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  • Open Access

    ARTICLE

    Murine double minute gene 2 (MDM2) promoted hepatocellular carcinoma (HCC) cell growth by targeting fructose-1,6-bisphosphatase (FBP1) for degradation

    YAO XU1,#, BIN WU2,#, JING YANG3, SHENG ZHANG2, LONGGEN LIU4, SUOBAO XU2,*, JIAKAI JIANG2,*

    BIOCELL, Vol.46, No.6, pp. 1483-1491, 2022, DOI:10.32604/biocell.2022.017745

    Abstract To study the roles and association of murine double minute gene 2 (MDM2) and fructose-1,6-biphosphatase (FBP1) in human hepatocellular carcinoma (HCC), growth response of human HCC cells was assessed using proliferation and apoptosis assay. Pro-survival AKT signaling associated proteins (p-AKT, survivin and cleaved caspase 3) were assessed using western blotting. The correlation between MDM2 and FBP1 was assessed using co-immunoprecipitation combined with ubiquitination assay. Our data suggested that low expression of FBP1 was correlated with high levels of MDM2 in HCC cell lines (Huh7 and Hep3B). Overexpression of FBP1 resulted in anti-proliferation, pro-apoptosis, the up-regulation of cleaved caspase 3 while… More >

  • Open Access

    ARTICLE

    The function of ubiquitin-specific protease 31 in intracerebral hemorrhage

    SUYING PU1,#, HUI ZHENG2,#, YUN TAO1, JING SHAO1, MINGNA YANG1, SHUNJUN LI1,*

    BIOCELL, Vol.46, No.6, pp. 1545-1555, 2022, DOI:10.32604/biocell.2022.017544

    Abstract Intracerebral hemorrhage (ICH) is the most serious type of stroke. High level of thrombin is found in the ICH. Ubiquitin-specific protease (USP) 31, a member of deubiquitinating enzymes family, has been found to negatively regulate the NF-κB pathway. However, the function of USP31 in ICH remains largely unknown. In the present study, the mRNA and protein expression levels of USP31 were measured by real-time PCR and western blot. Flow cytometry was used to measure cell apoptosis and the level of reactive oxygen species (ROS). In the current study, we found the mRNA level of USP31 was decreased in peripheral blood… More >

  • Open Access

    REVIEW

    Ubiquitin-like posttranslational modifications in NAFLD progression and treatment

    FUJI YANG1, YAN HUANG1, YOUWEN TAN2,*, YONGMIN YAN1,*

    BIOCELL, Vol.46, No.2, pp. 389-400, 2022, DOI:10.32604/biocell.2021.015899

    Abstract Nonalcoholic fatty liver disease (NAFLD) is a long-lasting condition that affects the liver, destroying its function. Liver injury can cause steatosis and inflammation, and further activation of hepatic stellate cells (HSCs) often leads to the development of nonalcoholic liver fibrosis. The patient with NAFLD is at risk of developing advanced liver disease and complications, such as liver failure, hepatocellular carcinoma (HCC), and portal hypertension. Although our understanding of the cellular and molecular mechanisms of NAFLD has greatly improved in recent years, treatment remains limited. Analysis and characterization of protein posttranslational modifications (PTMs) could improve our understanding of NAFLD pathology and… More >

  • Open Access

    ARTICLE

    Loss of the ubiquitin-conjugating enzyme Rad6B disturbs mitochondrial function and cellular homeostasis in mouse skin

    LINGHUI YU#, RONG SHEN#, YANAN GUO, YANXUAN GUO, CHEN LI, YANFENG SONG*, DEGUI WANG*

    BIOCELL, Vol.45, No.3, pp. 761-772, 2021, DOI:10.32604/biocell.2021.014602

    Abstract Various factors can induce cell degeneration by altering the phenotype and metabolism of cells. Mitochondria play an essential role in cellular homeostasis and function, rendering aging processes highly associated with mitochondrial function and status. Herein, we describe an aging-prone phenotype of murine skin cells caused by depletion of Rad6B (Ube2b), an E2 ubiquitin-conjugating enzyme. In this study, using Masson’s trichrome, we showed that loss of Rad6B causes physiological structure changes in mouse skin with age. In addition, a combination of western blotting experiments, transmission electron microscopy and employment of immunofluorescence staining revealed that depletion of Rad6B was characterized by an… More >

  • Open Access

    REVIEW

    Functions of ULK1 in autophagy and non-autophagy pathways and its implications in human physiology and disease

    LINNA TAN1,2, YUYONG TAN1,2, DELIANG LIU1,2,*

    BIOCELL, Vol.44, No.4, pp. 535-543, 2020, DOI:10.32604/biocell.2020.09171

    Abstract ULK1 (unc-51 like autophagy activating kinase 1), a mammalian serine/threonine kinase, is a key component of autophagy initiation complex and helps to induce all types of autophagy. Canonical autophagy is a process in which, through the interactions of a series of autophagy-related proteins, damaged organelles or misfolded proteins are engulfed by autophagosomes and then merged with lysosomes to be degraded. Thus, canonical autophagy is an important constituent part of the cellular “quality control.” Besides, accumulating evidence indicates that ULK1 exerts autophagy-independent effects in a cell-specific manner. For example, ULK1 facilitates neurite elongation through the regulation of endoplasmic reticulum (ER)–Golgi trafficking… More >

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