NAP1L1 Regulates Hepatitis C Virus Entry and Interacts with NS3

Yin, Peiqi; Li, Ye; Zhou, Liya; Zhang, Leiliang

doi:10.1007/s12250-018-0006-5

Cited by 4 publications

(5 citation statements)

References 16 publications

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“…NAP1L1 also attenuates NF‐kappaB signaling pathway to induce the anti‐apoptotic Mcl‐1 gene and functions as a tumor promoter in hepatocellular carcinoma (Tanaka et al, 2017; Zhang et al, 2021). In addition, NAP1L1 regulates the entry of both DNA and RNA viruses (Yin et al, 2018). Due to the aberrant expression of some cancers, NAP1L1 is a potential biomarker with diagnostic and prognostic purposes (Aydin et al, 2020; Queiroz et al, 2020; Shen et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

NAP1L1 is a novel microtubule‐associated protein

Peng

Zhang

et al. 2023

Cytoskeleton

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Microtubule‐associated proteins (MAPs) regulate assembly and stability of microtubules (MTs) during cell cytokinesis, cell migration, neuronal growth, axon guidance, and synapse formation. Using data mining of the Human Protein Atlas database and experimental screening, we identified nucleosome assembly protein 1 like 1 (NAP1L1) as a new MAP. The Human Protein Atlas and PubMed database screening identified 99 potential new MAPs. Twenty candidate proteins that highly co‐localized with MTs were exogenously expressed with green fluorescent protein (GFP) or hemagglutinin (HA) tags in tissue culture cells and MTs were co‐stained for immunofluorescent microscopy. We found that NAP1L1 is mainly localized in the cytosol with MTs during interphase. Using bacterially expressed recombinant NAP1L1 fragments and purified MTs, we biochemically mapped the MT‐binding site on the N‐terminal region (1–72aa) and the central region (164–269aa) of NAP1L1. NAP1L1 dimerizes through the long helix region (73–163aa), and full‐length NAP1L1 induces the formation of thick MTs, indicating that NAP1L1 has the ability to bundle MTs in cells. Analysis of publicly available RNA‐seq data of NAP1L1 depleted cells suggested that NAP1L1 is involved in cell adhesion and migration in agreement with the function of NAP1L1 as a MAP.

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Section: Introductionmentioning

confidence: 99%

NAP1L1 is a novel microtubule‐associated protein

Peng

Zhang

et al. 2023

Cytoskeleton

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“…Ovarian cancer (OC) is the most deadly gynecological tumor in female reproductive organs in China [ 1 ], and the underlying molecular mechanisms in OC development remain unclear. It is difficult to diagnose OC at an early stage, and the treatment options following diagnosis are limited.…”

Section: Introductionmentioning

confidence: 99%

“…Nucleosome assembly protein 1-like 1 (NAP1L1) is a member of the nucleosome assembly protein l-like family that includes NAP1L1, NAP1L2, NAP1L3, NAP1L4, and NAP1L5 [ 1 ], which was first detected in human thymus tissue [ 2 ]. The functions attributed to NAP1L1 proteins include nucleosome assembly, histone transport, histone eviction, transcriptional regulation, and cell cycle progression [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

NAP1L1 promotes tumor proliferation through HDGF/C-JUN signaling in ovarian cancer

et al. 2022

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Background Nucleosome assembly protein 1-like 1 (NAP1L1) is highly expressed in various types of cancer and plays an important role in carcinogenesis, but its specific role in tumor development and progression remains largely unknown. In this study, we suggest the potential of NAP1L1 as a prognostic biomarker and therapeutic target for the treatment of ovarian cancer (OC). Methods In our study, a tissue microarray (TMA) slide containing specimens from 149 patients with OC and 11 normal ovarian tissues underwent immunohistochemistry (IHC) to analyze the correlation between NAP1L1 expression and clinicopathological features. Loss-of- function experiments were performed by transfecting siRNA and following lentiviral gene transduction into SKOV3 and OVCAR3 cells. Cell proliferation and the cell cycle were assessed by the Cell Counting Kit-8, EDU assay, flow cytometry, colony formation assay, and Western blot analysis. In addition, co-immunoprecipitation (Co-IP) and immunofluorescence assays were performed to confirm the relationship between NAP1L1 and its potential targets in SKOV3/OVCAR3 cells. Results High expression of NAP1L1 was closely related to poor clinical outcomes in OC patients. After knocking down NAP1L1 by siRNA or shRNA, both SKOV3 and OVCAR3 cells showed inhibition of cell proliferation, blocking of the G1/S phase, and increased apoptosis in vitro. Mechanism analysis indicated that NAP1L1 interacted with hepatoma-derived growth factor (HDGF) and they were co-localized in the cytoplasm. Furthermore, HDGF can interact with jun proto-oncogene (C-JUN), an oncogenic transformation factor that induces the expression of cyclin D1 (CCND1). Overexpressed HDGF in NAP1L1 knockdown OC cells not only increased the expression of C-JUN and CCND1, but it also reversed the suppressive effects of si-NAP1L1 on cell proliferation. Conclusions Our data demonstrated that NAP1L1 could act as a prognostic biomarker in OC and can interact with HDGF to mediate the proliferation of OC, and this process of triggered proliferation may contribute to the activation of HDGF/C-JUN signaling in OC cells.

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“…In addition to a role in assisting H2A-H2B dimer incorporation into nucleosome, NAP1L1 also participates in gene expression regulation through epigenetic mechanisms (24,25). Recently, NAP1L family members have been found to be functionally involved in cell proliferation and differentiation during development and human diseases, such as carcinoma and virus infection (26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40). In contrast, our knowledge about other family members is still limited.…”

Section: Introductionmentioning

confidence: 99%

NAP1L5 Promotes Nucleolar Hypertrophy and Is Required for Translation Activation During Cardiomyocyte Hypertrophy

Guo

Zheng

Sun

et al. 2021

Front. Cardiovasc. Med.

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Pathological growth of cardiomyocytes during hypertrophy is characterized by excess protein synthesis; however, the regulatory mechanism remains largely unknown. Using a neonatal rat ventricular myocytes (NRVMs) model, here we find that the expression of nucleosome assembly protein 1 like 5 (Nap1l5) is upregulated in phenylephrine (PE)-induced hypertrophy. Knockdown of Nap1l5 expression by siRNA significantly blocks cell size enlargement and pathological gene induction after PE treatment. In contrast, Adenovirus-mediated Nap1l5 overexpression significantly aggravates the pro-hypertrophic effects of PE on NRVMs. RNA-seq analysis reveals that Nap1l5 knockdown reverses the pro-hypertrophic transcriptome reprogramming after PE treatment. Whereas, immune response is dominantly enriched in the upregulated genes, oxidative phosphorylation, cardiac muscle contraction and ribosome-related pathways are remarkably enriched in the down-regulated genes. Although Nap1l5-mediated gene regulation is correlated with PRC2 and PRC1, Nap1l5 does not directly alter the levels of global histone methylations at K4, K9, K27 or K36. However, puromycin incorporation assay shows that Nap1l5 is both necessary and sufficient to promote protein synthesis in cardiomyocyte hypertrophy. This is attributable to a direct regulation of nucleolus hypertrophy and subsequent ribosome assembly. Our findings demonstrate a previously unrecognized role of Nap1l5 in translation control during cardiac hypertrophy.

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NAP1L1 Regulates Hepatitis C Virus Entry and Interacts with NS3

Cited by 4 publications

References 16 publications

NAP1L1 is a novel microtubule‐associated protein

NAP1L1 is a novel microtubule‐associated protein

NAP1L1 promotes tumor proliferation through HDGF/C-JUN signaling in ovarian cancer

NAP1L5 Promotes Nucleolar Hypertrophy and Is Required for Translation Activation During Cardiomyocyte Hypertrophy

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