Affinage

HBZ

Hemoglobin subunit zeta · UniProt P02008

Length
142 aa
Mass
15.6 kDa
Annotated
2026-06-10
100 papers in source corpus 43 papers cited in narrative 43 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HTLV-1 HBZ is a viral bZIP factor that drives proviral latency and leukemogenesis by reprogramming host transcription, signaling, and protein turnover, and it is the HBZ protein — not its mRNA stem-loop — that is the critical determinant of viral persistence and leukemogenesis in vivo (PMID:12937177, PMID:37327244). HBZ heterodimerizes through its bZIP domain with the Jun/ATF/Maf families to selectively rewire AP-1 output: it suppresses c-Jun by both blocking its DNA binding and tethering it to the 26S proteasome for ubiquitin-independent degradation, sequesters JunB into HBZ nuclear bodies, yet cooperates with JunD (and Sp1) to activate targets such as the hTERT promoter (PMID:12937177, PMID:17306025, PMID:18078517, PMID:18805793, PMID:19595408). In parallel, HBZ targets the p300/CBP coactivator: its N-terminal activation domain folds into an α-helix bearing tandem (L/V)(V/L)DGLL motifs that engage the MLL-binding surface of the KIX domain, competitively displacing Tax, while its bZIP domain directly inhibits p300/CBP histone acetyltransferase activity, reducing H3K18 acetylation and repressing viral sense-strand transcription (PMID:18599479, PMID:22434882, PMID:30232260). Through this coactivator inhibition together with binding and inhibition of HBO1, HBZ represses p53-dependent activation of p21/CDKN1A and GADD45A (PMID:26625199). HBZ stability is controlled by UBR5-mediated ubiquitination at multiple lysines (PMID:29441057). HBZ shuttles between compartments via a CRM1-dependent NES; in the cytoplasm it binds GADD34 to activate mTOR signaling and suppress autophagy, and its subcellular distribution tracks disease state — exclusively cytoplasmic in asymptomatic carriers and HAM/TSP but nuclear/dual in ATL, with TGF-β/JunB/pSmad3 driving its cytoplasm-to-nucleus translocation in ATL cells (PMID:23708656, PMID:28095504, PMID:31080441, PMID:33626865, PMID:40549917). HBZ also enforces latency by inhibiting Rex-dependent export of intron-containing structural mRNAs (PMID:24699669) and promotes infection and oncogenic phenotypes through transcriptional programs including myoferlin induction, CCR4/GATA3-driven T-cell migration, and RANKL-dependent bone lesions (PMID:27402079, PMID:36827461, PMID:31578308).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 2003 High

    Establishing that HBZ is a bZIP protein that physically heterodimerizes with Jun-family factors defined its core molecular activity as a host transcription modulator rather than a conventional viral transactivator.

    Evidence Reciprocal Co-IP, colocalization, and luciferase/DNA-binding assays in CEM cells

    PMID:12937177

    Open questions at the time
    • Selectivity for c-Jun vs JunB vs JunD not yet mechanistically resolved
    • No structural basis for differential dimer outcomes
  2. 2004 Medium

    Identifying JunD as an activating partner showed HBZ's bZIP engagement produces opposite transcriptional outcomes depending on the partner, and mapped the N-terminus as the activation determinant.

    Evidence In vitro binding, Co-IP, and luciferase reporter assays

    PMID:15044019

    Open questions at the time
    • Single lab
    • Mechanism distinguishing activation from repression unresolved at this stage
  3. 2005 Medium

    Discovery that HBZ both blocks c-Jun DNA binding and promotes its proteasomal degradation revealed a dual repression strategy, and subnuclear mapping placed HBZ in nuclear speckles/heterochromatin via multiple NLS.

    Evidence Deletion-mutant reporter and Western assays with proteasome inhibitors; fluorescence and immunogold EM localization

    PMID:15592508 PMID:15755797

    Open questions at the time
    • Degradation pathway (ubiquitin dependence) not yet defined
    • Functional consequence of heterochromatin localization unclear
  4. 2006 Medium

    Chimera and mutagenesis studies pinpointed the DNA-binding region and a charged-residue cluster controlling Jun transcriptional potency, refining how HBZ tunes AP-1 output, and a spliced isoform was shown to occupy distinct subnuclear sites.

    Evidence HBZ/c-Fos chimeras, mutagenesis with reporters; RACE and immunofluorescence of isoforms

    PMID:16474156 PMID:16717281

    Open questions at the time
    • Functional difference between spliced and unspliced isoforms not yet established
  5. 2007 Medium

    Demonstrating sequestration of JunB into HBZ nuclear bodies and HBZ/JunD cooperation at the hTERT promoter clarified the structural and DNA-occupancy basis of partner-specific outcomes.

    Evidence FRAP and co-transfection reporters; ChIP at the proximal hTERT promoter

    PMID:17306025 PMID:18078517

    Open questions at the time
    • Single lab
    • Composition of HBZ nuclear bodies not fully defined
  6. 2008 High

    Mapping HBZ's LXXLL-like motifs to the KIX domain of p300/CBP and reconstituting an HBZ–c-Jun–26S proteasome complex established two mechanistically distinct repressive activities: coactivator hijacking and ubiquitin-independent substrate delivery.

    Evidence In vitro binding/pulldown with motif mutagenesis and reporters; Co-IP with 26S proteasome plus ubiquitination assays

    PMID:18599479 PMID:18805793

    Open questions at the time
    • Whether KIX binding and HAT inhibition are separable not yet tested
    • Proteasome tethering mechanism not structurally resolved
  7. 2010 Medium

    Extending HBZ's bZIP partner repertoire to Maf, ATF2, CEBPG, and CREBZF, with biophysical confirmation, broadened the host network HBZ rewires beyond Jun proteins.

    Evidence Yeast two-hybrid, Co-IP, coiled-coil peptide arrays, circular dichroism, and DNA-binding assays

    PMID:20102225 PMID:20506502

    Open questions at the time
    • In vivo relevance of MafB/MafG, ATF2, CREBZF interactions not established
  8. 2011 Medium

    Refined KIX-surface mapping showed HBZ simultaneously blocks MLL-dependent transcription while allosterically enhancing c-Myb/CREB, and HBZ was shown to blunt Tax-induced senescence via NF-κB downregulation.

    Evidence In vitro binding with domain mutagenesis and reporters; shRNA knockdown with NF-κB and senescence assays

    PMID:21497608 PMID:21552325

    Open questions at the time
    • Allosteric model not structurally proven at this stage
  9. 2012 High

    Demonstrating that HBZ directly inhibits p300/CBP HAT activity, lowering H3K18ac in infected cells, established an enzymatic (not just competitive) mechanism of transcriptional repression.

    Evidence In vitro HAT assay with domain mutagenesis and H3K18ac Western in infected vs uninfected cells

    PMID:22434882

    Open questions at the time
    • Genome-wide acetylation consequences not mapped
    • Single lab
  10. 2013 Medium

    Identifying a CRM1-dependent NES and cytoplasmic GADD34 binding revealed HBZ as a spatially regulated signaling effector that activates mTOR and suppresses autophagy outside the nucleus.

    Evidence Leptomycin B treatment, Co-IP domain mapping, S6K phosphorylation and autophagy assays

    PMID:23708656

    Open questions at the time
    • Signals controlling nuclear vs cytoplasmic partitioning not yet defined
    • CREB-mediated cyclin D1 repression (idx 41) rests on a single low-confidence study
  11. 2014 Medium

    Showing HBZ inhibits Rex-mediated export of unspliced viral mRNAs and induces BDNF/TrkB survival signaling connected HBZ to both latency maintenance and infected-cell survival.

    Evidence shRNA knockdown, Rex overexpression, viral mRNA export and RT-PCR; ectopic expression with TrkB inhibitor and apoptosis assays

    PMID:24699669 PMID:25210182

    Open questions at the time
    • Direct HBZ–Rex contact not demonstrated
    • Single lab for each
  12. 2015 Medium

    Endogenous-protein imaging and quantification validated speckle localization and physiological interactions with p300, JunD, CBP, and CREB2 at native expression levels far below overexpression systems.

    Evidence Monoclonal-antibody immunofluorescence, endogenous Co-IP, single-molecule quantification

    PMID:26140924

    Open questions at the time
    • Stoichiometry of native complexes not resolved
  13. 2016 High

    Linking HBZ to p53 repression via inhibition of both p300/CBP and HBO1 HAT activity, plus GATA3/CCR4-driven T-cell migration, connected HBZ's coactivator targeting to tumor-suppressor inactivation and an ATL homing phenotype.

    Evidence Co-IP, in vitro HAT assays, cell-cycle analysis in HCT116; promoter reporters and HBZ-transgenic mouse migration model

    PMID:26625199 PMID:27402079

    Open questions at the time
    • Relative contribution of p300/CBP vs HBO1 inhibition to p53 silencing not dissected
  14. 2017 Medium

    Patient-cell imaging defined disease-stage-specific localization (cytoplasmic in HAM/TSP), a ΔJunD translation-switch mechanism via RPS25 mRNA retention, and selective modulation of IRF7/IRF3 interferon responses.

    Evidence Validated monoclonal-antibody confocal imaging of PBMCs; ribosomal-protein/JunD isoform biochemistry; Co-IP and IFN reporter/ELISA assays

    PMID:28095504 PMID:28260789 PMID:28768861

    Open questions at the time
    • Determinants forcing exclusive cytoplasmic retention not identified
    • Single lab for each mechanism
  15. 2018 High

    The crystal structure of the KIX:c-Myb:HBZ ternary complex provided atomic-level proof that the HBZ AD folds into a helix with cooperative tandem (L/V)(V/L)DGLL motifs, and UBR5 was identified as the E3 ligase controlling HBZ stability.

    Evidence X-ray crystallography and ITC; affinity-MS, endogenous Co-IP, ubiquitination-site mapping, shRNA knockdown

    PMID:29441057 PMID:30232260

    Open questions at the time
    • Whether UBR5 turnover is regulated by upstream signals not addressed
  16. 2019 Medium

    Discovery of HBZ interactions with SWI/SNF (BRG1/PBAF) and PRC2, and RANKL-driven bone pathology, extended HBZ's reach into chromatin-remodeling control of the viral promoter and to in vivo osteolytic disease.

    Evidence GST pulldown, Co-IP, ChIP-qPCR; Drosophila genetic epistasis with PRC2 Co-IP; HBZ-transgenic/humanized mice with denosumab rescue

    PMID:31142665 PMID:31578308 PMID:33471856

    Open questions at the time
    • NF90/NF110 antagonism (idx 29) is low-confidence and unconfirmed
    • Direct vs indirect PRC2 effects not fully separated
  17. 2020 Medium

    Separating RNA from protein functions showed HBZ RNA epigenetically silences 5' LTR sense transcription, while cytoplasmic HBZ protein stabilizes anti-apoptotic HAX-1 by blocking FBXO25-mediated ubiquitination.

    Evidence RNA-vs-protein functional/silencing assays; Co-IP, ubiquitination assays, caspase-9 readouts

    PMID:32893878 PMID:33170933

    Open questions at the time
    • Molecular basis of RNA-mediated silencing not resolved
    • Single lab
  18. 2021 Medium

    Mapping the HBZ interactome to splicing machinery (U2AF2) and documenting dual ATL localization tied HBZ to genome-wide exon exclusion and to the nuclear translocation associated with transformation.

    Evidence AP-MS interactome, RNA-seq splicing analysis with patient validation; validated-antibody confocal imaging of ATL cells

    PMID:33626865 PMID:34543356

    Open questions at the time
    • Trigger for nuclear translocation in ATL not yet identified at this stage
  19. 2023 High

    Genetic dissection in two animal models proved HBZ protein (not mRNA stem-loop) drives persistence and leukemogenesis, and HBZ was shown to transcriptionally induce myoferlin to protect viral Env from lysosomal degradation.

    Evidence Proviral mutants in rabbit and humanized-mouse infection models; ChIP, shRNA, pharmacological and lysosomal-rescue assays

    PMID:36827461 PMID:37327244

    Open questions at the time
    • In vivo contribution of individual HBZ molecular activities not yet partitioned
  20. 2025 Medium

    Defining TGF-β/JunB/pSmad3-driven nuclear import in ATL and Tax-mediated splicing control of HBZ expression explained how HBZ activity is switched on during transformation and constrained during early infection.

    Evidence Proximity ligation assay on primary cells, Co-IP, shRNA, xenografts; RNA-seq and competitive splicing-factor binding assays

    PMID:40549917 PMID:40720552

    Open questions at the time
    • Why TGF-β-triggered import occurs only in ATL and not carriers not mechanistically resolved
    • Single lab for each

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how HBZ's many parallel activities — coactivator inhibition, bZIP rewiring, RNA silencing, and cytoplasmic signaling — are coordinated and individually weighted to drive persistence versus transformation in vivo.
  • No integrated model linking subcellular localization switching to specific oncogenic outputs
  • Individual molecular activities not yet mutationally separated in animal models
  • Structural basis of bZIP partner selectivity (c-Jun vs JunB vs JunD) incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0098772 molecular function regulator activity 4 GO:0003677 DNA binding 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0003723 RNA binding 1
Localization
GO:0005829 cytosol 5 GO:0005634 nucleus 4 GO:0005654 nucleoplasm 4 GO:0005730 nucleolus 1
Pathway
R-HSA-74160 Gene expression (Transcription) 5 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-4839726 Chromatin organization 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-168256 Immune System 2

Evidence

Reading pass · 43 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 HBZ dimerizes with JunB and c-Jun via bZIP domains, suppresses c-Jun-mediated AP-1 transcription by decreasing its DNA-binding activity, enhances JunB transcriptional activity, and inhibits c-Jun-mediated basal expression of the HTLV-1 promoter. Co-immunoprecipitation, cellular colocalization, reporter gene (luciferase) assays, DNA-binding assays in CEM cells The Journal of biological chemistry High 12937177
2004 HBZ interacts with JunD in vitro and in vivo via the bZIP domains of both proteins, and stimulates JunD-dependent transcription; the amino-terminus of HBZ is required for transcriptional activation. In vitro binding assay, co-immunoprecipitation, luciferase reporter assay FEBS letters Medium 15044019
2005 HBZ suppresses AP-1 activity through a dual mechanism: (1) inhibiting c-Jun DNA-binding activity and (2) promoting proteasome-dependent degradation of c-Jun; both the N-terminal and leucine-zipper regions of HBZ are required for c-Jun elimination. Luciferase assays, Western blotting with proteasome inhibitor treatment, HBZ deletion mutant analysis Oncogene Medium 15592508
2005 HBZ nuclear targeting is mediated by three distinct nuclear localization signals (NLS); at least two NLS are necessary for nuclear translocation; wild-type HBZ accumulates in nuclear speckles (not Cajal bodies, splicing factor compartments, or PML bodies); the integrity of the full protein is required for speckle localization; immunogold EM localizes HBZ to heterochromatin. Deletion mutant analysis in mammalian cells, fluorescence microscopy, immunogold electron microscopy Journal of cell science Medium 15755797
2006 The DNA-binding domain of HBZ is responsible for its inhibitory effect on c-Jun trans-activation; a cluster of six charged amino acids adjacent to the DNA-contact region (a modified Fos-associated cluster) is critical for regulating Jun transcriptional potency, including HBZ's ability to stimulate JunD activity. HBZ/c-Fos chimera construction, reporter gene assays, mutagenesis Nucleic acids research Medium 16717281
2006 A spliced isoform of HBZ (HBZ-SI/HBZ-SP1) localizes to distinct subnuclear structures (intense nuclear spots/HBZ-NBs and nucleoli) distinct from the unspliced HBZ isoform, indicating isoform-specific subnuclear targeting. RT-PCR, 5'/3' RACE, Western blotting, immunofluorescence microscopy Journal of virology Medium 16474156
2007 HBZ-SP1 represses JunB transcriptional activity by sequestering JunB into HBZ nuclear bodies (HBZ-NBs); the ZIP domain of HBZ-SP1 is required for association with HBZ-NBs; JunB co-expression redistributes into HBZ-NBs whereas JunD co-expression results in diffuse nucleoplasmic distribution without NB formation. Fluorescence microscopy, FRAP, co-transfection/reporter assays in COS and HeLa cells Retrovirology Medium 17306025
2007 HBZ cooperates with JunD to activate hTERT promoter transcription; HBZ/JunD heterodimers interact with Sp1 and activate hTERT transcription through GC-rich Sp1 binding sites in the proximal hTERT promoter; ChIP confirms HBZ and JunD co-occupy the proximal hTERT promoter region. Co-transfection luciferase assays, RT-PCR for hTERT transcripts, chromatin immunoprecipitation (ChIP) Retrovirology Medium 18078517
2008 HBZ binds directly to the KIX domain of p300/CBP via two LXXLL-like motifs in its N-terminal activation domain; this interaction specifically targets the MLL-binding surface of KIX, competing with Tax for p300/CBP binding and inhibiting coactivator recruitment to the viral promoter — a second mechanism of HTLV-1 transcriptional repression distinct from CREB dimerization. Co-immunoprecipitation, in vitro binding/pulldown assays, luciferase reporter assays, mutagenesis of LXXLL-like motifs The Journal of biological chemistry High 18599479
2008 HBZ promotes ubiquitin-independent proteasomal degradation of c-Jun: HBZ directly interacts with both the 26S proteasome and c-Jun, acting as a tethering factor that delivers c-Jun to the proteasome without requiring polyubiquitination. Co-immunoprecipitation with the 26S proteasome, ubiquitination assays, proteasome inhibitor treatment, in vitro binding The Journal of biological chemistry High 18805793
2008 The spliced HBZ (sHBZ) isoform shows stronger suppression of Tax-mediated transcriptional activation and promotes T-cell proliferation, while unspliced HBZ (usHBZ) does not promote proliferation; sHBZ transcription from a TATA-less promoter is driven by Sp1 sites and is upregulated by Tax via Tax-responsive elements in the 3' LTR. Luciferase promoter assays, Sp1 site mutagenesis, T-cell proliferation assays Journal of virology Medium 18653454
2009 Repression of c-Jun transcriptional activity by HBZ-SP1 is predominantly due to sequestration of c-Jun into HBZ nuclear bodies rather than inhibition of DNA-binding activity; a DNA-binding-improved HBZ-SP1 chimera retains repressive activity through sequestration. Chimeric mutant construction, DNA-binding assays, fluorescence microscopy, reporter gene assays Virology Medium 19595408
2010 HBZ interacts with MafB via bZIP domains, abrogates MafB DNA-binding at Maf recognition elements (MARE), and promotes proteasomal degradation of MafB; identified by yeast two-hybrid screen and confirmed by co-immunoprecipitation and luciferase assays. Yeast two-hybrid screen, co-immunoprecipitation, luciferase reporter assay, proteasome inhibitor treatment Journal of cellular biochemistry Medium 20506502
2010 HBZ interacts with MAFB and MAFG via its basic region in a coiled-coil array system; HBZ also forms heterodimers with ATF2, CEBPG, and CREBZF; all new interactions confirmed by circular dichroism in solution; HBZ-MAFB/MAFG heterocomplexes can associate with MARE-site DNA. Coiled-coil peptide arrays, circular dichroism spectroscopy, DNA-binding assays Biochemistry Medium 20102225
2011 HBZ down-regulates NF-κB activity induced by Tax, thereby alleviating Tax-induced cellular senescence driven by p21(CIP1/WAF1) and p27(KIP1); shRNA-mediated knockdown confirmed that HBZ delays or prevents the onset of Tax-induced senescence. shRNA knockdown, NF-κB reporter assays, senescence assays, cell proliferation assays PLoS pathogens Medium 21552325
2011 HBZ binds to the KIX domain of p300/CBP via two φXXφφ motifs targeting the MLL-binding surface; this simultaneously inhibits MLL-mediated transcription and enhances c-Myb and CREB transcriptional activity by allosterically promoting their binding to the opposite KIX surface. In vitro binding assays, luciferase reporter assays, domain mutagenesis Journal of molecular biology Medium 21497608
2012 HBZ directly inhibits the histone acetyltransferase (HAT) activity of p300/CBP through its bZIP domain, leading to reduced H3K18 acetylation in HBZ-expressing cells and in HTLV-1-infected cells; HBZ also inhibits acetylation of NF-κB p65 and p53. In vitro HAT activity assay, Western blotting for H3K18ac, comparison of HTLV-1-infected vs. uninfected cells Nucleic acids research High 22434882
2013 HBZ is exported from the nucleus to the cytoplasm via a CRM1-dependent nuclear export signal (NES) in its N-terminal region; in the cytoplasm, HBZ interacts with GADD34 (N-terminal region of HBZ binds C-terminal region of GADD34), activates mTOR signaling (increased S6 kinase phosphorylation), and suppresses starvation-induced autophagy. CRM1 inhibitor (leptomycin B) treatment, co-immunoprecipitation, domain mapping, phosphorylation assays, autophagy assays Oncogene Medium 23708656
2014 HBZ inhibits Rex-mediated nuclear export of intron-containing (unspliced) viral mRNAs; shRNA-mediated knockdown of HBZ or overexpression of Rex reactivates viral structural protein expression, indicating HBZ maintains HTLV-1 latency partly by blocking Rex function. shRNA knockdown of HBZ, Rex overexpression, viral mRNA nuclear export assays, RT-PCR for viral transcripts PLoS pathogens Medium 24699669
2014 HBZ activates BDNF expression in HTLV-1-infected T cells; elevated BDNF and its receptor TrkB are found in HTLV-1-infected T-cell lines; chemical inhibition of TrkB signaling increases apoptosis in HTLV-1-infected cells and reduces phosphorylation of GSK-3β, demonstrating a functional BDNF/TrkB autocrine/paracrine survival signaling loop promoted by HBZ. Ectopic HBZ expression, RT-PCR/Western blotting for BDNF and TrkB, TrkB chemical inhibitor treatment, apoptosis assays, phosphorylation assays Journal of virology Medium 25210182
2015 Endogenous HBZ protein in HTLV-1-infected and ATL cells localizes in speckle-like nuclear structures; endogenous HBZ interacts with p300, JunD, and partially co-localizes with CBP and CREB2 in vivo; quantified at 17,000–40,000 molecules per cell (20–50-fold less than in overexpression systems). Monoclonal antibody immunofluorescence, confocal microscopy, co-immunoprecipitation with endogenous protein, single-molecule quantification Retrovirology Medium 26140924
2016 HBZ represses p53 activity by directly inhibiting the HAT activity of p300/CBP (reducing p53 acetylation) and by binding to and inhibiting the HAT activity of HBO1 (a p53 coactivator at the p21/CDKN1A promoter), leading to impaired p53-dependent activation of p21/CDKN1A and GADD45A and delay in G2 arrest. Co-immunoprecipitation, in vitro HAT activity assay, luciferase/gene expression assays, cell cycle analysis in HCT116 p53+/+ cells Oncotarget High 26625199
2016 HBZ induces CCR4 expression in CD4+ T cells by activating GATA3, which in turn activates CCR4 promoter transcription; HBZ silencing in ATL cell lines inhibits CCR4 expression; in HBZ-transgenic mice, CD4+ T cells migrate preferentially and proliferate in response to CCR4 ligands CCL17/CCL22 and CD103 ligand E-cadherin. Ectopic HBZ expression, shRNA knockdown, promoter reporter assays, HBZ-transgenic mouse air-pouch migration model, CCR4 antagonist treatment Cancer research Medium 27402079
2017 HBZ induces expression of the ΔJunD isoform (N-terminal truncated, oncogenic) by causing nuclear retention of RPS25 mRNA and loss of RPS25 protein, a small ribosomal subunit component; loss of RPS25 bypasses translational control of the JunD upstream open reading frame (uORF), shifting translation initiation to produce ΔJunD, which promotes cell proliferation and transformation. Western blotting for JunD isoforms, qRT-PCR for RPS25 mRNA, ChIP for JunD promoter, cell proliferation and transformation assays, nuclear fractionation Leukemia Medium 28260789
2017 HBZ localizes exclusively in the cytoplasm of PBMCs from HAM/TSP patients; in ATL cell lines it localizes in the nucleus; HBZ and Tax-1 are rarely co-expressed in the same cell in HAM/TSP patients; cytoplasmic HBZ is found almost exclusively in CD4+ T cells. Immunofluorescence with validated monoclonal antibody 4D4-F3, confocal microscopy, PBMC fractionation and cell-type analysis PLoS neglected tropical diseases Medium 28095504
2017 HBZ enhances IRF7-induced IFN-α and ISRE promoter activity and IFN-α production, and enhances IRF7 activation by TBK1/IKKε; conversely, HBZ cooperates with Tax to suppress IRF3-induced IFN-β; HBZ physically interacts with IRF7 and IKKε but not with IRF3 or TBK1. Co-immunoprecipitation, luciferase reporter assays, IFN-α ELISA, IRF3 nuclear accumulation assays Journal of virology Medium 28768861
2018 Crystal structure of ternary KIX:c-Myb:HBZ complex shows HBZ activation domain (AD) folds into a long α-helix upon KIX binding, with two tandem amphipathic (L/V)(V/L)DGLL motifs binding the MLL site cooperatively; ITC demonstrates strong cooperativity between c-Myb AD and HBZ for KIX; HBZ bridges two KIX:c-Myb entities simultaneously. X-ray crystallography, isothermal titration calorimetry (ITC) Proceedings of the National Academy of Sciences of the United States of America High 30232260
2018 UBR5 (an E3 ubiquitin-protein ligase) is a novel HBZ-binding partner; UBR5 ubiquitinates HBZ at seven lysine residues; shRNA knockdown of UBR5 stabilizes HBZ protein by reducing its ubiquitination; UBR5 knockdown decreases T-cell proliferation in transformed lines. Affinity-tagged protein pulldown with shotgun proteomics, co-immunoprecipitation (overexpression and endogenous), shRNA knockdown, MS/MS identification of ubiquitination sites, proliferation assays Frontiers in microbiology High 29441057
2019 HBZ physically interacts with BRG1 (ATPase subunit of SWI/SNF), BAF200, and BAF180 (PBAF signature subunits); BRG1 expression translocates HBZ into distinct nuclear foci; HBZ represses HTLV-1 LTR activation by Tax/BRG1 by deregulating SWI/SNF complex recruitment to the viral promoter (shown by ChIP-qPCR); HBZ also reverses Tax-mediated stabilization of BRG1. GST pulldown, co-immunoprecipitation, fluorescence microscopy, ChIP-qPCR, luciferase reporter assays Journal of virology Medium 31142665
2019 HBZ interacts with NF90/NF110 (NFAR proteins) via specific protein domains; HBZ abolishes NF90/110-mediated enhancement of Tax LTR activation; HBZ modulates survivin promoter activity and antagonizes NF110-mediated survivin activation. GST pulldown, co-immunoprecipitation, luciferase reporter assays Virology Low 27110706
2019 HBZ is exclusively cytoplasmic in asymptomatic carriers (AC) as well as HAM/TSP patients; the cytoplasmic localization in AC and HAM/TSP is not dependent on THEMIS expression; cells from an HTLV-1-immortalized HAM/TSP cell line confirm HBZ as a cytoplasmic resident protein that does not shuttle to the nucleus. Immunofluorescence with monoclonal antibody 4D4-F3, confocal microscopy on primary PBMCs and cell lines Frontiers in microbiology Medium 31080441
2020 HBZ RNA (independent of protein) interferes with the basal transcription machinery to epigenetically silence HTLV-1 sense (5' LTR) transcription, enabling proviral latency. RNA expression/functional assays distinguishing RNA vs. protein contributions, transcriptional silencing assays Blood advances Medium 33170933
2020 HBZ-US (but not HBZ-SI) interacts with HAX-1 in the cytoplasm; HBZ suppresses polyubiquitination of HAX-1 by inhibiting its association with FBXO25 (an SCF E3 ubiquitin ligase component), thereby stabilizing HAX-1 protein; enhanced HAX-1 correlates with suppression of caspase-9 processing, suggesting anti-apoptotic function. Co-immunoprecipitation, ubiquitination assays, Western blotting with proteasome inhibitor treatment Journal of cellular physiology Medium 32893878
2021 HBZ localizes in both cytoplasm and nucleus of ATL patient cells (dual localization), in contrast to exclusive cytoplasmic localization in asymptomatic carriers and HAM/TSP; nuclear translocation of HBZ is associated with neoplastic transformation in ATL. Immunofluorescence with monoclonal antibody 4D4-F3, confocal microscopy on primary ATL patient cells Haematologica Medium 33626865
2021 HBZ interacts with U2AF2 (a key pre-mRNA splicing regulator) as part of its interactome; HBZ perturbs the cellular splicing landscape by inducing exon exclusion (opposite to Tax which induces exon inclusion), altering cassette exons in genes also changed in ATLL patient samples. Interactome mapping (affinity purification-MS), RNA-seq splicing analysis, patient cohort validation PLoS pathogens Medium 34543356
2021 In a Drosophila transgenic model, HBZ does not induce transformation, NF-κB activation, or enhanced PRC2 activity on its own; overexpression of HBZ in tax transgenic flies prevents Tax-induced NF-κB activation, PRC2 activation, transformation, and senescence; both Tax and HBZ directly interact with PRC2 complex core components. Drosophila transgenic models (hbz-Tg and tax-Tg flies), NF-κB reporter assays, H3K27me3 ChIP, co-immunoprecipitation with PRC2 components PLoS pathogens Medium 33471856
2023 HBZ activates myoferlin (MyoF) expression by forming a complex with c-Jun or JunB at two enhancer sites within the MYOF gene and recruiting p300/CBP coactivator (shown by ChIP); MyoF restricts HTLV-1 envelope (Env) SU trafficking to lysosomes for degradation, thereby maintaining SU levels; MyoF knockdown or inhibition reduces HTLV-1 infection efficiency, cell adhesion, and SU in virus particles. ChIP assays, qRT-PCR, shRNA knockdown, pharmacological inhibition (WJ460), lysosomal protease inhibitors, LAMP-2 co-localization PLoS pathogens High 36827461
2023 HBZ protein (not hbz mRNA or its stem-loop structure) is critical for HTLV-1 persistence in vivo and leukemogenesis; proviral mutants lacking HBZ protein showed significantly lower proviral loads in rabbits and increased survival of humanized mice, while mRNA stem-loop mutations had no effect. Proviral mutant viruses, rabbit infection model, humanized immune system (HIS) mouse infection model PLoS pathogens High 37327244
2025 TGF-β stimulation triggers cytoplasm-to-nucleus translocation of HBZ in ATL cells but not in HTLV-1 carriers; nuclear translocation is mediated by JunB and pSmad3 interacting with HBZ; JUNB knockdown inhibits ATL cell proliferation in vitro and in vivo and promotes apoptosis in ATL but not in non-leukemic HTLV-1-infected cells. Proximity Ligation Assay on primary cells, co-immunoprecipitation, shRNA knockdown, TGF-β treatment, in vivo xenograft experiments Proceedings of the National Academy of Sciences of the United States of America Medium 40549917
2025 Tax inhibits HBZ RNA splicing by competitively binding splicing factors WDR83 and GPATCH1 (components of the spliceosome), thereby constraining HBZ expression during HTLV-1 early/productive infection; in Tax-negative cells, HBZ is predominantly spliced and active, driving mitotic propagation. RNA-seq splicing analysis, co-immunoprecipitation of Tax with splicing factors, competitive binding assays PLoS pathogens Medium 40720552
2019 HBZ regulates RANKL expression in a c-Fos-dependent manner; HBZ transgenic mice develop osteolytic bone lesions and hypercalcemia; RANKL, PTHrP, and DKK1 are upregulated in HBZ-expressing T cells; denosumab (anti-RANKL antibody) alleviates HBZ-driven bone loss in HTLV-1-infected humanized mice. HBZ-transgenic mice, humanized mouse HTLV-1 infection model, gene expression arrays, pharmacological antibody treatment, patient-derived xenografts JCI insight Medium 31578308
2013 HBZ suppresses cyclin D1 transcription via its bZIP domain by binding CREB and inhibiting cyclin D1 promoter activity through the CRE site; confirmed by immunoprecipitation and GST pulldown showing HBZ-bZIP–CREB interaction. Luciferase reporter assay, RT-PCR, Western blotting, co-immunoprecipitation, GST pulldown Molecular biology reports Low 24065533
2010 hbz mRNA (not HBZ protein) indirectly promotes Tax expression by down-regulating p30(II) mRNA levels; proviral splice-acceptor mutants that eliminate hbz mRNA reduce tax mRNA, and this is restored by heterologous hbz expression; protein-disrupting mutants alone do not affect tax mRNA levels. Proviral splice-acceptor and protein-coding mutants, RT-PCR for tax and p30(II) mRNA, heterologous hbz expression rescue Virology Medium 21176937

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 Human T-cell leukemia virus type 1 (HTLV-1) and leukemic transformation: viral infectivity, Tax, HBZ and therapy. Oncogene 205 21119600
2003 The HBZ factor of human T-cell leukemia virus type I dimerizes with transcription factors JunB and c-Jun and modulates their transcriptional activity. The Journal of biological chemistry 171 12937177
2008 Human T-cell leukemia virus type-1 antisense-encoded gene, Hbz, promotes T-lymphocyte proliferation. Blood 166 18689544
2006 Enhancement of infectivity and persistence in vivo by HBZ, a natural antisense coded protein of HTLV-1. Blood 161 16424388
2009 In vivo expression of the HBZ gene of HTLV-1 correlates with proviral load, inflammatory markers and disease severity in HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). Retrovirology 137 19228429
2009 The HBZ gene, a key player in HTLV-1 pathogenesis. Retrovirology 135 19650892
2008 An interaction between the human T cell leukemia virus type 1 basic leucine zipper factor (HBZ) and the KIX domain of p300/CBP contributes to the down-regulation of tax-dependent viral transcription by HBZ. The Journal of biological chemistry 126 18599479
2016 HTLV-1 Infection and Adult T-Cell Leukemia/Lymphoma-A Tale of Two Proteins: Tax and HBZ. Viruses 125 27322308
2010 HLA class I binding of HBZ determines outcome in HTLV-1 infection. PLoS pathogens 120 20886101
2011 NF-κB hyper-activation by HTLV-1 tax induces cellular senescence, but can be alleviated by the viral anti-sense protein HBZ. PLoS pathogens 117 21552325
2008 Transcriptional control of spliced and unspliced human T-cell leukemia virus type 1 bZIP factor (HBZ) gene. Journal of virology 115 18653454
2005 HTLV-1 HBZ suppresses AP-1 activity by impairing both the DNA-binding ability and the stability of c-Jun protein. Oncogene 113 15592508
2004 HBZ interacts with JunD and stimulates its transcriptional activity. FEBS letters 110 15044019
2016 Multifaceted functions and roles of HBZ in HTLV-1 pathogenesis. Retrovirology 108 26979059
2008 Characteristic expression of HTLV-1 basic zipper factor (HBZ) transcripts in HTLV-1 provirus-positive cells. Retrovirology 103 18426605
2007 HTLV-1 HBZ cooperates with JunD to enhance transcription of the human telomerase reverse transcriptase gene (hTERT). Retrovirology 102 18078517
2006 A novel alternative splicing isoform of human T-cell leukemia virus type 1 bZIP factor (HBZ-SI) targets distinct subnuclear localization. Journal of virology 102 16474156
2005 Nuclear localization of HTLV-I bZIP factor (HBZ) is mediated by three distinct motifs. Journal of cell science 72 15755797
2014 HTLV-1 bZIP factor HBZ promotes cell proliferation and genetic instability by activating OncomiRs. Cancer research 71 25205102
2017 Role of HTLV-1 Tax and HBZ in the Pathogenesis of HAM/TSP. Frontiers in microbiology 67 29312243
2006 HBZ, a new important player in the mystery of adult T-cell leukemia. Blood 65 16917009
2012 HBZ and its roles in HTLV-1 oncogenesis. Frontiers in microbiology 63 22787458
2016 HTLV-1 Viral Factor HBZ Induces CCR4 to Promote T-cell Migration and Proliferation. Cancer research 58 27402079
2011 Effects of valproate on Tax and HBZ expression in HTLV-1 and HAM/TSP T lymphocytes. Blood 56 21505188
2009 HBZ is an immunogenic protein, but not a target antigen for human T-cell leukemia virus type 1-specific cytotoxic T lymphocytes. The Journal of general virology 56 19423550
2010 Identification of bZIP interaction partners of viral proteins HBZ, MEQ, BZLF1, and K-bZIP using coiled-coil arrays. Biochemistry 54 20102225
2007 The HBZ-SP1 isoform of human T-cell leukemia virus type I represses JunB activity by sequestration into nuclear bodies. Retrovirology 54 17306025
2014 Regulation of human T-lymphotropic virus type I latency and reactivation by HBZ and Rex. PLoS pathogens 51 24699669
2016 Human T-cell leukemia virus type-1-encoded protein HBZ represses p53 function by inhibiting the acetyltransferase activity of p300/CBP and HBO1. Oncotarget 41 26625199
2013 HTLV-1 HBZ positively regulates the mTOR signaling pathway via inhibition of GADD34 activity in the cytoplasm. Oncogene 38 23708656
2016 The Role of HBZ in HTLV-1-Induced Oncogenesis. Viruses 37 26848677
2012 The HTLV-1-encoded protein HBZ directly inhibits the acetyl transferase activity of p300/CBP. Nucleic acids research 36 22434882
2016 Functional Comparison of HBZ and the Related APH-2 Protein Provides Insight into Human T-Cell Leukemia Virus Type 1 Pathogenesis. Journal of virology 35 26819304
2013 Humoral immune response to HTLV-1 basic leucine zipper factor (HBZ) in HTLV-1-infected individuals. Retrovirology 35 23405908
2017 Cytoplasmic Localization of HTLV-1 HBZ Protein: A Biomarker of HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). PLoS neglected tropical diseases 34 28095504
2011 HTLV-1 HBZ protein deregulates interactions between cellular factors and the KIX domain of p300/CBP. Journal of molecular biology 34 21497608
2015 Localization, quantification and interaction with host factors of endogenous HTLV-1 HBZ protein in infected cells and ATL. Retrovirology 33 26140924
2015 Roles of HTLV-1 basic Zip Factor (HBZ) in Viral Chronicity and Leukemic Transformation. Potential New Therapeutic Approaches to Prevent and Treat HTLV-1-Related Diseases. Viruses 33 26690203
2008 Human T-cell leukemia virus type 1 HBZ protein bypasses the targeting function of ubiquitination. The Journal of biological chemistry 32 18805793
2017 HTLV-1 HBZ Viral Protein: A Key Player in HTLV-1 Mediated Diseases. Frontiers in microbiology 29 29312275
2021 The HTLV-1 viral oncoproteins Tax and HBZ reprogram the cellular mRNA splicing landscape. PLoS pathogens 27 34543356
2014 HBZ stimulates brain-derived neurotrophic factor/TrkB autocrine/paracrine signaling to promote survival of human T-cell leukemia virus type 1-Infected T cells. Journal of virology 27 25210182
2015 Triple Therapy with Prednisolone, Pegylated Interferon and Sodium Valproate Improves Clinical Outcome and Reduces Human T-Cell Leukemia Virus Type 1 (HTLV-1) Proviral Load, Tax and HBZ mRNA Expression in Patients with HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics 25 26174324
2010 HTLV-1 basic leucine-zipper factor, HBZ, interacts with MafB and suppresses transcription through a Maf recognition element. Journal of cellular biochemistry 25 20506502
2006 A modified version of a Fos-associated cluster in HBZ affects Jun transcriptional potency. Nucleic acids research 25 16717281
2017 HBZ-mediated shift of JunD from growth suppressor to tumor promoter in leukemic cells by inhibition of ribosomal protein S25 expression. Leukemia 24 28260789
2019 HTLV-1 HBZ Protein Resides Exclusively in the Cytoplasm of Infected Cells in Asymptomatic Carriers and HAM/TSP Patients. Frontiers in microbiology 23 31080441
2019 NF-κB and MicroRNA Deregulation Mediated by HTLV-1 Tax and HBZ. Pathogens (Basel, Switzerland) 23 31835460
2018 Interferon Lambda Family along with HTLV-1 Proviral Load, Tax, and HBZ Implicated in the Pathogenesis of Myelopathy/Tropical Spastic Paraparesis. Neuro-degenerative diseases 22 29990995
2012 Strong correlation between tax and HBZ mRNA expression in HAM/TSP patients: distinct markers for the neurologic disease. Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology 22 23127563
2018 The TP53-Induced Glycolysis and Apoptosis Regulator mediates cooperation between HTLV-1 p30II and the retroviral oncoproteins Tax and HBZ and is highly expressed in an in vivo xenograft model of HTLV-1-induced lymphoma. Virology 21 29777913
2016 Impaired expression of DICER and some microRNAs in HBZ expressing cells from acute adult T-cell leukemia patients. Oncotarget 21 26849145
2021 Dual cytoplasmic and nuclear localization of HTLV-1-encoded HBZ protein is a unique feature of adult T-cell leukemia. Haematologica 20 33626865
2016 Absolute quantification of HTLV-1 basic leucine zipper factor (HBZ) protein and its plasma antibody in HTLV-1 infected individuals with different clinical status. Retrovirology 20 27117327
2010 The HTLV-1 hbz antisense gene indirectly promotes tax expression via down-regulation of p30(II) mRNA. Virology 19 21176937
2009 Propensity for HBZ-SP1 isoform of HTLV-I to inhibit c-Jun activity correlates with sequestration of c-Jun into nuclear bodies rather than inhibition of its DNA-binding activity. Virology 19 19595408
2020 Epigenetic silencing of HTLV-1 expression by the HBZ RNA through interference with the basal transcription machinery. Blood advances 18 33170933
2019 HTLV-1 viral oncogene HBZ drives bone destruction in adult T cell leukemia. JCI insight 18 31578308
2021 In vivo antagonistic role of the Human T-Cell Leukemia Virus Type 1 regulatory proteins Tax and HBZ. PLoS pathogens 17 33471856
2022 Interplay between innate immunity and the viral oncoproteins Tax and HBZ in the pathogenesis and therapeutic response of HTLV-1 associated adult T cell leukemia. Frontiers in immunology 16 35935975
2020 Human T-cell lymphotropic virus HBZ and tax mRNA expression are associated with specific clinicopathological features in adult T-cell leukemia/lymphoma. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 15 32973330
2018 Structural basis for cooperative regulation of KIX-mediated transcription pathways by the HTLV-1 HBZ activation domain. Proceedings of the National Academy of Sciences of the United States of America 15 30232260
2017 HTLV-1 viral oncogene HBZ induces osteolytic bone disease in transgenic mice. Oncotarget 15 29050201
2018 Stability of the HTLV-1 Antisense-Derived Protein, HBZ, Is Regulated by the E3 Ubiquitin-Protein Ligase, UBR5. Frontiers in microbiology 14 29441057
2016 The effect of HTLV-1 virulence factors (HBZ, Tax, proviral load), HLA class I and plasma neopterin on manifestation of HTLV-1 associated myelopathy tropical spastic paraparesis. Virus research 14 27845163
2015 A vaccine against HTLV-1 HBZ makes sense. Blood 14 26316613
2013 Increased expression of HBZ and Foxp3 mRNA in bronchoalveolar lavage cells taken from human T-lymphotropic virus type 1-associated lung disorder patients. Internal medicine (Tokyo, Japan) 14 24292748
2011 Molecular and Cellular Mechanism of Leukemogenesis of ATL: Emergent Evidence of a Significant Role for HBZ in HTLV-1-Induced Pathogenesis. Leukemia research and treatment 14 23198153
2022 CARD11 mutation and HBZ expression induce lymphoproliferative disease and adult T-cell leukemia/lymphoma. Communications biology 13 36446869
2017 Evaluation of the role of TAX, HBZ, and HTLV-1 proviral load on the survival of ATLL patients. Blood research 13 28698846
2007 Does the HBZ gene represent a new potential target for the treatment of adult T-cell leukemia? International reviews of immunology 13 18027202
2011 Detection of HTLV-1 by means of HBZ gene in situ hybridization in formalin-fixed and paraffin-embedded tissues. Cancer science 12 21453388
2024 High level of genomic divergence in orf-I p12 and hbz genes of HTLV-1 subtype-C in Central Australia. Retrovirology 11 39014486
2019 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. Journal of virology 11 31142665
2016 Novel interactions between the HTLV antisense proteins HBZ and APH-2 and the NFAR protein family: Implications for the HTLV lifecycles. Virology 11 27110706
2010 [Adult T-cell leukemia induced by HTLV-1: before and after HBZ]. Medecine sciences : M/S 11 20412744
2023 HTLV-1 Hbz protein, but not hbz mRNA secondary structure, is critical for viral persistence and disease development. PLoS pathogens 10 37327244
2016 Evaluation of HTLV-1 HBZ and proviral load, together with host IFN λ3, in pathogenesis of HAM/TSP. Journal of medical virology 9 27787900
2013 The HTLV-1 HBZ protein inhibits cyclin D1 expression through interacting with the cellular transcription factor CREB. Molecular biology reports 9 24065533
2022 Coevolution of HTLV-1-HBZ, Tax, and proviral load with host IRF-1 and CCNA-2 in HAM/TSP patients. Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases 8 35835355
2020 HTLV-1 viral oncoprotein HBZ contributes to the enhancement of HAX-1 stability by impairing the ubiquitination pathway. Journal of cellular physiology 8 32893878
2014 Identification and characterization of HTLV-1 HBZ post-translational modifications. PloS one 7 25389759
2023 HBZ upregulates myoferlin expression to facilitate HTLV-1 infection. PLoS pathogens 6 36827461
2022 The Expression of Tax and HBZ Genes in Serum-Derived Extracellular Vesicles From HTLV-1 Carriers Correlates to Proviral Load and Inflammatory Markers. Frontiers in microbiology 6 35586867
2017 Positive and Negative Regulation of Type I Interferons by the Human T Cell Leukemia Virus Antisense Protein HBZ. Journal of virology 6 28768861
2016 New mouse model of acute adult T-cell leukemia generated by transplantation of AKT, BCLxL, and HBZ-transduced T cells. Cancer science 6 27223899
2013 Molecular study of HBZ and gp21 human T cell leukemia virus type 1 proteins isolated from different clinical profile infected individuals. AIDS research and human retroviruses 6 23800288
2025 YTHDF1 and YTHDC1 m6A reader proteins regulate HTLV-1 tax and hbz activity. Journal of virology 5 39902961
2023 Retroviral b-Zip protein (HBZ) contributes to the release of soluble and exosomal immune checkpoint molecules in the context of neuroinflammation. Journal of extracellular biology 5 37547182
2016 Impact of the SCF signaling pathway on leukemia stem cell-mediated ATL initiation and progression in an HBZ transgenic mouse model. Oncotarget 5 27340921
2025 JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis. Proceedings of the National Academy of Sciences of the United States of America 4 40549917
2025 Splicing-dependent restriction of the HBZ gene by Tax underlies biphasic HTLV-1 infection. PLoS pathogens 3 40720552
2025 High expression of Rex-orf-I and HBZ mRNAs and bronchiectasis in lung of HTLV-1A/C infected macaques. Nature communications 3 41006234
2023 Targeted zinc-finger repressors to the oncogenic HBZ gene inhibit adult T-cell leukemia (ATL) proliferation. NAR cancer 3 36644398
2023 Preclinical assessment of an anti-HTLV-1 heterologous DNA/MVA vaccine protocol expressing a multiepitope HBZ protein. Virology journal 3 38115107
2022 TAX and HBZ: hFc Ɣ 1 proteins as targets for passive immunotherapy. Iranian journal of basic medical sciences 3 35911645
2021 Molecular characterization of HTLV-1 genomic region hbz from patients with different clinical conditions. Journal of medical virology 2 33835501
2017 Methods for Identifying and Examining HTLV-1 HBZ Post-translational Modifications. Methods in molecular biology (Clifton, N.J.) 2 28357666
2026 Real-time diagnosis of adult T-cell leukemia/lymphoma using HBZ RNA in situ hybridization. American journal of clinical pathology 1 42106909
2022 The Road to HTLV-1-Induced Leukemia by Following the Subcellular Localization of HTLV-1-Encoded HBZ Protein. Frontiers in immunology 1 35812456

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