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Articles by X He
Total Records ( 6 ) for X He
  J Lan , S Hua , X He and Y. Zhang

In mammals, DNA methylation, characterized by the transfer of the methyl group from S-adenosylmethionines to a base (mainly referred to cytosine), acts as a major epigenetic modification. In parallel to DNA sequences arrangement, modification of methylation to DNA sequences has far-reaching influence on biological functions and activities, for it involves controlling gene transcription, regulating chromatin structure, sustaining genome stability and integrity, maintaining parental imprinting and X-chromosome inactivation, suppressing homologous recombination as well as limiting transposable elements, during which DNA methyltransferases (DNMTs) and methyl-binding proteins play important roles. Their aberrance can give rise to dysregulation of gene expression, cell maltransformation and so on. Hence, it is necessary to gain a good understanding of these two important kinds of proteins, which will help to better investigate the epigenetic mechanisms and manipulate the modifications according to our will based on its reversibility. Here we briefly review our current understanding of DNMTs and methyl-binding proteins in mammals.

  D Ouyang , X He , L Xu , X Wang , Q Gao and H. Guo

The major histocompatibility complex class I allele Mamu-B*17 of rhesus macaques is an elite controller of simian immunodeficiency virus (SIV) infection whereas Mamu-B*01 has no inhibitory effect on SIV replication. The mechanism is still elusive. In this study, the so-called ‘missing G’ in the leading peptide sequence of Mamu-B*1703 allele was artificially inserted back through PCR amplification, and the new sequence was renamed as Mamu-B*1703(+G). The plasmids harboring Mamu-B*1703, Mamu-B*1703(+G) and Mamu-B*0101 cDNA sequence fused to EGFP gene were transfected into K562 and Cos-7 cells, respectively. Our data showed that these plasmids had similar transfection efficiencies and expression potentials in K562 cells, but the surface density of Mamu-B*1703 complexes, which was slightly influenced by the artificial change of the leading peptide length, was much higher than that of Mamu-B*0101 molecules. These results might partially account for the differential effects of Mamu-B*17 and Mamu-B*01 alleles on SIV replication in rhesus macaques.

  P Liu , A Khurana , R Rattan , X He , S Kalloger , S Dowdy , B Gilks and V. Shridhar

We recently identified HSulf-1 as a down-regulated gene in ovarian carcinomas. Our previous analysis indicated that HSulf-1 inactivation in ovarian cancers is partly mediated by loss of heterozygosity and epigenetic silencing. Here, we show that variant hepatic nuclear factor 1 (vHNF1), encoded by transcription factor 2 gene (TCF2, HNF1β), negatively regulates HSulf-1 expression in ovarian cancer. Immunoblot assay revealed that vHNF1 is highly expressed in HSulf-1–deficient OV207, SKOV3, and TOV-21G cell lines but not in HSulf-1–expressing OSE, OV167, and OV202 cells. By short hairpin RNA–mediated down-regulation of vHNF1 in TOV-21G cells and transient enhanced vHNF1 expression in OV202 cells, we showed that vHNF1 suppresses HSulf-1 expression in ovarian cancer cell lines. Reporter assay and chromatin immunoprecipitation experiments showed that vHNF1 is specifically recruited to HSulf-1 promoter at two different vHNF1-responsive elements in OV207 and TOV-21G cells. Additionally, down-regulation of vHNF1 expression in OV207 and TOV-21G cells increased cisplatin- or paclitaxel-mediated cytotoxicity as determined by both 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and clonogenic assays and this effect was reversed by down-regulation of HSulf-1. Moreover, nude mice bearing TOV-21G cell xenografts with stably down-regulated vHNF1 were more sensitive to cisplatin- or paclitaxel-induced cytotoxicity compared with xenografts of TOV-21G clonal lines with nontargeted control short hairpin RNA. Finally, immunohistochemical analysis of 501 ovarian tumors including 140 clear-cell tumors on tissue microarrays showed that vHNF1 inversely correlates to HSulf-1 expression. Collectively, these results indicate that vHNF1 acts as a repressor of HSulf-1 expression and might be a molecular target for ovarian cancer therapy. [Cancer Res 2009;69(11):4843–50]

  X He , Z Gu and Y. Zhu

We consider the task model of periodic tasks running on a network of processor nodes connected by a bus based on the time-triggered protocol, an industry-standard bus protocol designed for safety-critical automotive and avionics distributed embedded systems, and present an integrated optimization framework that jointly considers one or more of the following attributes: task-to-processor allocation, task priority assignment, task period assignment and bus access configuration. We adopt a hierarchical optimization framework, where each possible task allocation and priority assignment is treated as one top-level coarse-grained state, which may contain many lower-level fine-grained states defined by different task period assignments and bus access configurations. Simulated annealing is used to explore the top-level states, which calls a geometric programming solver as a subroutine to explore the lower-level states contained within a given top-level state. Performance evaluation shows that our framework has good performance in terms of solution quality and scalability.

  Z. A Rasheed , J Yang , Q Wang , J Kowalski , I Freed , C Murter , S. M Hong , J. B Koorstra , N. V Rajeshkumar , X He , M Goggins , C Iacobuzio Donahue , D. M Berman , D Laheru , A Jimeno , M Hidalgo , A Maitra and W. Matsui

Specific populations of highly tumorigenic cells are thought to exist in many human tumors, including pancreatic adenocarcinoma. However, the clinical significance of these tumor-initiating (ie, cancer stem) cells remains unclear. Aldehyde dehydrogenase (ALDH) activity can identify tumor-initiating cells and normal stem cells from several human tissues. We examined the prognostic significance and functional features of ALDH expression in pancreatic adenocarcinoma.


ALDH expression was analyzed by immunohistochemistry in 269 primary surgical specimens of pancreatic adenocarcinoma and examined for association with clinical outcomes and in paired primary tumors and metastatic lesions from eight pancreatic cancer patients who had participated in a rapid autopsy program. The clonogenic growth potential of ALDH-positive pancreatic adenocarcinoma cells was assessed in vitro by a colony formation assay and by tumor growth in immunodeficient mice (10–14 mice per group). Mesenchymal features of ALDH-positive pancreatic tumor cells were examined by using quantitative reverse transcription–polymerase chain reaction and an in vitro cell invasion assay. Gene expression levels and the invasive potential of ADLH-positive pancreatic cancer cells relative to the bulk cell population were examined by reverse transcription–polymerase chain reaction and an in vitro invasion assays, respectively. All statistical tests were two-sided.


ALDH-positive tumor cells were detected in 90 of the 269 primary surgical specimens, and their presence was associated with worse survival (median survival for patients with ALDH-positive vs ALDH-negative tumors: 14 vs 18 months, hazard ratio of death = 1.28, 95% confidence interval = 1.02 to 1.68, P = .05). Six (75%) of the eight patients with matched primary and metastatic tumor samples had ALDH-negative primary tumors, and in four (67%) of these six patients, the matched metastatic lesions (located in liver and lung) contained ALDH-positive cells. ALDH-positive cells were approximately five- to 11-fold more clonogenic in vitro and in vivo compared with unsorted or ALHD-negative cells, expressed genes consistent with a mesenchymal state, and had in vitro migratory and invasive potentials that were threefold greater than those of unsorted cells.


ALDH expression marks pancreatic cancer cells that have stem cell and mesenchymal features. The enhanced clonogenic growth and migratory properties of ALDH-positive pancreatic cancer cells suggest that they play a key role in the development of metastatic disease that negatively affects the overall survival of patients with pancreatic adenocarcinoma.

  I Engel , K Hammond , B. A Sullivan , X He , I Taniuchi , D Kappes and M. Kronenberg

Mouse natural killer T (NKT) cells with an invariant V14-J18 rearrangement (V14 invariant [V14i] NKT cells) are either CD4+CD8 or CD4CD8. Because transgenic mice with forced CD8 expression in all T cells exhibited a profound NKT cell deficit, the absence of CD8 has been attributed to negative selection. We now present evidence that CD8 does not serve as a coreceptor for CD1d recognition and that the defect in development in CD8 transgene homozygous mice is the result of a reduction in secondary T cell receptor rearrangements. Thymocytes from mice hemizygous for the CD8 transgene have a less severe rearrangement defect and have functional CD8+ V14i NKT cells. Furthermore, we demonstrate that the transcription factor Th, Poxviruses and Zinc finger, and Krüppel family (Th-POK) is expressed by V14i NKT cells throughout their differentiation and is necessary both to silence CD8 expression and for the functional maturity of V14i NKT cells. We therefore suggest that Th-POK expression is required for the normal development of V14i NKT cells and that the absence of CD8 expression by these cells is a by-product of such expression, as opposed to the result of negative selection of CD8-expressing V14i NKT cells.

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