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  1. AU="Shinzo Iwashita"
  2. AU="Lucena, M I"
  3. AU="Colas, Luc"
  4. AU="Ramos, Paula S"
  5. AU="Song, Zhenzhi"
  6. AU="Shah, Peter"
  7. AU="Fullarton, John"
  8. AU="Jacobsen, Elisabet"
  9. AU="Sándor Hosztafi"
  10. AU="Hayder, Z."
  11. AU="Taylor, Evangeline"
  12. AU="Thomas E Morrison"
  13. AU="Hernandez-Cuebas, Lisa"
  14. AU="Juliann E Aukema"
  15. AU="Guy Melamed"
  16. AU="Raikhel, Marina"
  17. AU="Bhatti, Hakikat Bir Singh"
  18. AU="Christian Molnár"
  19. AU="Montarello, Natalie"
  20. AU="Phan Nu Dieu Hong"
  21. AU="Polliack, Michael"
  22. AU="Ye, Tianai"
  23. AU="Galenson, Walter"
  24. AU="Nisar, Muhammad K"
  25. AU="Keshavarzi, Nahid"
  26. AU="Gabig, Theodore G"
  27. AU="Nixon, Ian J"
  28. AU="Huang Xiaoting"
  29. AU="Colturato, Virgílio Antônio Rensi"
  30. AU="Mahfouz, Amira Y"
  31. AU="Ayyappan, Sabarish"
  32. AU=Wang Kevin L-C
  33. AU="Lukas T. Hirschwald"
  34. AU="Morley-Davies, A"
  35. AU="Felsberg, Gary J"
  36. AU="Bogen, Oliver"
  37. AU="de Portu, Simona"
  38. AU="Janssens, Rick"

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  1. Artikel ; Online: Loss of the fragile X mental retardation protein causes aberrant differentiation in human neural progenitor cells

    Naohiro Sunamura / Shinzo Iwashita / Kei Enomoto / Taisuke Kadoshima / Fujio Isono

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Band 13

    Abstract: Abstract Fragile X syndrome (FXS) is caused by transcriptional silencing of the FMR1 gene during embryonic development with the consequent loss of the encoded fragile X mental retardation protein (FMRP). The pathological mechanisms of FXS have been ... ...

    Abstract Abstract Fragile X syndrome (FXS) is caused by transcriptional silencing of the FMR1 gene during embryonic development with the consequent loss of the encoded fragile X mental retardation protein (FMRP). The pathological mechanisms of FXS have been extensively studied using the Fmr1-knockout mouse, and the findings suggest important roles for FMRP in synaptic plasticity and proper functioning of neural networks. However, the function of FMRP during early development in the human nervous system remains to be confirmed. Here we describe human neural progenitor cells (NPCs) as a model for studying FMRP functions and FXS pathology. Transcriptome analysis of the NPCs derived from FMR1-knockout human induced pluripotent stem cells (iPSCs) showed altered expression of neural differentiation markers, particularly a marked induction of the astrocyte marker glial fibrillary acidic protein (GFAP). When induced to differentiate, FMRP-deficient neurons continued to express GFAP, and showed less spontaneous calcium bursts than the parental iPSC-derived neurons. Interestingly, the aberrant expression of GFAP and the impaired firing was corrected by treatment with the protein kinase inhibitor LX7101. These findings underscore the modulatory roles of FMRP in human neurogenesis, and further demonstrate that the defective phenotype of FXS could be reversed at least partly by small molecule kinase inhibitors.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2018-08-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Ecrg4 peptide is the ligand of multiple scavenger receptors

    Tetsuo Moriguchi / Shuji Takeda / Shinzo Iwashita / Kei Enomoto / Tatsuya Sawamura / Uichi Koshimizu / Toru Kondo

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Band 9

    Abstract: Abstract Esophageal cancer-related gene 4 (Ecrg4) encodes a hormone-like peptide that is believed to be involved in a variety of physiological phenomena, including tumour suppression. Recent progress in the study of Ecrg4 has shown that Ecrg4 is a ... ...

    Abstract Abstract Esophageal cancer-related gene 4 (Ecrg4) encodes a hormone-like peptide that is believed to be involved in a variety of physiological phenomena, including tumour suppression. Recent progress in the study of Ecrg4 has shown that Ecrg4 is a proinflammatory factor and induces the expression of several cytokines and chemokines in macrophages/microglia. However, the detailed molecular mechanisms of Ecrg4 signalling, especially the Ecrg4 receptors, remain poorly understood. Here, using retrovirus-mediated expression cloning, we identified lectin-like oxidised low-density lipoprotein receptor-1 (LOX-1) as a membrane protein that binds amino acid residues 71–132 of Ecrg4 (Ecrg4(71–132)). Moreover, in addition to LOX-1, several scavenger receptors, such as Scarf1, Cd36 and Stabilin-1, facilitated the efficient internalisation of Ecrg4(71–132) into cells. A broad competitive inhibitor of scavenger receptors, polyinosinic acid, reduced both the binding of Ecrg4(71–132) and the activation of NF-κB in microglia. This activation was dependent on MyD88, an adaptor protein that recruits signalling proteins to Toll-like receptors (TLRs), with the consequent induction of various immune responses. These data suggest that multiple scavenger receptors recognise Ecrg4(71–132) and transduce its signals, together with TLRs, in microglia.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2018-03-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: cGMP signaling pathway that modulates NF-κB activation in innate immune responses

    Hirotaka Kanoh / Shinzo Iwashita / Takayuki Kuraishi / Akira Goto / Naoyuki Fuse / Haruna Ueno / Mariko Nimura / Tomohito Oyama / Chang Tang / Ryo Watanabe / Aki Hori / Yoshiki Momiuchi / Hiroki Ishikawa / Hiroaki Suzuki / Kumiko Nabe / Takeshi Takagaki / Masataka Fukuzaki / Li-Li Tong / Sinya Yamada /
    Yoshiteru Oshima / Toshiro Aigaki / Julian A.T. Dow / Shireen-Anne Davies / Shoichiro Kurata

    iScience, Vol 24, Iss 12, Pp 103473- (2021)

    2021  

    Abstract: Summary: The nuclear factor-kappa B (NF-κB) pathway is an evolutionarily conserved signaling pathway that plays a central role in immune responses and inflammation. Here, we show that Drosophila NF-κB signaling is activated via a pathway in parallel with ...

    Abstract Summary: The nuclear factor-kappa B (NF-κB) pathway is an evolutionarily conserved signaling pathway that plays a central role in immune responses and inflammation. Here, we show that Drosophila NF-κB signaling is activated via a pathway in parallel with the Toll receptor by receptor-type guanylate cyclase, Gyc76C. Gyc76C produces cyclic guanosine monophosphate (cGMP) and modulates NF-κB signaling through the downstream Tollreceptor components dMyd88, Pelle, Tube, and Dif/Dorsal (NF-κB). The cGMP signaling pathway comprises a membrane-localized cGMP-dependent protein kinase (cGK) called DG2 and protein phosphatase 2A (PP2A) and is crucial for host survival against Gram-positive bacterial infections in Drosophila. A membrane-bound cGK, PRKG2, also modulates NF-κB activation via PP2A in human cells, indicating that modulation of NF-κB activation in innate immunity by the cGMP signaling pathway is evolutionarily conserved.
    Schlagwörter Biological sciences ; Immune response ; Genomics ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2021-12-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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