LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Zurück zur letzten Suche Suchhistorie
Erweiterte Suche

Ihre letzten Suchen

  1. AU="Philip D King"
  2. AU="Yan, Zhongyu"
  3. AU="Cicalini, Carolina" AU="Cicalini, Carolina"
  4. AU="Magdalena Lange"
  5. AU="Riley, Julie"
  6. AU="Benherrif, Oussama"
  7. AU="Grau, A."
  8. AU=Tao Qiushan
  9. AU="Qin, Guole"
  10. AU="Reis, Jennifer"
  11. AU=Rothstein Eric S
  12. AU="Bruszel, Bella"
  13. AU="Edwin R. Chilvers"
  14. AU="Marco Heredia-R"
  15. AU="Barbora Chladkova"
  16. AU=Chen Yi-Ning
  17. AU="Dirce Maria Lobo Marchioni"
  18. AU="Martínez Fernández, Lidia"
  19. AU="Graham J. T"
  20. AU="Płońska-Gościniak, Edyta"
  21. AU="Shackira, A M"
  22. AU="Fukui, Mototaka"
  23. AU="Jones, Clare A"
  24. AU="Chen, Yonghua"
  25. AU=Das Nilay Kanti
  26. AU="Christine Brittsan"
  27. AU="Skinner, Henry"
  28. AU=Wang Wan-Ying
  29. AU="Ingrid Natalia Muñoz Quijano"
  30. AU="Xu, Jianrong"
  31. AU="Klutts, Abigail"
  32. AU="Corumlu, Ufuk"
  33. AU="Frank Dickmann"
  34. AU="Paz-Priel, Ido"
  35. AU=Budhraja Anshul

Suchergebnis

Treffer 1 - 7 von insgesamt 7

Suchoptionen

  1. Artikel ; Online: Mechanisms and functions of endocytosis in T cells

    John C. Charpentier / Philip D. King

    Cell Communication and Signaling, Vol 19, Iss 1, Pp 1-

    2021  Band 12

    Abstract: Abstract Once thought of primarily as a means to neutralize pathogens or to facilitate feeding, endocytosis is now known to regulate a wide range of eukaryotic cell processes. Among these are regulation of signal transduction, mitosis, lipid homeostasis, ...

    Abstract Abstract Once thought of primarily as a means to neutralize pathogens or to facilitate feeding, endocytosis is now known to regulate a wide range of eukaryotic cell processes. Among these are regulation of signal transduction, mitosis, lipid homeostasis, and directed migration, among others. Less well-appreciated are the roles various forms of endocytosis plays in regulating αβ and, especially, γδ T cell functions, such as T cell receptor signaling, antigen discovery by trogocytosis, and activated cell growth. Herein we examine the contribution of both clathrin-mediated and clathrin-independent mechanisms of endocytosis to T cell biology. Video Abstract
    Schlagwörter Endocytosis ; Macropinocytosis ; T lymphocytes ; TCR signaling ; Cell growth ; Medicine ; R ; Cytology ; QH573-671
    Sprache Englisch
    Erscheinungsdatum 2021-09-01T00:00:00Z
    Verlag BMC
    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: Macropinocytosis drives T cell growth by sustaining the activation of mTORC1

    John C. Charpentier / Di Chen / Philip E. Lapinski / Jackson Turner / Irina Grigorova / Joel A. Swanson / Philip D. King

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Band 9

    Abstract: Macropinocytosis has been implicated in the expansion of transformed cells when nutrient-depleted. Here the authors show that macropinocytosis also contributes to the expansion of primary T cells even under nutrient-replete conditions, potentially by ... ...

    Abstract Macropinocytosis has been implicated in the expansion of transformed cells when nutrient-depleted. Here the authors show that macropinocytosis also contributes to the expansion of primary T cells even under nutrient-replete conditions, potentially by providing access of extracellular amino acids to an endolysosomal compartment to sustain mTORC1 activation.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2020-01-01T00:00:00Z
    Verlag Nature Publishing Group
    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: Macropinocytosis drives T cell growth by sustaining the activation of mTORC1

    John C. Charpentier / Di Chen / Philip E. Lapinski / Jackson Turner / Irina Grigorova / Joel A. Swanson / Philip D. King

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Band 9

    Abstract: Macropinocytosis has been implicated in the expansion of transformed cells when nutrient-depleted. Here the authors show that macropinocytosis also contributes to the expansion of primary T cells even under nutrient-replete conditions, potentially by ... ...

    Abstract Macropinocytosis has been implicated in the expansion of transformed cells when nutrient-depleted. Here the authors show that macropinocytosis also contributes to the expansion of primary T cells even under nutrient-replete conditions, potentially by providing access of extracellular amino acids to an endolysosomal compartment to sustain mTORC1 activation.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2020-01-01T00:00:00Z
    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.

  4. Artikel ; Online: Deletion of SHP-2 in mesenchymal stem cells causes growth retardation, limb and chest deformity, and calvarial defects in mice

    Philip E. Lapinski / Melissa F. Meyer / Gen-Sheng Feng / Nobuhiro Kamiya / Philip D. King

    Disease Models & Mechanisms, Vol 6, Iss 6, Pp 1448-

    2013  Band 1458

    Abstract: SUMMARY In mice, induced global disruption of the Ptpn11 gene, which encodes the SHP-2 tyrosine phosphatase, results in severe skeletal abnormalities. To understand the extent to which skeletal abnormalities can be attributed to perturbation of SHP-2 ... ...

    Abstract SUMMARY In mice, induced global disruption of the Ptpn11 gene, which encodes the SHP-2 tyrosine phosphatase, results in severe skeletal abnormalities. To understand the extent to which skeletal abnormalities can be attributed to perturbation of SHP-2 function in bone-forming osteoblasts and chondrocytes, we generated mice in which disruption of Ptpn11 is restricted to mesenchymal stem cells (MSCs) and their progeny, which include both cell types. MSC-lineage-specific SHP-2 knockout (MSC SHP-2 KO) mice exhibited postnatal growth retardation, limb and chest deformity, and calvarial defects. These skeletal abnormalities were associated with an absence of mature osteoblasts and massive chondrodysplasia with a vast increase in the number of terminally differentiated hypertrophic chondrocytes in affected bones. Activation of mitogen activated protein kinases (MAPKs) and protein kinase B (PKB; also known as AKT) was impaired in bone-forming cells of MSC SHP-2 KO mice, which provides an explanation for the skeletal defects that developed. These findings reveal a cell-autonomous role for SHP-2 in bone-forming cells in mice in the regulation of skeletal development. The results add to our understanding of the pathophysiology of skeletal abnormalities observed in humans with germline mutations in the PTPN11 gene (e.g. Noonan syndrome and LEOPARD syndrome).
    Schlagwörter Medicine ; R ; Pathology ; RB1-214
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2013-11-01T00:00:00Z
    Verlag The Company of Biologists
    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.

  5. Artikel ; Online: The FERM and PDZ domain-containing protein tyrosine phosphatases, PTPN4 and PTPN3, are both dispensable for T cell receptor signal transduction.

    Timothy J Bauler / Wiljan J A J Hendriks / Philip D King

    PLoS ONE, Vol 3, Iss 12, p e

    2008  Band 4014

    Abstract: PTPN3 and PTPN4 are two closely-related non-receptor protein tyrosine phosphatases (PTP) that, in addition to a PTP domain, contain FERM (Band 4.1, Ezrin, Radixin, and Moesin) and PDZ (PSD-95, Dlg, ZO-1) domains. Both PTP have been implicated as negative- ...

    Abstract PTPN3 and PTPN4 are two closely-related non-receptor protein tyrosine phosphatases (PTP) that, in addition to a PTP domain, contain FERM (Band 4.1, Ezrin, Radixin, and Moesin) and PDZ (PSD-95, Dlg, ZO-1) domains. Both PTP have been implicated as negative-regulators of early signal transduction through the T cell antigen receptor (TCR), acting to dephosphorylate the TCRzeta chain, a component of the TCR complex. Previously, we reported upon the production and characterization of PTPN3-deficient mice which show normal TCR signal transduction and T cell function. To address if the lack of a T cell phenotype in PTPN3-deficient mice can be explained by functional redundancy of PTPN3 with PTPN4, we generated PTPN4-deficient and PTPN4/PTPN3 double-deficient mice. As in PTPN3 mutants, T cell development and homeostasis and TCR-induced cytokine synthesis and proliferation were found to be normal in PTPN4-deficient and PTPN4/PTPN3 double-deficient mice. PTPN13 is another FERM and PDZ domain-containing non-receptor PTP that is distantly-related to PTPN3 and PTPN4 and which has been shown to function as a negative-regulator of T helper-1 (Th1) and Th2 differentiation. Therefore, to determine if PTPN13 might compensate for the loss of PTPN3 and PTPN4 in T cells, we generated mice that lack functional forms of all three PTP. T cells from triple-mutant mice developed normally and showed normal cytokine secretion and proliferative responses to TCR stimulation. Furthermore, T cell differentiation along the Th1, Th2 and Th17 lineages was largely unaffected in triple-mutants. We conclude that PTPN3 and PTPN4 are dispensable for TCR signal transduction.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2008-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    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.

  6. Artikel ; Online: Evidence for SH2 domain-containing 5'-inositol phosphatase-2 (SHIP2) contributing to a lymphatic dysfunction.

    Germaine D Agollah / Manuel L Gonzalez-Garay / John C Rasmussen / I-Chih Tan / Melissa B Aldrich / Chinmay Darne / Caroline E Fife / Renie Guilliod / Erik A Maus / Philip D King / Eva M Sevick-Muraca

    PLoS ONE, Vol 9, Iss 11, p e

    2014  Band 112548

    Abstract: The lymphatic vasculature plays a critical role in a number of disease conditions of increasing prevalence, such as autoimmune disorders, obesity, blood vascular diseases, and cancer metastases. Yet, unlike the blood vasculature, the tools available to ... ...

    Abstract The lymphatic vasculature plays a critical role in a number of disease conditions of increasing prevalence, such as autoimmune disorders, obesity, blood vascular diseases, and cancer metastases. Yet, unlike the blood vasculature, the tools available to interrogate the molecular basis of lymphatic dysfunction/disease have been lacking. More recently, investigators have reported that dysregulation of the PI3K pathway is involved in syndromic human diseases that involve abnormal lymphatic vasculatures, but there have been few compelling results that show the direct association of this molecular pathway with lymphatic dysfunction in humans. Using near-infrared fluorescence lymphatic imaging (NIRFLI) to phenotype and next generation sequencing (NGS) for unbiased genetic discovery in a family with non-syndromic lymphatic disease, we discovered a rare, novel mutation in INPPL1 that encodes the protein SHIP2, which is a negative regulator of the PI3K pathway, to be associated with lymphatic dysfunction in the family. In vitro interrogation shows that SHIP2 is directly associated with impairment of normal lymphatic endothelial cell (LEC) behavior and that SHIP2 associates with receptors that are associated in lymphedema, implicating its direct involvement in the lymphatic vasculature.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    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.

  7. Artikel ; Online: Development of severe skeletal defects in induced SHP-2-deficient adult mice

    Timothy J. Bauler / Nobuhiro Kamiya / Philip E. Lapinski / Eric Langewisch / Yuji Mishina / John E. Wilkinson / Gen-Sheng Feng / Philip D. King

    Disease Models & Mechanisms, Vol 4, Iss 2, Pp 228-

    a model of skeletal malformation in humans with SHP-2 mutations

    2011  Band 239

    Abstract: SUMMARY SHP-2 (encoded by PTPN11) is a ubiquitously expressed protein tyrosine phosphatase required for signal transduction by multiple different cell surface receptors. Humans with germline SHP-2 mutations develop Noonan syndrome or LEOPARD syndrome, ... ...

    Abstract SUMMARY SHP-2 (encoded by PTPN11) is a ubiquitously expressed protein tyrosine phosphatase required for signal transduction by multiple different cell surface receptors. Humans with germline SHP-2 mutations develop Noonan syndrome or LEOPARD syndrome, which are characterized by cardiovascular, neurological and skeletal abnormalities. To study how SHP-2 regulates tissue homeostasis in normal adults, we used a conditional SHP-2 mouse mutant in which loss of expression of SHP-2 was induced in multiple tissues in response to drug administration. Induced deletion of SHP-2 resulted in impaired hematopoiesis, weight loss and lethality. Most strikingly, induced SHP-2-deficient mice developed severe skeletal abnormalities, including kyphoses and scolioses of the spine. Skeletal malformations were associated with alterations in cartilage and a marked increase in trabecular bone mass. Osteoclasts were essentially absent from the bones of SHP-2-deficient mice, thus accounting for the osteopetrotic phenotype. Studies in vitro revealed that osteoclastogenesis that was stimulated by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa B ligand (RANKL) was defective in SHP-2-deficient mice. At least in part, this was explained by a requirement for SHP-2 in M-CSF-induced activation of the pro-survival protein kinase AKT in hematopoietic precursor cells. These findings illustrate an essential role for SHP-2 in skeletal growth and remodeling in adults, and reveal some of the cellular and molecular mechanisms involved. The model is predicted to be of further use in understanding how SHP-2 regulates skeletal morphogenesis, which could lead to the development of novel therapies for the treatment of skeletal malformations in human patients with SHP-2 mutations.
    Schlagwörter Medicine ; R ; Pathology ; RB1-214
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2011-03-01T00:00:00Z
    Verlag The Company of Biologists
    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