LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Zurück zur letzten Suche Suchhistorie
Erweiterte Suche

Ihre letzten Suchen

  1. AU="Yoshiaki Yasumizu"
  2. AU=Arendt Lisa M.
  3. AU=BATTEN P J AU=BATTEN P J
  4. AU="Konieczny, S F"
  5. AU="Riches, Lucy"
  6. AU=Sozkes Sarkis AU=Sozkes Sarkis
  7. AU="Patrignelli, Robert"
  8. AU="Muzamil shah"
  9. AU="Bhat, Aishwarya"
  10. AU="Hossain, Md Zakir"
  11. AU=Jiang Xianhan
  12. AU="Mousavi, Seyyed Meysam"
  13. AU=Paulson J C
  14. AU="Saif, Tahir"
  15. AU=Alam Sabiha AU=Alam Sabiha
  16. AU="Braniff, Julia"
  17. AU="Kasim, Sazzli"
  18. AU=Brown Samuel M
  19. AU="Daubenberger, Claudia A."
  20. AU="Esteban, L"
  21. AU=Tyrka Audrey R.
  22. AU="Álvarez-Valenzuela, Francisco D"
  23. AU="Akrofi, M.M."
  24. AU="Torres, Daiana Rodrigues"
  25. AU="Bercovici, Nicholas"
  26. AU="Di Maio, Ginevra"
  27. AU="Indelicarto, Matthew"
  28. AU="Ma, Yan"
  29. AU="Ngan, CDR Kelly"
  30. AU="Arzamendi, Dabit"
  31. AU="Rezende, Carlos Eduardo Borges"
  32. AU="Brunvand, E."
  33. AU="Gateno, Jaime"

Suchergebnis

Treffer 1 - 3 von insgesamt 3

Suchoptionen

  1. Artikel ; Online: Localization of KRAS downstream target ARL4C to invasive pseudopods accelerates pancreatic cancer cell invasion

    Akikazu Harada / Shinji Matsumoto / Yoshiaki Yasumizu / Kensaku Shojima / Toshiyuki Akama / Hidetoshi Eguchi / Akira Kikuchi

    eLife, Vol

    2021  Band 10

    Abstract: Pancreatic cancer has a high mortality rate due to metastasis. Whereas KRAS is mutated in most pancreatic cancer patients, controlling KRAS or its downstream effectors has not been succeeded clinically. ARL4C is a small G protein whose expression is ... ...

    Abstract Pancreatic cancer has a high mortality rate due to metastasis. Whereas KRAS is mutated in most pancreatic cancer patients, controlling KRAS or its downstream effectors has not been succeeded clinically. ARL4C is a small G protein whose expression is induced by the Wnt and EGF–RAS pathways. In the present study, we found that ARL4C is frequently overexpressed in pancreatic cancer patients and showed that its localization to invasive pseudopods is required for cancer cell invasion. IQGAP1 was identified as a novel interacting protein for ARL4C. ARL4C recruited IQGAP1 and its downstream effector, MMP14, to invasive pseudopods. Specific localization of ARL4C, IQGAP1, and MMP14 was the active site of invasion, which induced degradation of the extracellular matrix. Moreover, subcutaneously injected antisense oligonucleotide against ARL4C into tumor-bearing mice suppressed metastasis of pancreatic cancer. These results suggest that ARL4C–IQGAP1–MMP14 signaling is activated at invasive pseudopods of pancreatic cancer cells.
    Schlagwörter ARL4C ; invasion ; pancreatic cancer ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2021-09-01T00:00:00Z
    Verlag eLife Sciences Publications Ltd
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  2. Artikel ; Online: IL‐27 produced during acute malaria infection regulates Plasmodium‐specific memory CD4+ T cells

    Maria Lourdes Macalinao / Shin‐Ichi Inoue / Sanjaadorj Tsogtsaikhan / Hirotaka Matsumoto / Ganchimeg Bayarsaikhan / Jiun‐Yu Jian / Kazumi Kimura / Yoshiaki Yasumizu / Tsuyoshi Inoue / Hiroki Yoshida / Julius Hafalla / Daisuke Kimura / Katsuyuki Yui

    EMBO Molecular Medicine, Vol 15, Iss 12, Pp n/a-n/a (2023)

    2023  

    Abstract: Abstract Malaria infection elicits both protective and pathogenic immune responses, and IL‐27 is a critical cytokine that regulate effector responses during infection. Here, we identified a critical window of CD4+ T cell responses that is targeted by IL‐ ... ...

    Abstract Abstract Malaria infection elicits both protective and pathogenic immune responses, and IL‐27 is a critical cytokine that regulate effector responses during infection. Here, we identified a critical window of CD4+ T cell responses that is targeted by IL‐27. Neutralization of IL‐27 during acute infection with Plasmodium chabaudi expanded specific CD4+ T cells, which were maintained at high levels thereafter. In the chronic phase, Plasmodium‐specific CD4+ T cells in IL‐27‐neutralized mice consisted mainly of CD127+KLRG1− and CD127−KLRG1+ subpopulations that displayed distinct cytokine production, proliferative capacity, and are maintained in a manner independent of active infection. Single‐cell RNA‐seq analysis revealed that these CD4+ T cell subsets formed independent clusters that express unique Th1‐type genes. These IL‐27‐neutralized mice exhibited enhanced cellular and humoral immune responses and protection. These findings demonstrate that IL‐27, which is produced during the acute phase of malaria infection, inhibits the development of unique Th1 memory precursor CD4+ T cells, suggesting potential implications for the development of vaccines and other strategic interventions.
    Schlagwörter CD4+ T cells ; IL‐27 ; immunological memory ; malaria ; Th1 ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-12-01T00:00:00Z
    Verlag Wiley
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  3. Artikel ; Online: High cell surface expression and peptide binding affinity of HLA-DQA1*05:03, a susceptible allele of neuromyelitis optica spectrum disorders (NMOSD)

    Shohei Beppu / Makoto Kinoshita / Jan Wilamowski / Tadahiro Suenaga / Yoshiaki Yasumizu / Kotaro Ogawa / Teruyuki Ishikura / Satoru Tada / Toru Koda / Hisashi Murata / Naoyuki Shiraishi / Yasuko Sugiyama / Keigo Kihara / Tomoyuki Sugimoto / Hisashi Arase / Daron M. Standley / Tatsusada Okuno / Hideki Mochizuki

    Scientific Reports, Vol 12, Iss 1, Pp 1-

    2022  Band 12

    Abstract: Abstract Neuromyelitis optica spectrum disorder (NMOSD) is a relapsing autoimmune disease characterized by the presence of pathogenic autoantibodies, anti-aquaporin 4 (AQP4) antibodies. Recently, HLA-DQA1*05:03 was shown to be significantly associated ... ...

    Abstract Abstract Neuromyelitis optica spectrum disorder (NMOSD) is a relapsing autoimmune disease characterized by the presence of pathogenic autoantibodies, anti-aquaporin 4 (AQP4) antibodies. Recently, HLA-DQA1*05:03 was shown to be significantly associated with NMOSD in a Japanese patient cohort. However, the specific mechanism by which HLA-DQA1*05:03 is associated with the development of NMOSD has yet to be elucidated. In the current study, we revealed that HLA-DQA1*05:03 exhibited significantly higher cell surface expression levels compared to other various DQA1 alleles, and that its expression strongly depended on the amino acid sequence of the α1 domain, with a preference for leucine at position 75. Moreover, in silico analysis indicated that the HLA-DQ encoded by HLA-DQA1*05:03 preferentially presents immunodominant AQP4 peptides, and that the peptide major histocompatibility complexes (pMHCs) are more energetically stable in the presence of HLA-DQA1*05:03 than other HLA-DQA1 alleles. In silico 3D structural models were also applied to investigate the validity of the energetic stability of pMHCs. Taken together, our findings indicate that HLA-DQA1*05:03 possesses a distinct property to play a pathogenic role in the development of NMOSD.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2022-01-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

    Zusatzmaterialien

    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

Zum Seitenanfang