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  1. Article: Correction: Vacuolin‑1 enhances RA‑induced differentiation of human myeloblastic leukemia cells: evidence for involvement of a CD11b/FAK/LYN/SLP‑76 axis subject to endosomal regulation that drives late differentiation steps.

    Zhu, Kaiyuan / Kazim, Noor / Yue, Jianbo / Yen, Andrew

    Cell & bioscience

    2023  Volume 13, Issue 1, Page(s) 22

    Language English
    Publishing date 2023-02-03
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2593367-X
    ISSN 2045-3701
    ISSN 2045-3701
    DOI 10.1186/s13578-023-00965-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Vacuolin-1 enhances RA-induced differentiation of human myeloblastic leukemia cells: evidence for involvement of a CD11b/FAK/LYN/SLP-76 axis subject to endosomal regulation that drives late differentiation steps.

    Zhu, Kaiyuan / Kazim, Noor / Yue, Jianbo / Yen, Andrew

    Cell & bioscience

    2022  Volume 12, Issue 1, Page(s) 179

    Abstract: Background: Retinoic acid(RA), an embryonic morphogen, regulates cell differentiation. Endocytosis regulates receptor signaling that governs such RA-directed cellular processes. Vacuolin-1 is a small molecule that disrupts endocytosis, motivating ... ...

    Abstract Background: Retinoic acid(RA), an embryonic morphogen, regulates cell differentiation. Endocytosis regulates receptor signaling that governs such RA-directed cellular processes. Vacuolin-1 is a small molecule that disrupts endocytosis, motivating interest in its effect on RA-induced differentiation/arrest. In HL-60 myeloblastic-leukemia cells, RA causes differentiation evidenced by a progression of cell-surface and functional markers, CD38, CD11b, and finally reactive oxygen species(ROS) production and G1/0 cell cycle arrest in mature cells.
    Results: We found that Vacuolin-1 enhanced RA-induced CD11b, ROS and G1/0 arrest, albeit not CD38. Enhanced CD11b expression was associated with enhanced activation of Focal Adhesion Kinase(FAK). Adding vacuolin-1 enhanced RA-induced tyrosine phosphorylation of FAK, Src Family Kinases(SFKs), and the adaptor protein, SLP-76, expression of which is known to drive RA-induced differentiation. Depleting CD11b cripples late stages of progressive myeloid differentiation, namely G1/0 arrest and inducible ROS production, but not expression of CD38. Loss of NUMB, a protein that supports early endosome maturation, affected RA-induced ROS and G1/0 arrest, but not CD38 expression.
    Conclusion: Hence there appears to be a novel CD11b/FAK/LYN/SLP-76 axis subject to endosome regulation which contributes to later stages of RA-induced differentiation. The effects of vacuolin-1 thus suggest a model where RA-induced differentiation consists of progressive stages driven by expression of sequentially-induced receptors.
    Language English
    Publishing date 2022-11-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 2593367-X
    ISSN 2045-3701
    ISSN 2045-3701
    DOI 10.1186/s13578-022-00911-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Autophagy in host-microbe interactions.

    Wu, William K K / Yue, Jianbo

    Seminars in cell & developmental biology

    2020  Volume 101, Page(s) 1–2

    MeSH term(s) Autophagy/immunology ; Host-Pathogen Interactions/immunology ; Humans
    Language English
    Publishing date 2020-02-08
    Publishing country England
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2020.02.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2918: Show issues Location:
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  4. Article ; Online: Identification of Anhydrodebromoaplysiatoxin as a Dichotomic Autophagy Inhibitor

    Feng, Limin / Lu, Chung-Kuang / Wu, Jiajun / Chan, Leo Lai / Yue, Jianbo

    Mar Drugs. 2023 Jan. 10, v. 21, no. 1

    2023  

    Abstract: Dysfunctional autophagy is associated with various human diseases, e.g., cancer. The discovery of small molecules modulating autophagy with therapeutic potential could be significant. To this end, we screened the ability of a series of metabolites ... ...

    Abstract Dysfunctional autophagy is associated with various human diseases, e.g., cancer. The discovery of small molecules modulating autophagy with therapeutic potential could be significant. To this end, we screened the ability of a series of metabolites isolated from marine microorganisms to modulate autophagy. Anhydrodebromoaplysiatoxin (ADAT), a metabolite yielded by the marine red algae Gracilaria coronopifolia, inhibited autophagosome-lysosome fusion in mammalian cells, thereby inducing the accumulation of autophagosomes. Treatment of cells with ADAT alkalinized lysosomal pH. Interestingly, ADAT also activated the mTOR/p70S6K/FoxO3a signaling pathway, likely leading to the inhibition of autophagy induction. ADAT had little effect on apoptosis. Our results suggest that ADAT is a dichotomic autophagy inhibitor that inhibits both late-stage (autophagosome-lysosome fusion) and early-stage (autophagy induction) autophagy.
    Keywords Gracilaria ; apoptosis ; autophagosomes ; autophagy ; humans ; metabolites ; pH ; therapeutics
    Language English
    Dates of publication 2023-0110
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article ; Online
    ZDB-ID 2175190-0
    ISSN 1660-3397
    ISSN 1660-3397
    DOI 10.3390/md21010046
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: Identification of Anhydrodebromoaplysiatoxin as a Dichotomic Autophagy Inhibitor.

    Feng, Limin / Lu, Chung-Kuang / Wu, Jiajun / Chan, Leo Lai / Yue, Jianbo

    Marine drugs

    2023  Volume 21, Issue 1

    Abstract: Dysfunctional autophagy is associated with various human diseases, e.g., cancer. The discovery of small molecules modulating autophagy with therapeutic potential could be significant. To this end, we screened the ability of a series of metabolites ... ...

    Abstract Dysfunctional autophagy is associated with various human diseases, e.g., cancer. The discovery of small molecules modulating autophagy with therapeutic potential could be significant. To this end, we screened the ability of a series of metabolites isolated from marine microorganisms to modulate autophagy. Anhydrodebromoaplysiatoxin (ADAT), a metabolite yielded by the marine red algae
    MeSH term(s) Animals ; Humans ; Autophagosomes/metabolism ; Autophagy ; Lysosomes ; Mammals ; Signal Transduction
    Chemical Substances anhydrodebromoaplysiatoxin
    Language English
    Publishing date 2023-01-10
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2175190-0
    ISSN 1660-3397 ; 1660-3397
    ISSN (online) 1660-3397
    ISSN 1660-3397
    DOI 10.3390/md21010046
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The interplay of autophagy and enterovirus.

    Huang, Lihong / Yue, Jianbo

    Seminars in cell & developmental biology

    2019  Volume 101, Page(s) 12–19

    Abstract: Autophagy, an evolutional conserved lysosomal degradation process, has been implicated to play an important role in cellular defense against a variety of microbial infection. Interestingly, numerous studies found that some pathogens, especially positive- ... ...

    Abstract Autophagy, an evolutional conserved lysosomal degradation process, has been implicated to play an important role in cellular defense against a variety of microbial infection. Interestingly, numerous studies found that some pathogens, especially positive-single-strand RNA viruses, actually hijacked autophagy machinery to promote virus infection within host cells, facilitating different stages of viral life cycle, from replication, assembly to egress. Enterovirus, a genus of positive-strand RNA virus, can cause various human diseases and is one of main public health threat globally, yet no effective clinical intervention is available for enterovirus infection. Here we summarized recent literature on how enteroviruses regulate and utilize autophagy process to facilitate their propagation in the host cells. The studies on the interplay between enterovirus and autophagy not only shed light on the molecular mechanisms underlying how enterovirus hijacks cellular components and pathway for its own benefits, but also provide therapeutic option against enterovirus infection.
    MeSH term(s) Autophagy/immunology ; Enterovirus/immunology ; Host-Pathogen Interactions/immunology ; Humans
    Keywords covid19
    Language English
    Publishing date 2019-09-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1312473-0
    ISSN 1096-3634 ; 1084-9521
    ISSN (online) 1096-3634
    ISSN 1084-9521
    DOI 10.1016/j.semcdb.2019.08.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2918: Show issues Location:
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  7. Article ; Online: The temporal association of CapZ with early endosomes regulates endosomal trafficking and viral entry into host cells.

    Zhu, Huazhang / Wang, Dawei / Ye, Zuodong / Huang, Lihong / Wei, Wenjie / Chan, Kui Ming / Zhang, Rongxin / Zhang, Liang / Yue, Jianbo

    BMC biology

    2024  Volume 22, Issue 1, Page(s) 12

    Abstract: Background: Many viruses enter host cells by hijacking endosomal trafficking. CapZ, a canonical actin capping protein, participates in endosomal trafficking, yet its precise role in endocytosis and virus infection remains elusive.: Results: Here, we ... ...

    Abstract Background: Many viruses enter host cells by hijacking endosomal trafficking. CapZ, a canonical actin capping protein, participates in endosomal trafficking, yet its precise role in endocytosis and virus infection remains elusive.
    Results: Here, we showed that CapZ was transiently associated with early endosomes (EEs) and was subsequently released from the matured EEs after the fusion of two EEs, which was facilitated by PI(3)P to PI(3,5)P2 conversion. Vacuolin-1 (a triazine compound) stabilized CapZ at EEs and thus blocked the transition of EEs to late endosomes (LEs). Likewise, artificially tethering CapZ to EEs via a rapamycin-induced protein-protein interaction system blocked the early-to-late endosome transition. Remarkably, CapZ knockout or artificially tethering CapZ to EEs via rapamycin significantly inhibited flaviviruses, e.g., Zika virus (ZIKV) and dengue virus (DENV), or beta-coronavirus, e.g., murine hepatitis virus (MHV), infection by preventing the escape of RNA genome from endocytic vesicles.
    Conclusions: These results indicate that the temporal association of CapZ with EEs facilitates early-to-late endosome transition (physiologically) and the release of the viral genome from endocytic vesicles (pathologically).
    MeSH term(s) Animals ; Humans ; Mice ; Endocytosis/physiology ; Endosomes/metabolism ; Phosphatidylinositol Phosphates ; Sirolimus/pharmacology ; Sirolimus/metabolism ; Transport Vesicles ; Virus Internalization ; Zika Virus ; Zika Virus Infection/metabolism
    Chemical Substances phosphatidylinositol 3-phosphate ; Phosphatidylinositol Phosphates ; Sirolimus (W36ZG6FT64) ; Capza1 protein, mouse
    Language English
    Publishing date 2024-01-25
    Publishing country England
    Document type Journal Article
    ZDB-ID 2133020-7
    ISSN 1741-7007 ; 1741-7007
    ISSN (online) 1741-7007
    ISSN 1741-7007
    DOI 10.1186/s12915-024-01819-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: TPC2 mediates autophagy progression and extracellular vesicle secretion in cancer cells.

    Sun, Wei / Yue, Jianbo

    Experimental cell research

    2018  Volume 370, Issue 2, Page(s) 478–489

    Abstract: Autophagy is an evolutionarily conserved lysosomal degradation process, and is involved in various cellular processes. Here we studied the role of two pore channel 2 (TPC2), a lysosomal non-selective ... ...

    Abstract Autophagy is an evolutionarily conserved lysosomal degradation process, and is involved in various cellular processes. Here we studied the role of two pore channel 2 (TPC2), a lysosomal non-selective Na
    MeSH term(s) Autophagosomes/physiology ; Autophagy/physiology ; Calcium Channels/metabolism ; Cell Nucleus/metabolism ; Extracellular Vesicles/metabolism ; HeLa Cells ; Humans ; Lysosomes/metabolism ; Signal Transduction/physiology
    Chemical Substances Calcium Channels ; TPCN2 protein, human
    Language English
    Publishing date 2018-07-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2018.07.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 563: Show issues Location:
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  9. Article ; Online: Depleting interferon regulatory factor-1(IRF-1) with CRISPR/Cas9 attenuates inducible oxidative metabolism without affecting RA-induced differentiation in HL-60 human AML cells.

    Zhu, Kaiyuan / Yue, Jianbo / Yen, Andrew

    FASEB bioAdvances

    2020  Volume 2, Issue 6, Page(s) 354–364

    Abstract: The known collaboration between all-transretinoic acid and interferon motivates this study of the dependence of RA-induced leukemic cell differentiation on interferon regulatory factor-1 (IRF-1), a transcription factor that is the main mediator of ... ...

    Abstract The known collaboration between all-transretinoic acid and interferon motivates this study of the dependence of RA-induced leukemic cell differentiation on interferon regulatory factor-1 (IRF-1), a transcription factor that is the main mediator of interferon effects. In the HL-60 acute myeloid leukemia (AML) model that represents a rare RA-responsive subtype of AML, IRF-1 is not expressed until RA induces its prominent expression, and ectopic IRF-1 expression enhances RA-induced differentiation, motivating interest in how IRF-1 is putatively needed for RA response. Accordingly, we created CRISPR/Cas9-mediated IRF-1 knockout HL-60 cells. Contrary to expectation, loss of IRF-1 did not diminish RA-induced cellular signaling that propels differentiation, and RA-induced cell differentiation markers, including CD38 and CD11b expression and G1/G0cell cycle arrest, were unaffected. However, elimination of IRF-1 inhibited RA-induced p47phox expression and inducible oxidative metabolism detected by reactive oxygen species (ROS), suggesting IRF-1 is essential for mature granulocytic inducible oxidative metabolism. In the case of 1,25-Dihydroxyvitamin D3-induced differentiation to monocytes, IRF-1 loss did not affect D3-induced expression of CD38, CD11b, and CD14, and G1/0 arrest; but inhibited ROS production. Our data suggest that IRF-1 is inessential for differentiation but upregulates p47phox expression for mature-cell ROS production.
    Language English
    Publishing date 2020-05-22
    Publishing country United States
    Document type Journal Article
    ISSN 2573-9832
    ISSN (online) 2573-9832
    DOI 10.1096/fba.2020-00004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: VCP/p97 targets the nuclear export and degradation of p27

    Shi, Xianli / Zhu, Kaiyuan / Ye, Zuodong / Yue, Jianbo

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2020  Volume 34, Issue 4, Page(s) 5193–5207

    Abstract: One of the critical regulatory mechanisms for cell cycle progression is the timely degradation of CDK inhibitors, including ... ...

    Abstract One of the critical regulatory mechanisms for cell cycle progression is the timely degradation of CDK inhibitors, including p21
    MeSH term(s) Active Transport, Cell Nucleus ; Animals ; Apoptosis ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Female ; G1 Phase ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Proteolysis ; S Phase ; Tumor Cells, Cultured ; Valosin Containing Protein/genetics ; Valosin Containing Protein/metabolism ; Xenograft Model Antitumor Assays
    Chemical Substances Biomarkers, Tumor ; CDKN1A protein, human ; CDKN1B protein, human ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; VCP protein, human (EC 3.6.4.6) ; Valosin Containing Protein (EC 3.6.4.6)
    Language English
    Publishing date 2020-02-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.201901506R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 296: Show issues

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