kansasgrid.266515.3 Medical Center, Kansas City, Kansas, USA.

The Pim family of serine/threonine kinases promote tumorigenesis by enhancing cell survival and inhibiting apoptosis. Three isoforms exist, Pim-1, -2, and -3, that are highly expressed in hematological cancers, including Pim-1 in adult T-cell leukemia (ATL). Human T-cell leukemia virus type-1 (HTLV-1) is the etiological agent of ATL, a dismal lymphoproliferative disease known as adult T-cell leukemia. Read More

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February 2022

The HTLV-1 viral oncoproteins Tax and HBZ reprogram the cellular mRNA splicing landscape.

PLoS Pathog 2021 09 20;17(9):e1009919. Epub 2021 Sep 20.

Laboratory of Viral Interactomes, GIGA Institute, University of Liege, Liege, Belgium.

Viral infections are known to hijack the transcription and translation of the host cell. However, the extent to which viral proteins coordinate these perturbations remains unclear. Here we used a model system, the human T-cell leukemia virus type 1 (HTLV-1), and systematically analyzed the transcriptome and interactome of key effectors oncoviral proteins Tax and HBZ. Read More

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September 2021

Tax Induces the Recruitment of NF-κB to Unintegrated HIV-1 DNA To Rescue Viral Gene Expression and Replication.

J Virol 2021 06 10;95(13):e0028521. Epub 2021 Jun 10.

Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina, USA.

We previously reported that the normally essential step of integration of the HIV-1 proviral DNA intermediate into the host cell genome becomes dispensable in T cells that express the human T cell leukemia virus 1 (HTLV-1) Tax protein, a known activator of cellular NF-κB. The rescue of integrase (IN)-deficient HIV-1 replication by Tax results from the strong activation of transcription from the long terminal repeat (LTR) promoter on episomal HIV-1 DNA, an effect that is closely correlated with the recruitment of activating epigenetic marks, such as H3Ac, and depletion of repressive epigenetic marks, such as H3K9me3, from chromatinized unintegrated proviruses. In addition, activation of transcription from unintegrated HIV-1 DNA coincides with the recruitment of NF-κB to the two NF-κB binding sites found in the HIV-1 LTR enhancer. Read More

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NF-κB-induced R-loop accumulation and DNA damage select for nucleotide excision repair deficiencies in adult T cell leukemia.

Proc Natl Acad Sci U S A 2021 03;118(10)

Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814;

Constitutive NF-κB activation (NF-κB) confers survival and proliferation advantages to cancer cells and frequently occurs in T/B cell malignancies including adult T cell leukemia (ATL) caused by human T-cell leukemia virus type 1 (HTLV-1). Counterintuitively, NF-κB by the HTLV-1 transactivator/oncoprotein Tax induces a senescence response, and HTLV-1 infections in culture mostly result in senescence or cell-cycle arrest due to NF-κB How NF-κB induces senescence, and how ATL cells maintain NF-κB and avert senescence, remain unclear. Here we report that NF-κB by Tax increases R-loop accumulation and DNA double-strand breaks, leading to senescence. Read More

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In vivo dynamics and adaptation of HTLV-1-infected clones under different clinical conditions.

PLoS Pathog 2021 02 1;17(2):e1009271. Epub 2021 Feb 1.

Department of Hematology, Rheumatology, and Infectious Diseases, Graduate School of Medical Sciences, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.

Human T-cell leukemia virus type 1 (HTLV-1) spreads through cell contact. Therefore, this virus persists and propagates within the host by two routes: clonal proliferation of infected cells and de novo infection. The proliferation is influenced by the host immune responses and expression of viral genes. Read More

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February 2021

In vivo antagonistic role of the Human T-Cell Leukemia Virus Type 1 regulatory proteins Tax and HBZ.

PLoS Pathog 2021 01 20;17(1):e1009219. Epub 2021 Jan 20.

Department of Internal Medicine, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.

Adult T cell leukemia (ATL) is an aggressive malignancy secondary to chronic infection by the human T-cell leukemia virus type 1 (HTLV-1) infection. Two viral proteins, Tax and HBZ, play central roles in ATL leukemogenesis. Tax expression transforms T cells in vitro and induces ATL-like disease in mice. Read More

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January 2021

The E3/E4 ubiquitin conjugation factor UBE4B interacts with and ubiquitinates the HTLV-1 Tax oncoprotein to promote NF-κB activation.

PLoS Pathog 2020 12 23;16(12):e1008504. Epub 2020 Dec 23.

Department of Microbiology and Immunology, Penn State College School of Medicine, Hershey, Pennsylvania, United States of America.

Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATLL), and the neurological disease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax protein persistently activates the NF-κB pathway to enhance the proliferation and survival of HTLV-1 infected T cells. Lysine 63 (K63)-linked polyubiquitination of Tax provides an important regulatory mechanism that promotes Tax-mediated interaction with the IKK complex and activation of NF-κB; however, the host proteins regulating Tax ubiquitination are largely unknown. Read More

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December 2020

Epidemiology of Virus Infection and Human Cancer.

Recent Results Cancer Res 2021 ;217:13-45

Genomics Research Center, Academia Sinica, 128 Academia Road, Sect. 2, Taipei, 115, Taiwan.

Seven viruses including the Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), Kaposi's sarcoma herpes virus (KSHV), human immunodeficiency virus, type-1 (HIV-1), human T cell lymphotrophic virus, type-1 (HTLV-1), and human papillomavirus (HPV) have been classified as Group 1 human carcinogens by the International Agency for Research on Cancer (IARC). The conclusions are based on the findings of epidemiological and mechanistic studies. EBV, HPV, HTLV-1, and KSHV are direct carcinogens; HBV and HCV are indirect carcinogens through chronic inflammation; and HIV-1 is an indirect carcinogen through immune suppression. Read More

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January 2021

Restoration of ceramide de novo synthesis by the synthetic retinoid ST1926 as it induces adult T-cell leukemia cell death.

Biosci Rep 2020 10;40(10)

Department of Biochemistry and Molecular Genetics, American University of Beirut, Lebanon.

Ceramide (Cer) is a bioactive cellular lipid with compartmentalized and tightly regulated levels. Distinct metabolic pathways lead to the generation of Cer species with distinguishable roles in oncogenesis. Deregulation of Cer pathways has emerged as an important mechanism for acquired chemotherapeutic resistance. Read More

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October 2020

Regulation of Expression and Latency in BLV and HTLV.

Viruses 2020 09 25;12(10). Epub 2020 Sep 25.

Department of Biology, The University of Winnipeg, Winnipeg, MB R3B 2E9, Canada.

(HTLV-1) and (BLV) belong to the genus. HTLV-1 is the etiologic agent of the highly aggressive and currently incurable cancer adult T-cell leukemia (ATL) and a neurological disease HTLV-1-associated myelopathy (HAM)/tropical spastic paraparesis (TSP). BLV causes neoplastic proliferation of B cells in cattle: enzootic bovine leucosis (EBL). Read More

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September 2020

Human T-cell lymphotropic virus HBZ and tax mRNA expression are associated with specific clinicopathological features in adult T-cell leukemia/lymphoma.

Mod Pathol 2021 02 24;34(2):314-326. Epub 2020 Sep 24.

Department of Pathology, Kurume University School of Medicine, Kurume, Japan.

Adult T-cell leukemia/lymphoma (ATLL) is caused by human T-cell leukemia virus type 1 (HTLV-1). HTLV-1-associated mRNA, including HBZ and tax, is deeply involved in the pathogenesis of ATLL. Using 88 ATLL tissue samples, we performed in situ mRNA analysis of HBZ and tax, and investigated its association with clinicopathological characteristics of ATLL. Read More

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February 2021

North American Big Brown Bats (Eptesicus fuscus) Harbor an Exogenous .

mSphere 2020 09 23;5(5). Epub 2020 Sep 23.

Animal Disease Research and Diagnostic Laboratory, South Dakota State University, Brookings, South Dakota, USA.

Bats are the reservoir for a large number of zoonotic viruses, including members of (severe acute respiratory syndrome coronavirus [SARS-CoV] and SARS-CoV-2), (Hendra and Nipah viruses), (rabies virus), and (Ebola virus) as exemplars. Many retroviruses, such as human immunodeficiency virus, are similarly zoonotic; however, only infectious exogenous gammaretroviruses have recently been identified in bats. Here, viral metagenomic sequencing of samples from bats submitted for rabies virus testing, largely due to human exposure, identified a novel, highly divergent exogenous from a big brown bat () in South Dakota. Read More

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September 2020

A novel positive feedback-loop between the HTLV-1 oncoprotein Tax and NF-κB activity in T-cells.

Retrovirology 2020 09 10;17(1):30. Epub 2020 Sep 10.

Institute of Clinical and Molecular Virology, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.

Background: Human T-cell leukemia virus type 1 (HTLV-1) infects primarily CD4 T-lymphocytes and evoques severe diseases, predominantly Adult T-Cell Leukemia/ Lymphoma (ATL/L) and HTLV-1-associated Myelopathy/ Tropical Spastic Paraparesis (HAM/TSP). The viral transactivator of the pX region (Tax) is important for initiating malignant transformation, and deregulation of the major signaling pathway nuclear factor of kappa B (NF-κB) by Tax represents a hallmark of HTLV-1 driven cancer.

Results: Here we found that Tax mutants which are defective in NF-κB signaling showed diminished protein expression levels compared to Tax wildtype in T-cells, whereas Tax transcript levels were comparable. Read More

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September 2020

RNF8 Dysregulation and Down-regulation During HTLV-1 Infection Promote Genomic Instability in Adult T-Cell Leukemia.

PLoS Pathog 2020 05 26;16(5):e1008618. Epub 2020 May 26.

Department of Microbiology and Immunology Uniformed Services University of the Health Sciences Bethesda, MD, United States of America.

The genomic instability associated with adult T cell leukemia/lymphoma (ATL) is causally linked to Tax, the HTLV-1 viral oncoprotein, but the underlying mechanism is not fully understood. We have previously shown that Tax hijacks and aberrantly activates ring finger protein 8 (RNF8) - a lysine 63 (K63)-specific ubiquitin E3 ligase critical for DNA double-strand break (DSB) repair signaling - to assemble K63-linked polyubiquitin chains (K63-pUbs) in the cytosol. Tax and the cytosolic K63-pUbs, in turn, initiate additional recruitment of linear ubiquitin assembly complex (LUBAC) to produce hybrid K63-M1 pUbs, which trigger a kinase cascade that leads to canonical IKK:NF-κB activation. Read More

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Expression of TSLC1 in patients with HAM/TSP.

J Neurovirol 2020 06 13;26(3):404-414. Epub 2020 Apr 13.

Department of Neurology and Geriatrics, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, 890-8520, Japan.

Human T-lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is chronic myelopathy characterized by slowly progressive spastic paraparesis and urinary dysfunction. A few biomarkers in the cerebrospinal fluid are known to be related to disease activity, but no biomarker has been reported in peripheral blood. This study aims to explore the expression level of the adhesion molecule during the expression level of the adhesion molecule among HAM/TSP disease activity. Read More

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The IL-18, IL-12, and IFN-γ expression in HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients, HTLV-1 carriers, and healthy subjects.

J Neurovirol 2020 06 8;26(3):338-346. Epub 2020 Apr 8.

Immunology Research Center, Inflammation and Inflammatory Diseases Division, Faculty of Medicine, Mashhad University of Medical Sciences, Azadi-Square, Medical Campus, Mashhad, 9177948564, Iran.

Interleukin (IL)-12, IL-18, and interferon gamma (IFN-γ) can induce Th1-inflammatory responses in favor of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) manifestation. In this study, the gene expression and plasma levels of these cytokines were evaluated. The peripheral blood mononuclear cells (PBMCs) in 20 HAM/TSP patients, 21 asymptomatic carriers (ACs), and 21 healthy subjects (HSs) were assessed for the expression of IL-18, IL-12, and IFN-γ, using qRT-PCR. Read More

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Clinical features and treatment outcomes of opportunistic infections among human T-lymphotrophic virus type 1 (HTLV-1) carriers and patients with adult T-cell leukemia-lymphoma (ATL) at a single institution from 2006 to 2016.

J Clin Exp Hematop 2019 ;59(4):156-167

As opportunistic infections among human T-lymphotrophic virus type 1 (HTLV-1) carriers and patients with adult T-cell leukemia/lymphoma (ATL) pose a serious problem, it is necessary to clarify their clinical characteristics and outcomes in these patients. We retrospectively analyzed the clinical features and outcomes of opportunistic infections in 127 HTLV-1 carriers and 153 ATL patients between 2006 and 2016. The cumulative incidence rates of opportunistic infections among HTLV-1 carriers and ATL patients were 1. Read More

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EOS, an Ikaros family zinc finger transcription factor, interacts with the HTLV-1 oncoprotein Tax and is downregulated in peripheral blood mononuclear cells of HTLV-1-infected individuals, irrespective of clinical statuses.

Virol J 2019 12 19;16(1):160. Epub 2019 Dec 19.

Department of Microbiology, Kawasaki Medical School, 577 Matsushima, Okayama, 701-0192, Japan.

Background: EOS plays an important role in maintaining the suppressive function of regulatory T cells (Tregs), and induces a regulated transformation of Tregs into T helper-like cells, which are capable of secreting proinflammatory cytokines in response to specific inflammatory signals. Meanwhile, significant reduction in Treg activity along with production of proinflammatory cytokines has been reported in patients with HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

Methods: In this study, to examine whether there is an alteration in EOS expression in peripheral blood mononuclear cells (PBMCs) derived from HTLV-1-infected individuals especially HAM/TSP, we investigated the expression of HTLV-1 tax genotype, proviral load (PVL), and the mRNA expression of tax, HBZ and EOS in HTLV-1 infected individuals including adult T-cell leukemia/lymphoma (ATL), HAM/TSP, or asymptomatic carriers. Read More

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December 2019

SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.

Sci Rep 2019 11 5;9(1):16014. Epub 2019 Nov 5.

International Center for Research in Infectiology, Retroviral Oncogenesis Laboratory, INSERM U1111 - Université Claude Bernard Lyon 1, CNRS, UMR5308, École Normale Supérieure de Lyon, Université Lyon, Lyon, France.

The NF-κB pathway is constitutively activated in adult T cell leukemia, an aggressive malignancy caused by Human T Leukemia Virus type 1 (HTLV-1). The viral oncoprotein Tax triggers this constitutive activation by interacting with the ubiquitin-rich IKK complex. We previously demonstrated that Optineurin and TAX1BP1, two members of the ubiquitin-binding, Sequestosome-1 (SQSTM-1/p62)-like selective autophagy receptor family, are involved in Tax-mediated NF-κB signaling. Read More

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November 2019

The ESCRT-0 Protein HRS Interacts with the Human T Cell Leukemia Virus Type 2 Antisense Protein APH-2 and Suppresses Viral Replication.

J Virol 2019 12 12;94(1). Epub 2019 Dec 12.

Centre for Research in Infectious Diseases, School of Medicine, University College Dublin, Dublin, Ireland

The divergent clinical outcomes of human T cell leukemia virus type 1 (HTLV-1) and HTLV-2 infections have been attributed to functional differences in their antisense proteins. In contrast to HTLV-1 bZIP factor (HBZ), the role of the antisense protein of HTLV-2 (APH-2) in HTLV-2 infection is poorly understood. In previous studies, we identified the endosomal sorting complex required for transport 0 (ESCRT-0) subunit HRS as a novel interaction partner of APH-2 but not HBZ. Read More

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December 2019

Flow cytometric methodology for the detection of de novo human T-cell leukemia virus -1 infection in vitro: A tool to study novel infection inhibitors.

J Virol Methods 2019 12 8;274:113728. Epub 2019 Sep 8.

Department of Biology & Hull York Medical School, University of York, UK. Electronic address:

Methodology to detect and study de novo human T-cell leukemia virus (HTLV)-1 infection is required to further our knowledge of the viruses' mechanisms of infection and to study potential therapeutic interventions. Whilst methodology currently exists, utilisation of an anti-Tax antibody to detect de novo Tax expression in permissive cells labelled with cell tracker allowing for the detection by flow cytometry of new infection after co-culture with donor cell lines productively infected with HTLV-1 is an alternative strategy. Using this methodology, we have been able to detect de novo infection of the T cell line HUT78 following co-culture with the productively infected HTLV-1 donor cell line MT-2 and to confirm that infection can be effectively blocked with well characterised infection inhibitors. Read More

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December 2019

Prevalence of human T-cell lymphotropic virus and the socio-demographic and risk factors associated with the infection among post-natal clinics women in Zaria, Nigeria.

J Immunoassay Immunochem 2019 24;40(5):485-494. Epub 2019 Jul 24.

Department of Microbiology, Ahmadu Bello University , Zaria , Nigeria.

Human T-cell lymphotropic virus has long been associated with Adult T-cell leukemia/lymphoma, HTLV-associated myelopathy/tropical spastic paraparesis, and hairy cell leukemia. The aim was to determine the prevalence of HTLV antibodies as well as the socio-demographic and risk factors associated with HTLV among women attending postnatal clinics in Zaria. A total of 190 samples were collected within the months of January and June 2017 and qualitative determination of antibodies for HTLV in serum was performed by an antigen sandwich enzyme immunoassay method. Read More

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October 2019

The human T-cell leukemia virus type-1 tax oncoprotein dissociates NF-κB p65-Stathmin complexes and causes catastrophic mitotic spindle damage and genomic instability.

Virology 2019 09 3;535:83-101. Epub 2019 Jul 3.

Laboratory of Molecular Virology, Department of Biological Sciences, The Dedman College Center for Drug Discovery, Design & Delivery, Southern Methodist University, Dallas, TX, 75275-0376, United States. Electronic address:

Genomic instability is a hallmark of many cancers; however, the molecular etiology of chromosomal dysregulation is not well understood. The human T-cell leukemia virus type-1 (HTLV-1) oncoprotein Tax activates NF-κB-signaling and induces DNA-damage and aberrant chromosomal segregation through diverse mechanisms which contribute to viral carcinogenesis. Intriguingly, Stathmin/oncoprotein-18 (Op-18) depolymerizes tubulin and interacts with the p65 subunit and functions as a cofactor for NF-κB-dependent transactivation. Read More

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September 2019

HTLV-1 basic leucine zipper factor protects cells from oxidative stress by upregulating expression of Heme Oxygenase I.

PLoS Pathog 2019 06 28;15(6):e1007922. Epub 2019 Jun 28.

Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, North Carolina, United States of America.

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). Read More

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Novel Interactions between the Human T-Cell Leukemia Virus Type 1 Antisense Protein HBZ and the SWI/SNF Chromatin Remodeling Family: Implications for Viral Life Cycle.

J Virol 2019 08 30;93(16). Epub 2019 Jul 30.

Centre for Research in Infectious Diseases, School of Medicine, University College Dublin, Dublin, Ireland

The human T-cell leukemia virus type 1 (HTLV-1) regulatory proteins Tax and HBZ play indispensable roles in regulating viral and cellular gene expression. BRG1, the ATPase subunit of the SWI/SNF chromatin remodeling complex, has been demonstrated to be essential not only for Tax transactivation but also for viral replication. We sought to investigate the physical interaction between HBZ and BRG1 and to determine the effect of these interactions on Tax-mediated long terminal repeat (LTR) activation. Read More

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Human T-cell lymphotrophic virus in solid-organ transplant recipients: Guidelines from the American society of transplantation infectious diseases community of practice.

Clin Transplant 2019 09 12;33(9):e13575. Epub 2019 May 12.

Department of Pediatrics, Division of Infectious Diseases, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts.

These updated guidelines from the Infectious Diseases Community of Practice of the American Society of Transplantation review the diagnosis, prevention, and management of Human T-cell lymphotrophic virus 1 (HTLV)-1 in the pre- and post-transplant period. HTLV-1 is an oncogenic human retrovirus rare in North America but endemic in the Caribbean and parts of Africa, South America, Asia, and Oceania. While most infected persons do not develop disease, <5% will develop adult T-cell leukemia/lymphoma or neurological disease. Read More

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September 2019

HTLV-1 Tax-1 interacts with SNX27 to regulate cellular localization of the HTLV-1 receptor molecule, GLUT1.

PLoS One 2019 21;14(3):e0214059. Epub 2019 Mar 21.

Center for Retrovirus Research, The Ohio State University, Columbus, Ohio, United States of America.

An estimated 10-20 million people worldwide are infected with human T cell leukemia virus type 1 (HTLV-1), with endemic areas of infection in Japan, Australia, the Caribbean, and Africa. HTLV-1 is the causative agent of adult T cell leukemia (ATL) and HTLV-1 associated myopathy/tropic spastic paraparesis (HAM/TSP). HTLV-1 expresses several regulatory and accessory genes that function at different stages of the virus life cycle. Read More

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December 2019

Degradation of p47 by autophagy contributes to CADM1 overexpression in ATLL cells through the activation of NF-κB.

Sci Rep 2019 03 5;9(1):3491. Epub 2019 Mar 5.

Division of Tumor and Cellular Biochemistry, Department of Medical Sciences, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.

Cell adhesion molecule 1 (CADM1), a member of the immunoglobulin superfamily, is identified as a novel cell surface marker for human T-cell leukemia virus (HTLV-1)-infected T cells. Adult T-cell leukemia/lymphoma (ATLL) is developed in HTLV-1-infected T-cells after a long infection period. To examine the mechanism of CADM1 overexpression in ATLL, we first identified that CADM1 is transcriptionally up-regulated by a transcriptional enhancer element through NF-κB signaling pathway. Read More

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