共查询到20条相似文献，搜索用时 15 毫秒
1.
Hideki Hirose Atsushi Sasaki Nana Ishii Masaru Sekijima Takahiro Iyama Toshio Nojima Yoshikazu Ugawa 《Bioelectromagnetics》2010,31(2):104-112
Given the widespread use of the cellular phone today, investigation of potential biological effects of radiofrequency (RF) fields has become increasingly important. In particular, much research has been conducted on RF effects on brain function. To examine any biological effects on the central nervous system (CNS) induced by 1950 MHz modulation signals, which are controlled by the International Mobile Telecommunication‐2000 (IMT‐2000) cellular system, we investigated the effect of RF fields on microglial cells in the brain. We assessed functional changes in microglial cells by examining changes in immune reaction‐related molecule expression and cytokine production after exposure to a 1950 MHz Wideband Code Division Multiple Access (W‐CDMA) RF field, at specific absorption rates (SARs) of 0.2, 0.8, and 2.0 W/kg. Primary microglial cell cultures prepared from neonatal rats were subjected to an RF or sham field for 2 h. Assay samples obtained 24 and 72 h after exposure were processed in a blind manner. Results showed that the percentage of cells positive for major histocompatibility complex (MHC) class II, which is the most common marker for activated microglial cells, was similar between cells exposed to W‐CDMA radiation and sham‐exposed controls. No statistically significant differences were observed between any of the RF field exposure groups and the sham‐exposed controls in percentage of MHC class II positive cells. Further, no remarkable differences in the production of tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), and interleukin‐6 (IL‐6) were observed between the test groups exposed to W‐CDMA signal and the sham‐exposed negative controls. These findings suggest that exposure to RF fields up to 2 W/kg does not activate microglial cells in vitro. Bioelectromagnetics 31:104–112, 2010. © 2009 Wiley‐Liss, Inc. 相似文献
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《Chirality》2017,29(11):677-683
Circular dichroisms (CDs) of neutral and protonated [3.3]anthracenopyridinophane ( 1 and 1‐H + ) were investigated experimentally and theoretically. Introducing an anthracene moiety with extended conjugation affected the cyclophane structure with the bent angles being appreciably reduced from those of parent [3.3]pyridinophane. The Cotton effects (CEs) observed at the 1B b band for both 1 and 1‐H + were fairly strong and apparently bisignate, which, however, turned out not to be a simple exciton couplet but to be composed of multiple transitions. In contrast, the CEs were much weaker in the 1L a band region. The spectral changes upon protonation were less significant compared with the parent pyridinophane, being dominated by the local transitions of anthracene. Nevertheless, the CD spectra of 1 and 1‐H + were well reproduced by theoretical calculations to allow us an unambiguous absolute configuration determination of the first high‐performance liquid chromatography (HPLC) elute (from Chiralcel IB column) as S p. The transannular interactions between the anthracene and pyridine/pyridinium units were examined by UV‐vis and fluorescence spectroscopy to reveal a charge‐transfer (CT) band in the low‐energy region, particularly for 1‐H + . Despite the comparable CT interactions, the CE at the CT band was much stronger for the anthracenopyridinophane than for the parent pyridinophane, affording an anisotropy (g ) factor as large as 4 × 10‐3. 相似文献
3.
Athanassios Stavrakoudis Ioannis G. Tsoulos Zakhar O. Shenkarev Tatiana V. Ovchinnikova 《Peptide Science》2009,92(3):143-155
Arenicin‐2 is a 21 residue antimicrobial cyclic peptide, possessing one disulphide bond between residues Cys3 and Cys20. NMR and CD studies suggested that the structure of arenicin‐2 in water represented a well formed, but highly twisted β‐harpin. To investigate the spatial arrangement of the peptide side chains and to get a clear view of its possible amphipathic properties we performed molecular dynamics in explicit water. Four independent trajectories, 50 ns in length, were produced, starting from various initial conformations or by applying different simulation conditions. Arenicin‐2 retained its β‐hairpin structure during simulations, although the residues close to strand ends were found to escape from the ideal hairpin conformation. The type I′ β‐turn connecting the two strands fluctuated between type IV and II′ β‐turn. Conversely, the right‐handed twist of the β‐hairpin was well conserved with average twist value 203° ± 19° per eight residues. Several nonbonded interactions, like hydrophobic interactions between aliphatic side chains, cation/π‐aromatic interactions, CH…π aromatic bond and water bridges, contributed to the hairpin stabilization. © 2009 Wiley Periodicals, Inc. Biopolymers (Pept Sci) 92: 143–155, 2009. This article was originally published online as an accepted preprint. The “Published Online” date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com 相似文献
4.
Myrto Rizou Eleni A. Frangou Filio Marineli Niki Prakoura Jerome Zoidakis Harikleia Gakiopoulou George Liapis Panagiotis Kavvadas Christos Chatziantoniou Manousos Makridakis Antonia Vlahou John Boletis Demetrios Vlahakos Dimitrios Goumenos Evgenios Daphnis Christos Iatrou Aristidis S. Charonis 《Journal of cellular and molecular medicine》2018,22(9):4139-4149
5.
Jinyoung Son Misun Kim Ilo Jou Kyoung Chan Park Hee Young Kang 《Pigment cell & melanoma research》2014,27(2):201-208
Inflammatory cytokines are closely related to pigmentary changes. In this study, the effects of IFN‐γ on melanogenesis were investigated. IFN‐γ inhibits basal and α‐MSH‐induced melanogenesis in B16 melanoma cells and normal human melanocytes. MITF mRNA and protein expressions were significantly inhibited in response to IFN‐γ. IFN‐γ inhibited CREB binding to the MITF promoter but did not affect CREB phosphorylation. Instead, IFN‐γ inhibited the association of CBP and CREB through the increased association between CREB binding protein (CBP) and STAT1. These findings suggest that IFN‐γ inhibits both basal and α‐MSH‐induced melanogenesis by inhibiting MITF expression. The inhibitory action of IFN‐γ in α‐MSH‐induced melanogenesis is likely to be associated with the sequestration of CBP via the association between CBP and STAT1. These data suggest that IFN‐γ plays a role in controlling inflammation‐ or UV‐induced pigmentary changes. 相似文献
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Hyunju Kim Yu‐Ran Na So Yeon Kim Eun Gyeong Yang 《Journal of cellular biochemistry》2016,117(3):647-658
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Recent evidence implicates a central role for PI3K signalling in mediating cell survival during the process of neuronal differentiation. Although PI3K activity is stimulated by a wide range of growth factors and cytokines in different cell lines and tissues, activation of this pathway by insulin‐like growth factor I (IGF‐I) most likely represents the main survival signal during neuronal differentiation. IGF‐I is highly expressed during development of the central nervous system, and thus is a critical factor for the development and maturation of the cerebellum. Upon ligand binding, the IGF‐I receptor phosphorylates tyrosine residues in SHC and insulin receptor substrates (IRSs) initiating two main signalling cascades, the MAP kinase and the phosphatidylinositol 3‐kinase (PI3K) pathways. Activated PI3K is composed of a catalytic subunit (p110α or β) associated with one of a large family of regulatory subunits (p85α, p85β, p55γ, p55α, and p50α). To evaluate the contributions of these various regulatory subunits to neuronal differentiation, we have used antibodies specific for each of the PI3K subunits. Using these antisera, we now demonstrate that PI3K subunits are differentially regulated in cerebellar development, and that the expression level of the p55γ regulatory subunit reaches a maximum during postnatal development, decreasing thereafter to low levels in the adult cerebellum. Furthermore, our studies reveal that the distribution of the various PI3K regulatory subunits varies during development of the cerebellum. Interestingly, p55γ is expressed in both glial and neuronal cells; moreover, in Purkinje neurones, this subunit colocalises with the IGF‐IR. © 2001 John Wiley & Sons, Inc. J Neurobiol 47: 39–50, 2001 相似文献
11.
Yiyi Hu Xi Chen Huiqin Duan Yuanliang Hu Xiang Mu 《Cell biochemistry and function》2009,27(5):284-288
To investigate the pharmacological mechanism of the traditional Chinese medicine, Pulsatilla decoction (PD), the levels of nitric oxide (NO), endothelin‐1 (ET‐1), tumor necrosis factor‐α (TNF‐α), and interleukin‐1α (IL‐1α) secreted by cultured rat intestinal microvascular endothelial cells (RIMECs) were determined after treatment with PD and its seven active ingredients, namely anemoside B4, anemonin, berberine, jatrorrhizine, palmatine, aesculin, and esculetin. RIMECs were challenged with lipopolysaccharide (LPS) at 1 µg ml?1 for 3 h and then treated with PD at 1, 5, and 10 mg ml?1 and its seven ingredients at 1, 5, and 10 µg ml?1 for 21 h, respectively. The results revealed that PD, anemonin, berberine, and esculetin inhibited the production of NO; PD, anemonin, and esculetin inhibited the secretion of ET‐1; PD, anemoside B4, berberine, jatrorrhizine, and aesculin downregulated TNF‐α expression; PD, anemoside B4, berberine, and palmatine decreased the content of IL‐1α. It showed that PD and its active ingredients could significantly inhibit the secretion of NO, ET‐1, TNF‐α, and IL‐1α in LPS‐induced RIMECs and suggested they would reduce inflammatory response via these cytokines. Copyright © 2009 John Wiley & Sons, Ltd. 相似文献
12.
Mei Dai Ze‐Hong Miao Xuan Ren Lin‐Jiang Tong Na Yang Ting Li Li‐Ping Lin Yue‐Mao Shen Jian Ding 《Journal of cellular and molecular medicine》2010,14(9):2281-2291
The macrolide compound MFTZ‐1 has been identified as a novel topoisomerase II (Top2) inhibitor with potent in vitro and in vivo anti‐tumour activities. In this study, we further examined the effects of MFTZ‐1 on hypoxia‐inducible factor‐1α (HIF‐1α) accumulation, vascular endothelial growth factor (VEGF) secretion and angiogenesis. MFTZ‐1 reduced HIF‐1α accumulation driven by hypoxia or growth factors in human cancer cells. Mechanistic studies revealed that MFTZ‐1 did not affect the degradation of HIF‐1α protein or the level of HIF‐1α mRNA. By contrast, MFTZ‐1 apparently inhibited constitutive and inducible activation of both phosphatidylinositol‐3‐kinase (PI3K)‐Akt and p42/p44 mitogen‐activated protein kinase (MAPK) pathways. Further studies revealed that MFTZ‐1 abrogated the HIF‐1α‐driven increase in VEGF mRNA and protein secretion. MFTZ‐1 also lowered the basal level of VEGF secretion. The results reveal an important feature that MFTZ‐1 can reduce constitutive, HIF‐1α‐independent VEGF secretion and concurrently antagonize inducible, HIF‐1α‐dependent VEGF secretion. Moreover, MFTZ‐1 disrupted tube formation of human umbilical vein endothelial cells (HUVECs) stimulated by hypoxia with low‐concentration serum or by serum at normoxia, and inhibited HUVECs migration at normoxia. MFTZ‐1 also prevented microvessel outgrowth from rat aortic ring. These data reflect the potent anti‐angiogenesis of MFTZ‐1 under different conditions. Furthermore, using specific small interfering RNA targeting Top2α or Top2‐defective HL60/MX2 cells, we showed that MFTZ‐1 affected HIF‐1α accumulation and HUVECs tube formation irrelevant to its Top2 inhibition. Taken together, our data collectively reveal that MFTZ‐1 reduces constitutive and inducible HIF‐1α accumulation and VEGF secretion possibly via PI3K‐Akt and MAPK pathways, eliciting anti‐angiogenesis independently of its Top2 inhibition. 相似文献
13.
《Peptide Science》2017,108(3)
The conformational characteristics of protected homo‐oligomeric Boc‐[β3(R)Val]n‐OMe, n = 1, 2, 3, 4, 6, 9, and 12 have been investigated in organic solvents using nuclear magnetic resonance (NMR), Fourier transform infrared (FTIR) absorption spectroscopy and circular dichroism (CD) methods. The detailed 1H NMR analysis of Boc‐[β3(R)Val]12‐OMe reveals that the peptide aggregates extensively in CDCl3, but is disaggregated in 20%, (v/v) dimethyl sulfoxide (DMSO) in CDCl3 and in CD3OH. Limited assignment of the N‐terminus NH groups, together with solvent dependence of NH chemical shifts and temperature coefficients provides evidence for 14‐helix conformation in the 12‐residue peptide. FTIR analysis in CHCl3 establishes that the onset of folding and aggregation, as evidenced by NH stretching bands at 3375 cm−1 (intramolecular) and 3285 cm−1 (intermolecular), begins at the level of the tetrapeptide. The observed CD bands, 214 nm (negative) and 198 nm (positive), support 14‐helix formation in the 9 and 12 residue sequences. The folding and aggregation tendencies of homo‐oligomeric α‐, β‐, and γ‐ residues is compared in the model peptides Boc‐[ωVal]n‐NHMe, ω = α, β, and γ and n = 1, 2, and 3. Analysis of the FTIR spectra in CHCl3, establish that the tendency to aggregate at the di and tripeptide level follows the order β > α∼γ, while the tendency to fold follows the order γ > β > α. 相似文献
14.
Weifeng Cao Yujue Wang Jianquan Luo Junxiang Yin Yinhua Wan 《Engineering in Life Science》2018,18(3):196-203
α, ω‐Dodecanedioic acid (DC12) usually serves as a monomer of polyamides or some special nylons. During the biosynthesis, oxygenation cascaded in conversion of hydrophobic n‐dodecane to DC12, while the oxidation of n‐dodecane took place in the intracellular space. Therefore, it was important to investigate the role of oxygen supply on the cell growth and DC12 biosynthesis. It was found that stirring speed and aeration influenced the dissolved oxygen (DO) concentration which in turn affected cell growth as well as DC12 biosynthesis. However, the effect of culture redox potential (Orp) level on DC12 biosynthesis was more significant than that of DO level. For DC12 biosynthesis, the first step was to form the emulsion droplets through the interaction of n‐dodecane and the cell. When the stirring speed was enhanced, slits in the surface layer of the emulsion droplets would be increased. Thus, the substances transportation by water through the slits would be intensified, leading to an enhanced DC12 production. Compared with the batch culture at a lower stirring speed (400 rpm) without culture redox potential (Orp) control, the DC12 concentration was increased by 5 times up to 201.3 g/L with Orp controlled above 0 mV at a higher stirring speed (800 rpm). 相似文献
15.
Xiaohui Yu Baoyin Jia Faqiang Wang Xiuxiu Lv Xuemei Peng Yiyang Wang Hongmei Li Yanping Wang Daxiang Lu Huadong Wang 《Journal of cellular and molecular medicine》2014,18(2):263-273
Cardiomyocyte tumour necrosis factor α (TNF‐α) production contributes to myocardial depression during sepsis. This study was designed to observe the effect of norepinephrine (NE) on lipopolysaccharide (LPS)‐induced cardiomyocyte TNF‐α expression and to further investigate the underlying mechanisms in neonatal rat cardiomyocytes and endotoxaemic mice. In cultured neonatal rat cardiomyocytes, NE inhibited LPS‐induced TNF‐α production in a dose‐dependent manner. α1‐ adrenoceptor (AR) antagonist (prazosin), but neither β1‐ nor β2‐AR antagonist, abrogated the inhibitory effect of NE on LPS‐stimulated TNF‐α production. Furthermore, phenylephrine (PE), an α1‐AR agonist, also suppressed LPS‐induced TNF‐α production. NE inhibited p38 phosphorylation and NF‐κB activation, but enhanced extracellular signal‐regulated kinase 1/2 (ERK1/2) phosphorylation and c‐Fos expression in LPS‐treated cardiomyocytes, all of which were reversed by prazosin pre‐treatment. To determine whether ERK1/2 regulates c‐Fos expression, p38 phosphorylation, NF‐κB activation and TNF‐α production, cardiomyocytes were also treated with U0126, a selective ERK1/2 inhibitor. Treatment with U0126 reversed the effects of NE on c‐Fos expression, p38 mitogen‐activated protein kinase (MAPK) phosphorylation and TNF‐α production, but not NF‐κB activation in LPS‐challenged cardiomyocytes. In addition, pre‐treatment with SB202190, a p38 MAPK inhibitor, partly inhibited LPS‐induced TNF‐α production in cardiomyocytes. In endotoxaemic mice, PE promoted myocardial ERK1/2 phosphorylation and c‐Fos expression, inhibited p38 phosphorylation and IκBα degradation, reduced myocardial TNF‐α production and prevented LPS‐provoked cardiac dysfunction. Altogether, these findings indicate that activation of α1‐AR by NE suppresses LPS‐induced cardiomyocyte TNF‐α expression and improves cardiac dysfunction during endotoxaemia via promoting myocardial ERK phosphorylation and suppressing NF‐κB activation. 相似文献
16.
Ann L Cornish Caroline E Sutton Joanne O'Donnell Louise H Cengia Andrew W Roberts Ian P Wicks Kingston H G Mills Ben A Croker 《EMBO reports》2010,11(8):640-646
Reports describing the effect of interferon‐γ (IFNγ) on interleukin‐1β (IL‐1β) production are conflicting. We resolve this controversy by showing that IFNγ potentiates IL‐1β release from human cells, but transiently inhibits the production of IL‐1β from mouse cells. Release from this inhibition is dependent on suppressor of cytokine signalling 1. IL‐1β and Th17 cells are pathogenic in mouse models for autoimmune disease, which use Mycobacterium tuberculosis (MTB), in which IFNγ and IFNβ are anti‐inflammatory. We observed that these cytokines suppress IL‐1β production in response to MTB, resulting in a reduced number of IL‐17‐producing cells. In human cells, IFNγ increased IL‐1β production, and this might explain why IFNγ is detrimental for multiple sclerosis. In mice, IFNγ decreased IL‐1β and subsequently IL‐17, indicating that the adaptive immune response can provide a systemic, but transient, signal to limit inflammation. 相似文献
17.
Wooi Koon Wang Mark Bycroft Nicholas W. Foster Ashley M. Buckle Alan R. Fersht Yu Wai Chen 《Acta Crystallographica. Section D, Structural Biology》2001,57(4):545-551
p73 is a homologue of the tumour suppressor p53 and contains all three functional domains of p53. The α‐splice variant of p73 (p73α) contains near its C‐terminus an additional structural domain known as the sterile α‐motif (SAM) that is probably responsible for regulating p53‐like functions of p73. Here, the 2.54 Å resolution crystal structure of this protein domain is reported. The crystal structure and the published solution structure have the same five‐helix bundle fold that is characteristic of all SAM‐domain structures, with an overall r.m.s.d. of 1.5 Å for main‐chain atoms. The hydrophobic core residues are well conserved, yet some large local differences are observed. The crystal structure reveals a dimeric organization, with the interface residues forming a mini four‐helix bundle. However, analysis of solvation free energies and the surface area buried upon dimer formation indicated that this arrangement is more likely to be an effect of crystal packing rather than reflecting a physiological state. This is consistent with the solution structure being a monomer. The p73α SAM domain also contains several interesting structural features: a Cys‐X‐X‐Cys motif, a 310‐helix and a loop that have elevated B factors, and short tight inter‐helical loops including two β‐turns; these elements are probably important in the normal function of this domain. 相似文献
18.
Sang Hee Han Jun Yong Ha Kyoung Hoon Kim Sung Jin Oh Do Jin Kim Ji Yong Kang Hye Jin Yoon Se‐Hee Kim Ji Hae Seo Kyu‐Won Kim Se Won Suh 《Acta Crystallographica. Section F, Structural Biology Communications》2006,62(11):1127-1130
N‐terminal acetylation is one of the most common protein modifications in eukaryotes, occurring in approximately 80–90% of cytosolic mammalian proteins and about 50% of yeast proteins. ARD1 (arrest‐defective protein 1), together with NAT1 (N‐acetyltransferase protein 1) and possibly NAT5, is responsible for the NatA activity in Saccharomyces cerevisiae. In mammals, ARD1 is involved in cell proliferation, neuronal development and cancer. Interestingly, it has been reported that mouse ARD1 (mARD1225) mediates ɛ‐acetylation of hypoxia‐inducible factor 1α (HIF‐1α) and thereby enhances HIF‐1α ubiquitination and degradation. Here, the preliminary X‐ray crystallographic analyses of two N‐terminal acetyltransferase‐related proteins encoded by the Ta0058 and Ta1140 genes of Thermoplasma acidophilum are reported. The Ta0058 protein is related to an N‐terminal acetyltransferase complex ARD1 subunit, while Ta1140 is a putative N‐terminal acetyltransferase‐related protein. Ta0058 shows 26% amino‐acid sequence identity to both mARD1225 and human ARD1235.The sequence identity between Ta0058 and Ta1140 is 28%. Ta0058 and Ta1140 were overexpressed in Escherichia coli fused with an N‐terminal purification tag. Ta0058 was crystallized at 297 K using a reservoir solution consisting of 0.1 M sodium acetate pH 4.6, 8%(w/v) polyethylene glycol 4000 and 35%(v/v) glycerol. X‐ray diffraction data were collected to 2.17 Å. The Ta0058 crystals belong to space group P41 (or P43), with unit‐cell parameters a = b = 49.334, c = 70.384 Å, α = β = γ = 90°. The asymmetric unit contains a monomer, giving a calculated crystal volume per protein weight (VM) of 2.13 Å3 Da−1 and a solvent content of 42.1%. Ta1140 was also crystallized at 297 K using a reservoir solution consisting of 0.1 M trisodium citrate pH 5.6, 20%(v/v) 2‐propanol, 20%(w/v) polyethylene glycol 4000 and 0.2 M sodium chloride. X‐ray diffraction data were collected to 2.40 Å. The Ta1140 crystals belong to space group R3, with hexagonal unit‐cell parameters a = b = 75.174, c = 179.607 Å, α = β = 90, γ = 120°. Two monomers are likely to be present in the asymmetric unit, with a VM of 2.51 Å3 Da−1 and a solvent content of 51.0%. 相似文献
19.
Human α‐defensin 6 (HD6), unlike other mammalian defensins, does not exhibit bactericidal activity, particularly against aerobic bacteria. Monomeric HD6 has a tertiary structure similar to other α‐defensins in the crystalline state. However, the physico‐chemical reasons behind the lack of antibacterial activity of HD6 are yet to be established unequivocally. In this study, we have investigated the antimicrobial activity of HD6 analogs. A linear analog of HD6, in which the distribution of arginine residues was similar to active α‐defensins, shows broad‐spectrum antimicrobial activity, indicating that atypical distribution of arginine residues contributes to the inactivity of HD6. Peptides spanning the N‐terminal cationic segment were active against a wide range of organisms. Antimicrobial potency of these shorter analogs was further enhanced when myristic acid was conjugated at the N‐terminus. Cytoplasmic localization of the analogs without fatty acylation was observed to be necessary for bacterial killing, while they exhibited fungicidal activity by permeabilizing Candida albicans membranes. Myristoylated analogs and the linear full‐length arginine analog exhibited activity by permeabilizing bacterial and fungal membranes. Our study provides insights into the lack of bactericidal activity of HD6 against aerobic bacteria. Copyright © 2015 European Peptide Society and John Wiley & Sons, Ltd. 相似文献
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Neelesh Sharma Hirofumi Suzuki Quanren He Raghubir P. Sharma 《Journal of biochemical and molecular toxicology》2006,19(6):359-367
Fumonisin B1 is a mycotoxin produced by Fusarium verticillioides, frequently associated with corn. It produces species‐specific and organ‐specific toxicity, including equine leukoencephalomalacia, porcine pulmonary edema, and hepatic or renal damage in most animal species. Fumonisin B1 perturbs sphingolipid metabolism by inhibiting ceramide synthase. Our previous studies indicated that fumonisin B1 caused localized activation of cytokines in liver produced by macrophages and other cell types that modulate fumonisin B1 induced hepatic apoptosis in mice. The role of tumor necrosis factor α (TNFα) in fumonisin B1 mediated hepatocyte apoptosis has been established; not much is known about the downstream events leading to apoptosis. In the current study, fumonisin B1 induced apoptosis in primary culture of liver cells. In consistence with previous reports, fumonisin B1 caused accumulation of sphingoid bases and led to increase in TNFα expression. Phosphorylated and total c‐Jun NH2‐terminal kinase (JNK) activities were increased after 24 h fumonisin B1 treatment. JNK inhibitor (SP600125) and anti‐TNFα reduced the apoptosis induced by fumonisin B1. The role of JNK signaling in fumonisin B1 induced apoptosis is downstream of TNFα production, as fumonisin B1‐mediated activation of JNK was reduced by the presence of anti‐TNFα in the medium, whereas the presence of JNK inhibitor did not change the fumonisin B1 induced TNFα expression. Results of this study imply that generation of fumonisin B1 induced TNFα results in modulation of mitogen activated protein kinases, particularly of JNK, and provides a possible mechanism for apoptosis in murine hepatocytes. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 19:359‐367, 2005; Published online in Wiley InterScience ( www.interscience.wiley.com ). DOI 10.1002/jbt.20102 相似文献