Biomedical subjects

Wei Yi

Publications and source records attributed to Wei Yi.

At least 19 recordsLinked to original sources

PubMed2026

CTRP9 ameliorates heart failure with preserved ejection fraction by regulating lipid metabolism.

BACKGROUND: Heart failure with preserved ejection fraction (HFpEF) is a major clinical challenge, with cardiac lipotoxicity emerging as a key driver of disease progression. Despite CTRP9’s role in lipid metabolism and cardioprotective properties, its therapeutic potential in HFpEF remains unexplored. This study aimed to investigate whether CTRP9 ameliorates HFpEF by regulating cardiac lipid metabolism and to identify the underlying molecular mechanisms. METHODS: In the established two-hit HFpEF mouse model (induced by a high-fat diet and L-NAME), the mice were treated with either CTRP9 or saline. Cardiac function was evaluated by echocardiography, while hypertrophy, fibrosis, and lipid accumulation were assessed using histology and molecular assays. Proteomic sequencing was further employed to identify downstream targets of CTRP9. RESULTS: CTRP9 treatment significantly improved diastolic function and attenuated cardiac hypertrophy and fibrosis in HFpEF mice. Myocardial lipid accumulation was substantially reduced, accompanied by enhanced fatty acid oxidation. Proteomic analysis identified GPD1 as a key downstream target upregulated by CTRP9. Cardiac-specific knockdown of GPD1 partly abolished the therapeutic benefits of CTRP9. CONCLUSION: Our data suggest that CTRP9 ameliorates HFpEF through GPD1-mediated regulation of cardiac lipid metabolism, identifying the CTRP9-GPD1 axis as a promising therapeutic target for HFpEF.

Animals↗

PubMed2007

Emergency endovascular repair of iliac artery rupture caused by post-stenting angioplasty with an endograft.

Iliac artery rupture is a rare complication of post-stenting angioplasty and can lead to massive life-threatening haemorrhage. Conventional surgery can not repair the damaged vessel easily and may cause substantial blood loss and high operative morbidity and mortality. We report our experience with a self-expanding covered endoprosthesis for endovascular repair of the rupture of an iliac artery caused by stenting angioplasty.

Aged, 80 and over↗

PubMed2006

Radiotherapy-related typing in 842 patients in canton with nasopharyngeal carcinoma.

PURPOSE: The aim of this study was to propose the clinical radiotherapy-related typing and to summarize proportional distribution of radiotherapy-related types of nasopharyngeal carcinoma (NPC). METHODS AND MATERIALS: A total of 842 cases of NPC were randomly selected. According to 5-year follow-up results after radiotherapy, NPC was subdivided into four types: Type I (no primary and regional recurrence and no distant metastasis), Type II (primary or regional recurrence and no distant metastasis), Type III (no primary and regional recurrence, and distant metastasis), and Type IV (primary or regional recurrence, and distant metastasis). Proportion of the four types and relationship between this typing and Zhi-guang Xie typing were analyzed. RESULTS: Distribution of radiotherapy-related types of NPC were 50.6%, 23.2%, 20.7%, and 5.6% for Types I, II, III, and IV, respectively. For Types D and AD of Zhi-guang Xie typing system and Stage III and IV of the 1992 Fuzhou staging system, the proportion of Type III was greater than that of Type II; and for Type A and Stage I and II, there was a larger proportion of Type II than that of Type III. CONCLUSION: Radiotherapy-related typing, as a new clinical subclassification, could be supplementary for previous clinical typing and staging.

Adolescent↗

PubMed2006

Physical and functional interaction between hMSH5 and c-Abl.

Despite being a member of the mismatch repair family of proteins, the biological functions of hMSH5 in human cells are presently elusive. Here, we report a novel physical and functional interaction between hMSH5 and c-Abl; the latter is a critical non-receptor tyrosine kinase involved in many critical cellular functions including DNA damage response, in which the kinase activity is normally suppressed in the absence of biological challenges. Our data indicate that hMSH5 associates with c-Abl in vivo, which is mediated by a direct physical interaction between the NH2 terminus (residues 1-109) of hMSH5 and the c-Abl SH3 domain. This physical interaction facilitates the activation of c-Abl tyrosine kinase and the phosphorylation of hMSH5 in response to ionizing radiation. Our data also indicate that the hMSH5 P29S variant overactivates the c-Abl tyrosine kinase activity. Furthermore, it seems that the tyrosine phosphorylation of hMSH5 promotes the dissociation of hMSH4-hMSH5 heterocomplex. Together, the revealed physical and functional interaction of hMSH5 with c-Abl implies that the interplay between hMSH5 and c-Abl could manipulate cellular responses to ionizing radiation-induced DNA damages.

Cell Cycle Proteins↗

PubMed2006

[Experimental study on effects of electro-acupuncture in improving synaptic plasticity in focal cerebral ischemia rats].

OBJECTIVE: To explore the mechanisms of electro-acupuncture (EA) in improving synaptic plasticity after cerebral ischemic injury. METHODS: Focal cerebral ischemia (FCI) model was established by middle cerebral artery occlusion (MCAO) with heat-coagulation method. The changing rules of synaptic ultrastructure, synaptophysin (P38), growth-associated protein-43 (GAP-43), brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the ischemic cortex 2 and 5 weeks after FCI and the effects of EA on them were observed. RESULTS: Expression of numerical density (Nv), surface density (Sv), volume density (Vv), post synaptic density (PSD) and P38 in the ischemic cortex significantly decreased after MCAO (P<0.01). Among them, Nv and Sv were raised at the 5th week in FCI rats either treated or untreated with EA (P<0.01), but the increment of Sv was higher in those of the treated rats (P<0.01); PSD in the EA treated rats also showed a significant increase at the 5th week, which was significant higher than that in those untreated; EA showed insignificant influence on Vv and synaptic interfacial curvature; P38 lowered continuously after 2 weeks, but at the 5th week, it was higher in EA treated rats than that in untreated rats (P<0.01), while at the 2nd week, the levels in treated and untreated rats were equal. GAP-43 rose in the 2nd week after modeling, with no difference between EA treated and untreated animals, at the 5th week, it was lowered in untreated rats to near that in sham-operated rats, but maintained at higher level in EA treated rats; NGF and BDNF positive cells significantly increased after modeling (P<0.01), and showed a descending trend with the time going (P<0.01) both in rats treated or untreated with EA. CONCLUSION: EA can protect synaptic ultrastructure, promote the expression of P38, GAP-43, NGF and BDNF in the ischemic cerebral cortex, and thus improve synaptic plasticity in cerebral ischemic rats.

Acupuncture Therapy↗

PubMed2005

Formation of hMSH4-hMSH5 heterocomplex is a prerequisite for subsequent GPS2 recruitment.

Increasing evidence suggests that components of the DNA mismatch repair (MMR) pathway play multifunctional roles beyond the scope of mismatch correction, including the modulation of cellular responses to DNA damage and homologous recombination. The heterocomplex consisting of MutS homologous proteins, hMSH4 and hMSH5, is believed to play essential roles in meiotic DNA repair particularly during the process of meiotic homologous recombination (HR). In order to gain a better understanding of the mechanistic basis underlying the roles of these two human MutS proteins, we have identified G-protein pathway suppressor 2 (GPS2) (i.e., an integral component of a deacetylase complex) as an interacting protein partner specifically for the hMSH4-hMSH5 heterocomplex. The interaction with GPS2 is entirely dependent on the physical association between hMSH4 and hMSH5, as disruption of the interaction between hMSH4 and hMSH5 completely abolishes GPS2 recruitment. Our analysis further indicates that the association with GPS2 is mediated through the interface of hMSH4-hMSH5 complex and the N-terminal region of GPS2. Moreover, these three proteins interact in human cells, and analysis of microarray data suggested a coordinated expression pattern of these genes during the onset of meiosis. Together, the results of our present study suggest that the GPS2-associated deacetylase complex might function in concert with hMSH4-hMSH5 during the process of homologous recombination.

Blotting, Western↗

PubMed2005

Doubly ortho-linked quinoxaline/triarylamine hybrid as a bifunctional, dipolar electroluminescent template for optoelectronic applications.

The titled hybrid (Q-H) works as a clippable optoelectronic unit. Q-spacer-Q systems function as efficient orange emitters reaching EL intensities (L) of up to 6840 cd m-2 with etaext of 0.77% and operation efficiencies of 1.60 cd A-1 and 0.8 lm W-1. Notably, Q-An acts as a (bluish) green emitter, reaching L of 12347 cd m-2 with similar operational efficiency.

Journal Article↗

PubMed2005

Two variants of MutS homolog hMSH5: prevalence in humans and effects on protein interaction.

MSH5 is known to play functional roles in an array of cellular processes such as DNA damage response and meiotic homologous recombination. Here, we report the characterization of an hMSH5 splicing variant (hMSH5sv) that resulted from the retention of the last 51 bp of hMSH5 intron 6, in which the encoded 17-amino acid insertion between codons 179 and 180 does not compromise its capability to interact with hMSH4. We have also identified an hMSH5 polymorphism (C85T) [corrected] that altered codon 29 of the hMSH5 gene resulting in a proline-to-serine change (P29S). The interaction domains of hMSH4 and hMSH5 have also been resolved. The P29S alteration is located within the interacting domain and leads to a weakened protein interaction with hMSH4. Together, our present study revealed the existence of two forms of hMSH5 variants in human cells. The different properties associated with these two hMSH5 variants underscore the potential functional diversity of the human hMSH5 gene.

Amino Acid Sequence↗

PubMed2005

Basic fibroblast growth factor and fibroblast growth factor receptor-i in human meningiomas.

The expression of basic fibroblast growth factor (bFGF) and fibroblast growth factor receptor-1 (FGFR-1) in human meningiomas and the relationships between their expression and the tumors' histological features and angiogenesis were investigated by means of immunohistochemical technique. The expression of bFGF and FGFR-1 was detected by antibody of bFGF or FGFR-1. The tumors' angiogenesis was evaluated by microvascular density (MVD) and, which was observed by use of CD34-antibody immunohistochemically. The results showed that there were varied degrees of the expression of bFGF and FGFR-1 proteins in meningiomas. The expression was correlated with the tumors' histological characters and angiogenesis. It was concluded that bFGF and FGFR-1 might play important roles in meningiomas' angiogenesis and proliferation. The expression positive rate of bFGF and FGFR-1 may provide an indication of evaluating the histological and malignant degree of the tumor.

Adolescent↗

PubMed2005

Epstein-Barr virus encoded latent membrane protein 1 modulates nuclear translocation of telomerase reverse transcriptase protein by activating nuclear factor-kappaB p65 in human nasopharyngeal carcinoma cells.

Sustained proliferation of cancer cells requires that telomerase maintain chromosomal stability and prolong telomere length-regulated cell replication. Human telomerase reverse transcriptase (hTERT), the human telomerase catalytic subunit, and also the key determinant of the enzymatic activity of human telomerase, is regulated both at the transcriptional level and via phosphorylation and translocation. In this study, we show that latent membrane protein 1 (LMP1), the principal oncoprotein of Epstein-Barr virus (EBV), modulates telomerase activity by inducing the direct binding of hTERT to nuclear factor kappaB (NF-kappaB) p65 and translocation of both proteins from the cytoplasm to the nucleus in nasopharyngeal carcinoma cells (NPC). Conversely, a NF-kappaB nuclear translocation inhibitor, (benzylcarbonyl)-Leu-Leu-phenylalaninal (Z-LLF-CHO), and a dominant negative mutant of inhibitor of NFkappaB (IkappaBalpha), can block LMP1-induced hTERT nuclear translocation. These studies suggest a novel function of LMP1 and confirm that NF-kappaB plays an important role in regulating the activation and nuclear translocation of telomerase in NPC cells.

Antigens, Viral↗

PubMed2004

Epstein-Barr virus latent membrane protein 1 modulates epidermal growth factor receptor promoter activity in a nuclear factor kappa B-dependent manner.

The Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) oncoprotein may cause multiple cellular changes including the induction of epidermal growth factor receptor (EGFR) expression and activation of the NFkappaB transcription factor. LMP1 increases the levels of both EGFR protein and mRNA, but does not stabilize EGFR mRNA. Thus, the effects of LMP1 are likely to be mediated by the direct activation of the EGFR promoter. In this study, induction of LMP1 increased the EGFR in both protein and promoter levels in a dose-dependent manner using tetracycline-regulated LMP1 expression in nasopharyngeal carcinoma (NPC) cell line. Mutational analysis of the LMP1 protein indicated that the C-terminal activation region-1 (CTAR1) domain was mainly involved in the EGFR promoter induction, while CTAR2 was necessary but not sufficient to induce EGFR promoter. Inhibition of LMP1-mediated NFkappaB activation by constitutive repressive IkappaBalpha marginally decreased EGFR promoter activity using transiently transfected IkappaBalpha dominant negative mutant. Promoter mutagenesis analysis demonstrated that two putative NFkappaB binding sites of EGFR promoter were very necessary for the transcriptional activity of EGFR induced by LMP1, the proximal NFkappaB binding site was more important than the distal NFkappaB binding site, and both NFkappaB binding sites played a cooperative role. Taken together, Epstein-Barr virus latent membrane protein 1 modulated the EGFR promoter activity in a NFkappaB-dependent manner.

Base Sequence↗

PubMed2004

Nuclear factor kappa B (NFkappaB) dependent modulation of Epstein-Barr virus latent membrane protein 1 (LMP1) in epidermal growth factor receptor (EGFR) promoter activity.

The Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) oncoprotein may cause multiple cellular changes, including the induction of epidermal growth factor receptor (EGFR) expression and the activation of the nuclear factor kappa B (NFkappaB) transcription factor. LMP1 increases the levels of both EGFR protein and mRNA but does not stabilize EGFR mRNA. Thus the effects of LMP1 are likely to be mediated by direct activation of the EGFR promoter. In this study, induction of LMP1 increased the EGFR in both protein and promoter levels in a dose dependent manner using tetracycline-regulated LMP1 expression in nasopharyngeal carcinoma (NPC) cell line. Mutational analysis of the LMP1 protein indicated that the C-terminal activation region-1 (CTAR1) domain was mainly involved in the EGFR promoter induction, while CTAR2 was necessary but not sufficient to induce EGFR promoter. Inhibition of LMP1 mediated NFkappaB activation by constitutive repressive inhibitory kappa B alpha (IkappaBalpha) marginally decreased EGFR promoter activity using transiently transfected IkappaBalpha dominant negative mutant. Promoter mutagenesis analysis demonstrated that two putative NFkappaB binding sites of EGFR promoter were very necessary for the transcriptional activity of EGFR induced by LMP1, the proximal NFkappaB binding site was more important than the distal NFkappaB binding site. Taken together, Epstein-Barr virus latent membrane protein 1 modulated the EGFR promoter activity in a NFkappaB dependent manner.

Cell Line↗

PubMed2004

[Iodine-131 therapy for large goiter with hyperthyroidism: clinical observation of 38 cases].

OBJECTIVE: To evaluate the therapeutic efficacy and safety of iodine-131 therapy for large goiter complicated by hyperthyroidism. METHODS: After the diagnosis of large goiter complicated by hyperthyroidism was established, the weight of the patient's thyroid gland was determined, and the doses of iodine-131 calculated according to the formula currently available. After a single dose of oral iodine-131 capsule, the patients were observed for the therapeutic efficacy and side effects. Some patients were given the second or even the third dose of iodine-131. RESULTS: All of the 38 patients were cured by 1 to 3 single doses of iodine-131 therapy, of whom 23 (60.5%) needed only a single dose for the cure, 13 (34.2%) required the second dose, and 2 (5.3%) necessitate a third dose. Hypothyroidism occurred in 4 cases (10.5%), and none of the patients developed hyperthyroidism crisis and dyspnea. CONCLUSIONS: Iodine-131 therapy for serious goiter with hyperthyroidism is safe and effective, which can be used as a routine therapy for this condition.

Adult↗

PubMed2004

[Difference and significance of T-lymphocyte subsets in differential diagnosis between severe acute respiratory syndrome and common atypical pneumonia].

BACKGROUND: To clarify the difference and significance of T-lymphocyte subsets in differential diagnosis between severe acute respiratory syndrome SARS) and common atypical pneumonia. METHODS: Totally 100 patients hospitalized in Beijing Ditan Hospital since March to June 2003 with clinical diagnosis of SARS were involved in this study. These patients courses of disease were over 3 weeks. These patients were divided into two groups, SARS group and common atypical pneumonia group (non-SARS group). The counts of CD3+, CD4+ and CD8+ T-lymphocyte of two groups were systematically recorded and analyzed. RESULTS: Sixty-five of the patients were confirmed to have common type of SARS, including 26 males and 39 females, 50 cases received methylprednisolone treatment. Thirty-five cases had common atypical pneumonia (non-SARS), 21 were males while 14 were females, 20 cases received methylprednisolone treatment. All the cases of two groups were cured in the end. The SARS patients T-lymphocyte counts decreased first and then increased. Before 15 days of disease course, mean CD3+, CD4+, CD8+ T-lymphocyte counts of SARS patients were decreased apparently (694+/-568/microl, 441+/-356/microl, 309+/-462/microl). After 15th day of disease course, the counts gradually returned to normal CD3+, CD4+, CD8+ T-lymphocyte counts of non-SARS patients were normal. Compared with patients of the same group who were not treated with glucocorticoids, T-lymphocyte counts of non-SARS patients treated with glucocorticoids had no obvious difference. But glucocorticoids had some effect on SARS patients recovery of cellular immune function, i.e., it delayed the recovery by about 6 days. CONCLUSION: With or without treatment with glucocorticoids,the lowered CD3+, CD4+, CD8+ T-lymphocyte counts in the early stage are of very important significance in differential diagnosis between severe acute respiratory syndrome and common atypical pneumonia.

Adult↗

PubMed2003

Epstein-Barr virus encoded latent membrane protein 1 induces TRAF1 expression to promote anti-apoptosis activity via NF-kappaB signaling pathway in nasopharyngeal carcinoma.

OBJECTIVES: To identify whether Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor-associated factor 1 (TRAF1) expression and promote its anti-apoptosis activity via the NF-kappaB signaling pathway, and assess that LMP1 suppresses apoptosis in nasopharyngeal carcinoma (NPC). METHODS: A stable transfected cell line HNE2-LMP1 was established by introducing LMP1 cDNA into HNE2 cells. Transactivation of TRAF1 was determined by luciferase reporter assay, while expression of TRAF1 mRNA was detected by RT-PCR and expression of TRAF1 protein and caspase 3 by Western blot analysis. Apoptosis activity was observed through fluorescence staining. RESULTS: LMP1 induced TRAF1 expression in NPC cells and caused a decrease in apoptosis. This induction could be blocked by antisense LMP1. Moreover, LMP1-mediated induction of a TRAF1 promoter-driven reporter gene was significantly impaired when the kappaB site kappaB1 or kappaB5 was disrupted, whereas mutation of kappaB3 had only a minor effect on LMP1 dependent up-regulation of the reporter gene. CONCLUSION: LMP1 induces TRAF1 expression and promotes its anti-apoptosis activity via the NF-kappaB signaling pathway, which may be one of the mechanisms that LMP1 uses to suppress apoptosis in NPC cells.

Apoptosis↗

PubMed2003

[Epstein-Barr virus inhibits P16INK4a expression in human fetal nasopharyngeal epithelial cells escaping from the replicative senenscence].

Cell cycle deregulation is regarded as an important event to involve in cellular immortalization. To confirm the role of cell cycle deregulation in human fetal nasopharyngeal epithelial cells escaping from the replicative senescence induced by Epstein-Barr virus infection, we detected expression of cell cycle regulators, such as p16INK4a, p21WAF1/CIP1, p53, and E2F1 with Western blotting and immunocytochemisty in this study. Our results found that Epstein-Barr virus inhibited the expression of p16INK4a, at the same time, E2F1 expression were strongly increased in EBV-infected cells, however, as for the expression of p53 and p21WAF1/CIP1, there was no difference between EBV-infected cells and non-infected cells. The results show that EBV inactivates p16INK4a/pRB pathway and then induces E2F1 activity and it is implicated that Epstein-Barr virus-medicated cell cycle deregulation plays an important role in the immortalization of human nasopharyngeal epithelial cells. These data will be helpful for further studying the carcinogenesis of nasopharyngeal carcinoma.

Cell Transformation, Neoplastic↗

PubMed2002

[Matrix metalloproteinase 9 expression is induced by Epstein-Barr virus LMP1 via NF-kappa B or AP-1 signaling pathway in nasopharyngeal carcinoma cells].

OBJECTIVE: To clarify if Epstein-Barr virus encoded LMP1 induces matrix metalloproteinase 9 expression via NF-kappa B or AP-1 signaling pathway, which gives evidence to the elucidation of the mechanism of LMP1- mediated carcinogenesis. METHODS: To determine whether LMP1 or its mutants contribute to MMP9 production via NF-kappa B or AP-1 transcription factor, MMP9-chloramphenicol acetyl transferase (CAT), NF-kappa B mut 9-CAT, AP-1 mut MMP9-CAT were transfected into human nasopharyngeal carcinoma cells stably expressing LMP1 (HNE2-LMP1) or its mutants, [HNE2-LMP1 (1-185), HNE2-LMP1 (1-231), HNE2-LMP1 delta 187-351] by electroporation technic. The difference of MMP9 reporter activity among those cell lines was detected by CAT assay and expression of MMP9 was determined in nasopharyngeal carcinoma cells stably expressing LMP1 or its mutants by zymographic analysis. In the meantime, efforts were made to demonstrate if LMP1 regulates NF-kappa B or AP-1 activation using reporter gene analysis. RESULTS: In contrast with vector-transfected cells, MMP9 CAT activity in HNE2-LMP1, HNE2-LMP1 (1-185), HNE2-LMP1(1-231), HNE2-LMP1 delta 187-351 increased 7.2, 1.3, 3.3, 4.0 times respectively. Zymographic analysis demonstrated that the 92 kDa MMP9 expression was induced in HNE2-LMP1, HNE2-LMP1(1-231) and HNE2-LMP1 delta 187-351 cells, whereas it was negative in HNE2-pSG5 and HNE2-LMP1 (1-185) cells. As compared to the HNE2 cells, NF-kappa B or AP-1 reporter activity in HNE2-LMP1 cells were increased 13.8, 8.4 fold respectively. Moreover, In contrast with MMP9 CAT-transfected cells, MMP9 CAT activity in NF-kappa B mut MMP9-CAT or AP-1 mut MMP9-CAT transfected HNE2-LMP1, HNE2-LMP1 (1-185), HNE2-LMP1(1-231) and HNE2-LMP1 delta 187-351 cells were significantly decreased by 18.1% or 16.3%, 35.0% or 33.3%, 29.1% or 26.1% from the original level. However, there was no difference in NF-kappa B mut MMP9-CAT or AP-1 mut MMP9-CAT transfected HNE2-pSG5, HNE2-LMP1 (1-185) cells. CONCLUSION: In nasophargyngeal carcinoma, Epstein-Barr virus-encoded LMP1 induces MMP9 transcription and enzymatic activity via an NF-kappa B or AP-1 signaling pathway, which may contribute to invasiveness and metastasis.

Gene Expression↗

PubMed2002

[EB virus encoded latent membrane protein 1 modulates the phosphorylation of epidermal growth factor receptor in nasopharyngeal carcinoma cell line].

OBJECTIVE: To elucidate the regulation of the phosphorylation of epidermal growth factor receptor (EGFR) by the EB virus encoded latent membrane protein 1 (LMP1) in nasopharyngeal carcinoma cell line. METHODS: The levels of EGFR expression and phosphorylation in pTet-on LMP1 HNE2 cell, a nasopharyngeal carcinoma (NPC) cell line, in the dynamic expression of LMP1 induced by different concentrations of doxycycline (Dox) were observed. The EGFR dominant negative mutant and LMP1 antisense expression plasmid were transiently transfected into pTet-on LMP1 HNE2 cells by lipofectamine, and the changes in EGFR phosphorylation were observed by immunocoprecitation and Western blot. The changes in EGFR phosphorylation were observed after EGF treatment. RESULTS: In pTet-on LMP1 HNE2 cells, Dox-induced LMP1 upregulated EGFR expression and phosphorylation in a dose-dependent manner. After EGFR dominant negative mutant was transfected into pTet-on LMP1 HNE2 cells, the increase of EGFR phosphorylation was inhibited completely. When LMP1 antisense expression plasmid was transfected into pTet-on LMP1 HNE2 cells, the levels of EGFR phosphorylation were also inhibited significantly. Meanwhile, after EGF had been added into pTet-on LMP1 HNE2 cells, increase of EGFR phosphorylation was induced, but it was completely blocked by EGFR dominant negative mutant and the introduction of LMP1 antisense. CONCLUSION: EB virus encoded LMP1 not only induces the dose-dependent expression of EGFR, but also the dose-dependent phosphorylation of EGFR. The phosporylation of EGFR may play a vital role in the development of nasopharyngeal carcinoma.

Blotting, Western↗