1. Calreticulin promotes angiogenesis via activating nitric oxide signalling pathway in rheumatoid arthritis.

    Clinical and Experimental Immunology 178(2):236 (2014) PMID 24988887 PMCID PMC4233373

    Calreticulin (CRT) is a multi-functional endoplasmic reticulum protein implicated in the pathogenesis of rheumatoid arthritis (RA). The present study was undertaken to determine whether CRT was involved in angiogenesis via the activating nitric oxide (NO) signalling pathway. We explored the prof...
  2. Thiol peroxidases ameliorate LRRK2 mutant-induced mitochondrial and dopaminergic neuronal degeneration in Drosophila.

    Human Molecular Genetics 23(12):3157 (2014) PMID 24459295 PMCID PMC4030771

    Mutations in leucine-rich repeat kinase 2 (LRRK2) are common causes of familial Parkinson's disease (PD). LRRK2 has been shown to bind peroxiredoxin-3 (PRDX3), the most important scavenger of hydrogen peroxide in the mitochondria, in vitro. Here, we examined the interactions of LRRK2 and PRDX3 i...
  3. Thiol peroxidases ameliorate LRRK2 mutant-induced mitochondrial and dopaminergic neuronal degeneration in Drosophila.

    Human Molecular Genetics 23(12):3157 (2014) PMID 24459295 PMCID PMC4030771

    Mutations in leucine-rich repeat kinase 2 (LRRK2) are common causes of familial Parkinson's disease (PD). LRRK2 has been shown to bind peroxiredoxin-3 (PRDX3), the most important scavenger of hydrogen peroxide in the mitochondria, in vitro. Here, we examined the interactions of LRRK2 and PRDX3 i...
  4. Thiol peroxidases ameliorate LRRK2 mutant-induced mitochondrial and dopaminergic neuronal degeneration in Drosophila.

    Human Molecular Genetics 23(12):3157 (2014) PMID 24459295 PMCID PMC4030771

    Mutations in leucine-rich repeat kinase 2 (LRRK2) are common causes of familial Parkinson's disease (PD). LRRK2 has been shown to bind peroxiredoxin-3 (PRDX3), the most important scavenger of hydrogen peroxide in the mitochondria, in vitro. Here, we examined the interactions of LRRK2 and PRDX3 i...
  5. Ultrastructural features of endometrial-myometrial interface and its alteration in adenomyosis.

    International journal of clinical and experimen... 7(4):1469 (2014) PMID 24817942 PMCID PMC4014226

    The endometrial-myometrial interface (EMI) is a specific functional region of uterus. However, our knowledge on EMI ultrastructure both in normal uterus and adenomyosis is far from enough to understand its pathology. In this study, used the samples of EMI and outer myometrium (OM) from the adeno...
  6. Ultrastructural features of endometrial-myometrial interface and its alteration in adenomyosis.

    International journal of clinical and experimen... 7(4):1469 (2014) PMID 24817942 PMCID PMC4014226

    The endometrial-myometrial interface (EMI) is a specific functional region of uterus. However, our knowledge on EMI ultrastructure both in normal uterus and adenomyosis is far from enough to understand its pathology. In this study, used the samples of EMI and outer myometrium (OM) from the adeno...
  7. Ultrastructural features of endometrial-myometrial interface and its alteration in adenomyosis.

    International journal of clinical and experimen... 7(4):1469 (2014) PMID 24817942 PMCID PMC4014226

    The endometrial-myometrial interface (EMI) is a specific functional region of uterus. However, our knowledge on EMI ultrastructure both in normal uterus and adenomyosis is far from enough to understand its pathology. In this study, used the samples of EMI and outer myometrium (OM) from the adeno...
  8. Malignant transformation of CD4+ T lymphocytes mediated by oncogenic kinase NPM/ALK recapitulates IL-2-induced cell signaling and gene expression reprogramming.

    Journal of Immunology 191(12):6200 (2013) PMID 24218456 PMCID PMC3889215

    Anaplastic lymphoma kinase (ALK), physiologically expressed only by nervous system cells, displays a remarkable capacity to transform CD4(+) T lymphocytes and other types of nonneural cells. In this study, we report that activity of nucleophosmin (NPM)/ALK chimeric protein, the dominant form of ...
  9. Malignant transformation of CD4+ T lymphocytes mediated by oncogenic kinase NPM/ALK recapitulates IL-2-induced cell signaling and gene expression reprogramming.

    Journal of Immunology 191(12):6200 (2013) PMID 24218456 PMCID PMC3889215

    Anaplastic lymphoma kinase (ALK), physiologically expressed only by nervous system cells, displays a remarkable capacity to transform CD4(+) T lymphocytes and other types of nonneural cells. In this study, we report that activity of nucleophosmin (NPM)/ALK chimeric protein, the dominant form of ...
  10. Malignant transformation of CD4+ T lymphocytes mediated by oncogenic kinase NPM/ALK recapitulates IL-2-induced cell signaling and gene expression reprogramming.

    Journal of Immunology 191(12):6200 (2013) PMID 24218456 PMCID PMC3889215

    Anaplastic lymphoma kinase (ALK), physiologically expressed only by nervous system cells, displays a remarkable capacity to transform CD4(+) T lymphocytes and other types of nonneural cells. In this study, we report that activity of nucleophosmin (NPM)/ALK chimeric protein, the dominant form of ...
  11. Malignant transformation of CD4+ T lymphocytes mediated by oncogenic kinase NPM/ALK recapitulates IL-2-induced cell signaling and gene expression reprogramming.

    Journal of Immunology 191(12):6200 (2013) PMID 24218456 PMCID PMC3889215

    Anaplastic lymphoma kinase (ALK), physiologically expressed only by nervous system cells, displays a remarkable capacity to transform CD4(+) T lymphocytes and other types of nonneural cells. In this study, we report that activity of nucleophosmin (NPM)/ALK chimeric protein, the dominant form of ...
  12. Malignant transformation of CD4+ T lymphocytes mediated by oncogenic kinase NPM/ALK recapitulates IL-2-induced cell signaling and gene expression reprogramming.

    Journal of Immunology 191(12):6200 (2013) PMID 24218456 PMCID PMC3889215

    Anaplastic lymphoma kinase (ALK), physiologically expressed only by nervous system cells, displays a remarkable capacity to transform CD4(+) T lymphocytes and other types of nonneural cells. In this study, we report that activity of nucleophosmin (NPM)/ALK chimeric protein, the dominant form of ...
  13. Distribution of polybrominated diphenyl ethers and decabromodiphenylethane in surface sediments from the Bering Sea, Chukchi Sea, and Canada Basin

    Deep Sea Research Part II: Topical Studies in O... 81-84:95 (2012)

    24 surface sediment samples were collected from the Bering Sea, Chukchi Sea, and Canada Basin during the 3rd Chinese National Arctic Research Expedition in July–September 2008. To obtain information on the levels, spatial distribution, possible sources, and influences of total carbon a...
  14. Content and distribution of trace metals in surface sediments from the northern Bering Sea, Chukchi Sea and adjacent Arctic areas

    Marine Pollution Bulletin 63(5-12):523 (2011)

    Research highlights ► Compared to other sea area in the Arctic, there are still few studies on the environmental behaviors of pollutants in the study area. ► The study provided a good coverage of trace metals concentrations in surface sediments over a wide geographical extens...
  15. Content and distribution of trace metals in surface sediments from the northern Bering Sea, Chukchi Sea and adjacent Arctic areas.

    Marine Pollution Bulletin 63(5-12):523 (2011) PMID 21377172

    Concentrations of trace metals (Zn, Cr, Cu, V, Cd and Pb), total organic carbon (TOC), black carbon (BC) and their granulometry were examined in 25 surface sediment samples from the northern Bering Sea, Chukchi Sea and adjacent areas. Trace metal concentrations in the sediments varied from 21.06...
  16. Content and distribution of trace metals in surface sediments from the northern Bering Sea, Chukchi Sea and adjacent Arctic areas

    Marine Pollution Bulletin 63(5):523 (2011)

    Research highlights ► Compared to other sea area in the Arctic, there are still few studies on the environmental behaviors of pollutants in the study area. ► The study provided a good coverage of trace metals concentrations in surface sediments over a wide geographical extension of the...
  17. Lack of TNFalpha expression protects anaplastic lymphoma kinase-positive T-cell lymphoma (ALK+ TCL) cells from apoptosis.

    PNAS 106(37):15843 (2009) PMID 19717436 PMCID PMC2747206

    Here we report that T-cell lymphomas characterized by the expression of anaplastic lymphoma kinase (ALK+ TCL) fail to express the TNFalpha and frequently display DNA methylation of the TNFalpha gene promoter. While only a subset of the ALK+ TCL-derived cell lines showed a high degree of the prom...
  18. Lack of TNFalpha expression protects anaplastic lymphoma kinase-positive T-cell lymphoma (ALK+ TCL) cells from apoptosis.

    PNAS 106(37):15843 (2009) PMID 19717436 PMCID PMC2747206

    Here we report that T-cell lymphomas characterized by the expression of anaplastic lymphoma kinase (ALK+ TCL) fail to express the TNFalpha and frequently display DNA methylation of the TNFalpha gene promoter. While only a subset of the ALK+ TCL-derived cell lines showed a high degree of the prom...
  19. STAT5A is epigenetically silenced by the tyrosine kinase NPM1-ALK and acts as a tumor suppressor by reciprocally inhibiting NPM1-ALK expression.

    Nature Medicine 13(11):1341 (2007) PMID 17922009

    Although STAT5A and STAT5B have some nonredundant functional properties, their distinct contributions to carcinogenesis are not clearly defined. Here we report that STAT5A expression is selectively inhibited by DNA methylation of the STAT5A gene promoter region in cells expressing the oncogenic ...
  20. STAT3 induces transcription of the DNA methyltransferase 1 gene (DNMT1) in malignant T lymphocytes.

    Blood 108(3):1058 (2006) PMID 16861352 PMCID PMC1895864

    In this study, we demonstrated that STAT3, a well-characterized transcription factor expressed in continuously activated oncogenic form in the large spectrum of cancer types, induces in malignant T lymphocytes the expression of DNMT1, the key effector of epigenetic gene silencing. STAT3 binds in...