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Articles by J Wei
Total Records ( 3 ) for J Wei
  L Sun , X Shen , Y Liu , G Zhang , J Wei , H Zhang , E Zhang and F. Ma

The mechanism underlining human papillomaviruses (HPVs) causing cancer has been studied extensively, and it was concluded that the high-risk HPVs' E6 targeted and degraded tumor suppressor protein p53, leading to infected cells malignant transformation. In contrast, the low-risk HPVs only cause proliferative but non-invasive lesions of infected epithelia. Therefore, we hypothesized that low-risk HPVs' E6 might interact with p53 in a different pattern. We used a mammalian green fluorescent protein (GFP) expression system to express HPV-18E6 and HPV-6E6 fusion proteins in wild-type (wt) p53 cell lines, 293T and HEK293 cells, to investigate the traffic and location of E6s and p53. The results indicated GFP-18E6 was mainly expressed in nucleus, whereas GFP-6E6 was expressed exclusively in cytoplasm. Endogenous wt p53 was shown to be localized in the nuclei of cells transfected with GFP-18E6. Interestingly, for the first time, we observed that p53 was trapped in the cytoplasm and never translocated into the cell nuclei transfected with GFP-6E6. In conclusion, HPV-6E6 was responsible for the cytoplasmic localization of p53. Therefore, our experiments provide a new insight into the pathogenesis of HPV.

  J Wei , M Xu , D Zhang and H. Mi

Carotenoid isomerase (CRTISO) has been suggested to protect photosystem II (PS II) from photodamage, probably through its product lutein. However, the mechanism of the photoprotection still remains to be further elucidated. In this work, we cloned a point mutated gene reported to encode a CRTISO which is responsible for the accumulation of lutein in rice mutant zel1 by a map-based cloning approach. The mutant phenotype was rescued by transformation with the corresponding gene of the wild type (WT). The activity of photosynthetic oxygen evolution was evidently suppressed in zel1. The amount of the core protein of PS II CP47 was much lower in all the PS II complexes especially in the LHCII-PS II supercomplexes and CP43-free PS II of zel1 than that of WT. On the other hand, the amount of another core protein of PS II CP43 of zel1 was decreased in the higher supercomplexes, whereas it was increased in the lower ones and PS II monomer. The immunodetection displayed that CP43, CP47, and the oxygen-evolving extrinsic proteins PsbO and PsbP were reduced, but the amount of reaction center protein D1 did not show significant change in zel1. Northern blot analysis showed that the transcriptional level of CP43 was down-regulated but not that of CP47 or D1 in zel1. In addition, the plastoquinone (PQ) QA was in a reduced state in zel1. On the basis of the results, we suggest that CRTISO might function in regulating the transcription of CP43 and the translation of CP47 by affecting the redox state of the PQ to stabilize the extrinsic proteins of oxygen evolution complexes in the rice plant.

  X Huang , X Bai , Y Cao , J Wu , M Huang , D Tang , S Tao , T Zhu , Y Liu , Y Yang , X Zhou , Y Zhao , M Wu , J Wei , D Wang , G Xu , S Wang , D Ma and J. Zhou

Angiogenesis is increasingly recognized as an important prognosticator associated with the progression of lymphoma and as an attractive target for novel modalities. We report a previously unrecognized mechanism by which lymphoma endothelium facilitates the growth and dissemination of lymphoma by interacting with circulated T cells and suppresses the activation of CD4+ T cells. Global gene expression profiles of microdissected endothelium from lymphoma and reactive lymph nodes revealed that T cell immunoglobulin and mucin domain–containing molecule 3 (Tim-3) was preferentially expressed in lymphoma-derived endothelial cells (ECs). Clinically, the level of Tim-3 in B cell lymphoma endothelium was closely correlated to both dissemination and poor prognosis. In vitro, Tim-3+ ECs modulated T cell response to lymphoma surrogate antigens by suppressing activation of CD4+ T lymphocytes through the activation of the interleukin-6–STAT3 pathway, inhibiting Th1 polarization, and providing protective immunity. In a lymphoma mouse model, Tim-3–expressing ECs promoted the onset, growth, and dissemination of lymphoma by inhibiting activation of CD4+ T cells and Th1 polarization. Our findings strongly argue that the lymphoma endothelium is not only a vessel system but also a functional barrier facilitating the establishment of lymphoma immune tolerance. These findings highlight a novel molecular mechanism that is a potential target for enhancing the efficacy of tumor immunotherapy and controlling metastatic diseases.

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