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  1. AU="Gilbert J Cote"
  2. AU="Lumin, Qiao"
  3. AU=Ribeiro Rodrigo Antonini
  4. AU="Deschamps, Marie-Marcelle"
  5. AU="Kogler, Gesine"
  6. AU=Fehlings Michael G
  7. AU="Chouayekh, Hichem"
  8. AU="Beibei, Tao"
  9. AU="Lu, Kaifeng"
  10. AU="Hamade, Aline"
  11. AU="Pereira, Rickson"
  12. AU="Zou, Binbin"
  13. AU="Peng, Lingteng"
  14. AU="Zolotoukho, Anna"
  15. AU="Verhagen, E."
  16. AU=Butters Desley AU=Butters Desley
  17. AU="Hoffmann, Karl-Titus"
  18. AU="Iñiguez, Andrés"
  19. AU="Panaccione, Alexander"
  20. AU="Berube, Liliana L"

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  1. Artikel ; Online: Hydrogen peroxide alters splicing of soluble guanylyl cyclase and selectively modulates expression of splicing regulators in human cancer cells.

    Gilbert J Cote / Wen Zhu / Anthony Thomas / Emil Martin / Ferid Murad / Iraida G Sharina

    PLoS ONE, Vol 7, Iss 7, p e

    2012  Band 41099

    Abstract: Soluble guanylyl cyclase (sGC) plays a central role in nitric oxide (NO)-mediated signal transduction in the cardiovascular, nervous and gastrointestinal systems. Alternative RNA splicing has emerged as a potential mechanism to modulate sGC expression ... ...

    Abstract Soluble guanylyl cyclase (sGC) plays a central role in nitric oxide (NO)-mediated signal transduction in the cardiovascular, nervous and gastrointestinal systems. Alternative RNA splicing has emerged as a potential mechanism to modulate sGC expression and activity. C-α1 sGC is an alternative splice form that is resistant to oxidation-induced protein degradation and demonstrates preferential subcellular distribution to the oxidized environment of endoplasmic reticulum (ER).Here we report that splicing of C-α1 sGC can be modulated by H(2)O(2) treatment in BE2 neuroblastoma and MDA-MD-468 adenocarcinoma human cells. In addition, we show that the H(2)O(2) treatment of MDA-MD-468 cells selectively decreases protein levels of PTBP1 and hnRNP A2/B1 splice factors identified as potential α1 gene splicing regulators by in silico analysis. We further demonstrate that down-regulation of PTBP1 by H(2)O(2) occurs at the protein level with variable regulation observed in different breast cancer cells.Our data demonstrate that H(2)O(2) regulates RNA splicing to induce expression of the oxidation-resistant C-α1 sGC subunit. We also report that H(2)O(2) treatment selectively alters the expression of key splicing regulators. This process might play an important role in regulation of cellular adaptation to conditions of oxidative stress.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2012-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Mutaciones de línea germinal del proto-oncogen ret en pacientes chilenos con cáncer medular tiroideo hereditario y esporádico Germline mutations of the ret proto- oncogen in Chilean patients with hereditary and sporadic medullary thyroid carcinoma

    Nelson Wohllk G / Pedro Becker C / Ronald Youlton R / Gilbert J Cote / Robert F Gagel

    Revista Médica de Chile, Vol 129, Iss 7, Pp 713-

    2001  Band 718

    Abstract: Background: Medullary thyroid carcinoma (MTC) may occur either as a sporadic or familial disease. Multiple endocrine neoplasia (MEN) type 2, inherited as an autosomal dominant disease, is characterized by MTC only (FMTC) or coexistence of MTC with other ... ...

    Abstract Background: Medullary thyroid carcinoma (MTC) may occur either as a sporadic or familial disease. Multiple endocrine neoplasia (MEN) type 2, inherited as an autosomal dominant disease, is characterized by MTC only (FMTC) or coexistence of MTC with other endocrine neoplasia (NEM 2A, 2B). Germline mutations of the RET proto-oncogene (cRet) are found in the inherited forms and in some apparently sporadic MTC cases. Aim: To study RET mutations in 8 families with MEN 2. Material and methods: RET mutations were screened in peripheral blood DNA from 18 patients and 87 high risk carriers belonging to 8 MEN 2 families and 52 sporadic MTC. Exons 10, 11, 13, 14, 15 and 16 of the c-Ret were amplified by polymerase chain reaction (PCR) and examined by direct sequencing of PCR products and/or restriction enzyme analysis. Results: Five MEN 2A and one FMTC families with a germline mutation at codon 634, one MEN 2A and one FMTC family carrying a mutation at codon 620 were identified. Mutations were found in 23 out of 87 high risk carriers. In addition, we detected a S891A (exon 15) germline mutation in a sporadic MTC patient and in one out of her three sons and V804M (exon 14) in another sporadic MTC case and in one out of his six relatives, indicating in both cases the presence of a sporadic misclassified familial disease. Conclusions: These results underscore the importance of routine application of c-Ret testing in all cases of MTC either familial or sporadic. (Rev Méd Chile 2001; 129: 713-8).
    Schlagwörter Multiple endocrine neoplasia Type 2 ; Proto-oncogene proteins ; Thyroid neoplasms ; Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Thema/Rubrik (Code) 610
    Sprache Spanisch
    Erscheinungsdatum 2001-07-01T00:00:00Z
    Verlag Sociedad Médica de Santiago
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Calcium-Induced Activation of a Mutant G-Protein-Coupled Receptor Causes In Vitro Transformation of NIH/3T3 Cells

    Ana O. Hoff / Gilbert J. Cote / Herbert A. Fritsche, Jr. / Haiyan Qiu / Pamela N. Schultz / Robert F. Gagel

    Neoplasia : An International Journal for Oncology Research, Vol 1, Iss 6, Pp 485-

    1999  Band 491

    Abstract: The calcium-sensing receptor (CaR) is a G-proteincoupled receptor that is widely expressed, has tissuespecific functions, regulates cell growth. Activating mutations of this receptor cause autosomal dominant hypocalcemia, a syndrome characterized by ... ...

    Abstract The calcium-sensing receptor (CaR) is a G-proteincoupled receptor that is widely expressed, has tissuespecific functions, regulates cell growth. Activating mutations of this receptor cause autosomal dominant hypocalcemia, a syndrome characterized by hypocalcemia and hypercalciuria. The identification of a family with an activating mutation of the CaR (Thr151 Met) in which hypocalcemia cosegregates with several unusual neoplasms led us to examine the transforming effects of this mutant receptor. Transfection of NIH/3T3 cells with the mutant but not the normal receptor supported colony formation in soft agar at subphysiologic calcium concentrations. The mutant CaR causes a calcium-dependent activation of the extracellular signal-regulated protein kinase (ERK) 1/2 and Jun-N-terminal kinase/stress-activated (JNK/ SAPK) pathways, but not P38 MAP kinase. These findings contribute to a growing body of information suggesting that this receptor plays a role in the regulation of cellular proliferation, that aberrant activation of the mutant receptor in this family may play a role in the unusual neoplastic manifestations.
    Schlagwörter hypocalcemia ; Neoplasia ; G -protein receptor ; transformation ; MAP kinase ; Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
    Erscheinungsdatum 1999-12-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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