Journal of Cellular Biochemistry
0730-2312
1097-4644
Mỹ
Cơ quản chủ quản: WILEY , Wiley-Liss Inc.
Lĩnh vực:
BiochemistryMolecular BiologyCell Biology
Phân tích ảnh hưởng
Thông tin về tạp chí
The Journal of Cellular Biochemistry publishes descriptions of original research in which complex cellular, pathogenic, clinical, or animal model systems are studied by biochemical, molecular, genetic, epigenetic or quantitative ultrastructural approaches. Submission of papers reporting genomic, proteomic, bioinformatics and systems biology approaches to identify and characterize parameters of biological control in a cellular context are encouraged. The areas covered include, but are not restricted to, conditions, agents, regulatory networks, or differentiation states that influence structure, cell cycle & growth control, structure-function relationships.
Các bài báo tiêu biểu
Pathogenic <i>Vibrio harveyi</i>, in contrast to non‐pathogenic strains, intervenes with the p38 MAPK pathway to avoid an abalone haemocyte immune response Abstract Vibrio harveyi is a marine bacterial pathogen responsible for episodic abalone epidemics associated with massive mortalities in France, Japan, and Australia. The aim of this study was the understanding of a possible role of the p38 MAPK in abalone haemocyte responses towards this bacterium. First, the pathogenicity of different V. harveyi strains was compared in both immersion and injection trials, and clear differences were detected. The three strains, ORM4, 04/092, and 05/053, all isolated from moribund abalone, induced up to 80% mortalities in immersion or injection challenges (LD50 (ORM4) = 2.5 × 102 CFU animal−1 ). The two strains, LMG 4044T and LMG 7890 were non‐pathogenic towards abalone in immersion trials, and needed very high numbers for killing by intramuscular injections (LD50 = 8.9 × 104 and 1.6 × 105 CFU animal−1 , respectively). To start unraveling the mechanism explaining these differences, the p38‐MAPK, a keyplayer in antimicrobial immune response, was studied. The non‐pathogenic strain, LMG 7890 can be eliminated by abalone haemocytes and induces haemocyte phagocytosis and high ROS production. With different concentrations of a p38‐specific inhibitor, SB203580, p38 implication was shown. This inhibitor reduced phagocytosis and ROS induction leading to LMG 7890 proliferation. In the case of the pathogenic ORM4 which can not be eliminated by abalone haemocytes, no phagocytosis and ROS production was induced, and a retarded p38 activation was observed. Taken together, our results suggest that p38 MAPK modulation may be one of the ways of virulent V. harveyi to attack its host and escape abalone immune response. J. Cell. Biochem. 106: 152–160, 2009. © 2008 Wiley‐Liss, Inc.
Tập 106 Số 1 - Trang 152-160 - 2009
Long Non-Coding RNA MALAT1 Promotes Proliferation, Angiogenesis, and Immunosuppressive Properties of Mesenchymal Stem Cells by Inducing VEGF and IDO
Tập 118 Số 9 - Trang 2780-2791 - 2017
PTEN enters the nucleus by diffusion Abstract Despite much evidence for phosphatidylinositol phosphate (PIP)‐triggered signaling pathways in the nucleus, there is little understanding of how the levels and activities of these proteins are regulated. As a first step to elucidating this problem, we determined whether phosphatase and tensin homolog deleted on chromosome 10 (PTEN) enters the nucleus by passive diffusion or active transport. We expressed various PTEN fusion proteins in tsBN2, HeLa, LNCaP, and U87MG cells and determined that the largest PTEN fusion proteins showed little or no nuclear localization. Because diffusion through nuclear pores is limited to proteins of 60,000 Da or less, this suggests that nuclear translocation of PTEN occurs via diffusion. We examined PTEN mutants, seeking to identify a nuclear localization signal (NLS) for PTEN. Mutation of K13 and R14 decreased nuclear localization, but these amino acids do not appear to be part of an NLS. We used fluorescence recovery after photobleaching (FRAP) to demonstrate that GFP‐PTEN can passively pass through nuclear pores. Diffusion in the cytoplasm is retarded for the PTEN mutants that show reduced nuclear localization. We conclude that PTEN enters the nucleus by diffusion. In addition, sequestration of PTEN in the cytoplasm likely limits PTEN nuclear translocation. © 2005 Wiley‐Liss, Inc.
Tập 96 Số 2 - Trang 221-234 - 2005
Different cellular localization, translocation, and insulin‐induced phosphorylation of PKBα in HepG2 cells and hepatocytes Abstract Protein kinase B (PKB), a serine/threonine protein kinase, prevents apoptosis and promotes cellular transformation. PKB activity is stimulated by insulin. In this report, we examined the relative amounts of expression, location, and translocation upon insulin stimulation of PKBα in normal primary hepatocytes and carcinoma cells, HepG2 cells. Non‐phosphorylated PKBα was present in both types of unstimulated cells. The phosphorylated form of the enzyme was present in the nucleus of unstimulated HepG2 cells but not in normal hepatocytes. In the cytoplasm, PKBα was found in greater abundance in the hepatocytes as compared in HepG2 cells. Insulin induced the translocation of phosphorylated PKBα from the nucleus to the nuclear membrane in HepG2 cells. In contrast, insulin caused translocation and phosphorylation of PKBα from the cytosol to the plasma membrane in normal hepatocytes. In addition, there is a higher expression of PKBα in the HepG2 cells as compared to normal primary hepatocytes. These findings provide an important distinction between hepatocellular HepG2 cells and normal liver cells and suggest that the presence of constitutively active nuclear PKB in the transformed cells might be an important contributor in cell transformation and immortality of hepatoma cells. J. Cell. Biochem. 86: 118–127, 2002. © 2002 Wiley‐Liss, Inc.
Tập 86 Số 1 - Trang 118-127 - 2002
MicroRNA‐150 Protects Against Pressure Overload‐Induced Cardiac Hypertrophy ABSTRACT Cardiac hypertrophy is the response of the heart to a variety of hypertrophic stimuli; this condition progresses to heart failure and sudden death. MicroRNAs (miRs) are a family of small, non‐coding RNAs that mediate posttranscriptional gene silencing. Recent studies have identified miRs as important regulators in cardiac hypertrophy. One specific miR, miR‐150 has been reported to be downregulated in hypertrophic murine hearts. However, the role of miR‐150 as a regulator of cardiac hypertrophy remains unclear. In the present study, we used gain‐of‐function and loss‐of‐function approaches to investigate the functional roles of miR‐150 in cardiac hypertrophy induced by aortic banding. The extent of the cardiac hypertrophy was evaluated by echocardiography and by pathological and molecular analyses of heart samples. Our results revealed that transgenic mice that overexpress miR‐150 in the heart were resistant to cardiac hypertrophy and fibrosis through down‐regulation of serum response factor (SRF). Conversely, the loss of function of miR‐150 by genetic knockdown or antagomiR approaches produced the opposite effects. These studies suggest that miR‐150 plays an important role in the regulation of cardiac hypertrophy and SRF is involved in miR‐150 mediated anti‐hypertrophic effect. Thus, miR‐150 may be a new therapeutic target for cardiac hypertrophy. J. Cell. Biochem. 116: 2166–2176, 2015. © 2015 Wiley Periodicals, Inc.
Tập 116 Số 10 - Trang 2166-2176 - 2015
Differential regulation of cyclooxygenase‐2 and inducible nitric oxide synthase by 4‐hydroxynonenal in human osteoarthritic chondrocytes through ATF‐2/CREB‐1 transactivation and concomitant inhibition of NF‐κB signaling cascade Abstract 4‐hydroxynonenal (HNE), a lipid peroxidation end product, is produced abundantly in osteoarthritic (OA) articular tissues and was recently identified as a potent catabolic factor in OA cartilage. In this study, we provide additional evidence that HNE acts as an inflammatory mediator by elucidating the signaling cascades targeted in OA chondrocytes leading to cyclooxygenase‐2 (COX‐2) and inducible nitric oxide synthase (iNOS) gene expression. HNE induced COX‐2 protein and mRNA levels with accompanying increases in prostaglandin E2 (PGE2 ) production. In contrast, HNE had no effect on basal iNOS expression or nitric oxide (NO) release. However, HNE strongly inhibited IL‐1β‐induced iNOS or NO production. Transient transfection experiments revealed that the ATF/CRE site (−58/−53) is essential for HNE‐induced COX‐2 promoter activation and indeed HNE induced ATF‐2 and CREB‐1 phosphorylation as well as ATF/CRE binding activity. Overexpression of p38 MAPK enhanced the HNE‐induced ATF/CRE luciferase reporter plasmid activation, COX‐2 synthesis and promoter activity. HNE abrogated IL‐1β‐induced iNOS expression and promoter activity mainly through NF‐κB site (−5,817/−5,808) possibly via suppression of IKKα‐induced IκBα phosphorylation and NF‐κB/p65 nuclear translocation. Upon examination of upstream signaling components, we found that IKKα was inactivated through HNE/IKKα adduct formation. Taken together, these findings illustrate the central role played by HNE in the regulation of COX‐2 and iNOS in OA. The aldehyde induced selectively COX‐2 expression via ATF/CRE activation and inhibited iNOS via IKKα inactivation. J. Cell. Biochem. 100: 1217–1231, 2007. © 2006 Wiley‐Liss, Inc.
Tập 100 Số 5 - Trang 1217-1231 - 2007
Fracture healing as a post‐natal developmental process: Molecular, spatial, and temporal aspects of its regulation Abstract Fracture healing is a specialized post‐natal repair process that recapitulates aspects of embryological skeletal development. While many of the molecular mechanisms that control cellular differentiation and growth during embryogenesis recur during fracture healing, these processes take place in a post‐natal environment that is unique and distinct from those which exist during embryogenesis. This Prospect Article will highlight a number of central biological processes that are believed to be crucial in the embryonic differentiation and growth of skeletal tissues and review the functional role of these processes during fracture healing. Specific aspects of fracture healing that will be considered in relation to embryological development are: (1) the anatomic structure of the fracture callus as it evolves during healing; (2) the origins of stem cells and morphogenetic signals that facilitate the repair process; (3) the role of the biomechanical environment in controlling cellular differentiation during repair; (4) the role of three key groups of soluble factors, pro‐inflammatory cytokines, the TGF‐β superfamily, and angiogenic factors, during repair; and (5) the relationship of the genetic components that control bone mass and remodeling to the mechanisms that control skeletal tissue repair in response to fracture. J. Cell. Biochem. 88: 873–884, 2003. © 2003 Wiley‐Liss, Inc.
Tập 88 Số 5 - Trang 873-884 - 2003
Characterization of LipN (Rv2970c) of<i>Mycobacterium Tuberculosis</i>H37Rv and its Probable Role in Xenobiotic Degradation
Tập 117 Số 2 - Trang 390-401 - 2016
Bacterial resistances to mercury and copper Abstract Heavy metals are toxic to living organisms. Some have no known beneficial biological function, while others have essential roles in physiological reactions. Mechanisms which deal with heavy metal stress must protect against the deleterious effects of heavy metals, yet avoid depleting the cell of a heavy metal which is also an essential nutrient. We describe the mechanims of resistance in Escherichia coli to two different heavy metals, mercury and copper. Resistance of E. coli to mercury is reasonably well understood and is known to occur by transport of mercuric ions into the cytoplasmic compartment of the bacterial cell and subsequent reductive detoxification of mercuric ions. Recent mutational analysis has started to uncover the mechanistic detail of the mercuric ion transport processes, and has shown the essential nature of cysteine residues in transport of Hg(II). Resistance to copper is much less well understood, but is known to involve the increased export of copper from the bacterial cell and modification of the copper; the details of the process are still being elucidated. Expression of both metal resistance determinants is regulated by the corresponding cation. In each case the response enables the maintenance of cellular homeostasis for the metal. The conclusions drawn allow us to make testable predictions about the regulation of expression of resistance to other heavy metals.
Tập 46 Số 2 - Trang 106-114 - 1991
The various regulatory functions of long noncoding RNAs in apoptosis, cell cycle, and cellular senescence Abstract Long noncoding RNAs (lncRNAs) are a group of noncoding cellular RNAs involved in significant biological phenomena such as differentiation, cell development, genomic imprinting, adjusting the enzymatic activity, regulating chromosome conformation, apoptosis, cell cycle, and cellular senescence. The misregulation of lncRNAs interrupting normal biological processes has been implicated in tumor formation and metastasis, resulting in cancer. Apoptosis and cell cycle, two main biological phenomena, are highly conserved and intimately coupled mechanisms. Hence, some cell cycle regulators can influence both programmed cell death and cell division. Apoptosis eliminates defective and unwanted cells, and the cell cycle enables cells to replicate themselves. The improper regulation of apoptosis and cell cycle contributes to numerous disorders such as neurodegenerative and autoimmune diseases, viral infection, anemia, and mainly cancer. Cellular senescence is a tumor‐suppressing response initiated by environmental and internal stress factors. This phenomenon has recently attained more attention due to its therapeutic implications in the field of senotherapy. In this review, the regulatory roles of lncRNAs on apoptosis, cell cycle, and senescence will be discussed. First, the role of lncRNAs in mitochondrial dynamics and apoptosis is addressed. Next, the interaction between lncRNAs and caspases, pro/antiapoptotic proteins, and also EGFR/PI3K/PTEN/AKT/mTORC1 signaling pathway will be investigated. Furthermore, the effect of lncRNAs in the cell cycle is surveyed through interaction with cyclins, cdks, p21, and wnt/β‐catenin/c‐myc pathway. Finally, the function of essential lncRNAs in cellular senescence is mentioned.
Tập 123 Số 6 - Trang 995-1024 - 2022