The Experts below are selected from a list of 49584 Experts worldwide ranked by ideXlab platform
Takahiro Kunisada - One of the best experts on this subject based on the ideXlab platform.
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two distinct types of mouse melanocyte Differential Signaling requirement for the maintenance of non cutaneous and dermal versus epidermal melanocytes
Journal of Cell Science, 2009Co-Authors: Hitomi Aoki, Yasuhiro Yamada, Akira Hara, Takahiro KunisadaAbstract:1. Aoki et al. 2009. Development doi:10.1242/dev.037168 [OpenUrl][1][Abstract/FREE Full Text][2] [1]: {openurl}?query=rft.jtitle%253DDevelopment%26rft_id%253Dinfo%253Adoi%252F10.1242%252Fdev.037168%26rft_id%253Dinfo%253Apmid%252F19553284%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%
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Two distinct types of mouse melanocyte: Differential Signaling requirement for the maintenance of non-cutaneous and dermal versus epidermal melanocytes.
Development (Cambridge England), 2009Co-Authors: Hitomi Aoki, Yasuhiro Yamada, Akira Hara, Takahiro KunisadaAbstract:Unlike the thoroughly investigated melanocyte population in the hair follicle of the epidermis, the growth and differentiation requirements of the melanocytes in the eye, harderian gland and inner ear - the so-called non-cutaneous melanocytes - remain unclear. In this study, we investigated the in vitro and in vivo effects of the factors that regulate melanocyte development on the stem cells or the precursors of these non-cutaneous melanocytes. In general, a reduction in KIT receptor tyrosine kinase Signaling leads to disordered melanocyte development. However, melanocytes in the eye, ear and harderian gland were revealed to be less sensitive to KIT Signaling than cutaneous melanocytes. Instead, melanocytes in the eye and harderian gland were stimulated more effectively by endothelin 3 (ET3) or hepatocyte growth factor (HGF) signals than by KIT Signaling, and the precursors of these melanocytes expressed the lowest amount of KIT. The growth and differentiation of these non-cutaneous melanocytes were specifically inhibited by antagonists for ET3 and HGF. In transgenic mice induced to express ET3 or HGF in their skin and epithelial tissues from human cytokeratin 14 promoters, the survival and differentiation of non-cutaneous and dermal melanocytes, but not epidermal melanocytes, were enhanced, apparently irrespective of KIT Signaling. These results provide a molecular basis for the clear discrimination between non-cutaneous or dermal melanocytes and epidermal melanocytes, a difference that might be important in the pathogenesis of melanocyte-related diseases and melanomas.
Narumi Ogonuki - One of the best experts on this subject based on the ideXlab platform.
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the hippo Signaling pathway components lats and yap pattern tead4 activity to distinguish mouse trophectoderm from inner cell mass
Developmental Cell, 2009Co-Authors: Noriyuki Nishioka, Kenichi Inoue, Kenjiro Adachi, Hiroshi Kiyonari, Amy Ralston, Norikazu Yabuta, Shino Hirahara, Robert O Stephenson, Narumi Ogonuki, Ryosuke MakitaAbstract:Outside cells of the preimplantation mouse embryo form the trophectoderm (TE), a process requiring the transcription factor Tead4. Here, we show that transcriptionally active Tead4 can induce Cdx2 and other trophoblast genes in parallel in embryonic stem cells. In embryos, the Tead4 coactivator protein Yap localizes to nuclei of outside cells, and modulation of Tead4 or Yap activity leads to changes in Cdx2 expression. In inside cells, Yap is phosphorylated and cytoplasmic, and this involves the Hippo Signaling pathway component Lats. We propose that active Tead4 promotes TE development in outside cells, whereas Tead4 activity is suppressed in inside cells by cell contact- and Lats-mediated inhibition of nuclear Yap localization. Thus, Differential Signaling between inside and outside cell populations leads to changes in cell fate specification during TE formation.
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the hippo Signaling pathway components lats and yap pattern tead4 activity to distinguish mouse trophectoderm from inner cell mass
Developmental Cell, 2009Co-Authors: Noriyuki Nishioka, Kenichi Inoue, Kenjiro Adachi, Hiroshi Kiyonari, Amy Ralston, Norikazu Yabuta, Shino Hirahara, Robert O Stephenson, Mitsunori Ota, Narumi OgonukiAbstract:Outside cells of the preimplantation mouse embryo form the trophectoderm (TE), a process requiring the transcription factor Tead4. Here, we show that transcriptionally active Tead4 can induce Cdx2 and other trophoblast genes in parallel in embryonic stem cells. In embryos, the Tead4 coactivator protein Yap localizes to nuclei of outside cells, and modulation of Tead4 or Yap activity leads to changes in Cdx2 expression. In inside cells, Yap is phosphorylated and cytoplasmic, and this involves the Hippo Signaling pathway component Lats. We propose that active Tead4 promotes TE development in outside cells, whereas Tead4 activity is suppressed in inside cells by cell contact- and Lats-mediated inhibition of nuclear Yap localization. Thus, Differential Signaling between inside and outside cell populations leads to changes in cell fate specification during TE formation.
Matthew J Fenton - One of the best experts on this subject based on the ideXlab platform.
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tlr4 but not tlr2 mediates ifn beta induced stat1alpha beta dependent gene expression in macrophages
Nature Immunology, 2002Co-Authors: Vladimir Y Toshchakov, Bryan W Jones, Pinyu Perera, Karen E Thomas, Joshua M Cody, Shuling Zhang, Bryan R G Williams, Jennifer Major, Thomas A Hamilton, Matthew J FentonAbstract:Toll-like receptor 2 (TLR2) agonists induce a subset of TLR4-inducible proinflammatory genes, which suggests the use of Differential Signaling pathways. Murine macrophages stimulated with the TLR4 agonist Escherichia coli lipopolysaccharide (LPS), but not with TLR2 agonists, induced phosphorylation of signal transducer and activator of transcription 1alpha (STAT1alpha) and STAT1beta, which was blocked by antibodies to interferon beta (IFN-beta) but not IFN-alpha. All TLR2 agonists poorly induced IFN-beta, which is encoded by an immediate early LPS-inducible gene. Thus, the failure of TLR2 agonists to induce STAT1-dependent genes resulted, in part, from their inability to express IFN-beta. TLR4-induced IFN-beta mRNA was MyD88- and PKR (double-stranded RNA-dependent protein kinase)-independent, but TIRAP (Toll-interleukin 1 receptor domain-containing adapter protein)-dependent. Together, these findings provide the first mechanistic basis for Differential patterns of gene expression activated by TLR4 and TLR2 agonists.
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tlr4 but not tlr2 mediates ifn beta induced stat1alpha beta dependent gene expression in macrophages
Nature Immunology, 2002Co-Authors: Vladimir Y Toshchakov, Bryan W Jones, Pinyu Perera, Karen E Thomas, Joshua M Cody, Shuling Zhang, Bryan R G Williams, Jennifer Major, Thomas A Hamilton, Matthew J FentonAbstract:Toll-like receptor 2 (TLR2) agonists induce a subset of TLR4-inducible proinflammatory genes, which suggests the use of Differential Signaling pathways. Murine macrophages stimulated with the TLR4 agonist Escherichia coli lipopolysaccharide (LPS), but not with TLR2 agonists, induced phosphorylation of signal transducer and activator of transcription 1α (STAT1α) and STAT1β, which was blocked by antibodies to interferon β (IFN-β) but not IFN-α. All TLR2 agonists poorly induced IFN-β, which is encoded by an immediate early LPS-inducible gene. Thus, the failure of TLR2 agonists to induce STAT1-dependent genes resulted, in part, from their inability to express IFN-β. TLR4-induced IFN-β mRNA was MyD88- and PKR (double-stranded RNA–dependent protein kinase)-independent, but TIRAP (Toll–interleukin 1 receptor domain–containing adapter protein)-dependent. Together, these findings provide the first mechanistic basis for Differential patterns of gene expression activated by TLR4 and TLR2 agonists.
Tom S Wehrman - One of the best experts on this subject based on the ideXlab platform.
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biased agonism as a mechanism for Differential Signaling by chemokine receptors
Journal of Biological Chemistry, 2013Co-Authors: Sudarshan Rajagopal, Daniel Bassoni, James J Campbell, Norma P Gerard, Craig Gerard, Tom S WehrmanAbstract:Abstract Chemokines display considerable promiscuity with multiple ligands and receptors shared in common, a phenomenon that is thought to underlie their biochemical redundancy. Their receptors are part of a larger seven transmembrane receptor (7TMR) superfamily, commonly referred to as G protein-coupled receptors (GPCRs), which have been demonstrated to be able to signal with different efficacies to their multiple downstream Signaling pathways, a phenomenon referred to as biased agonism. Biased agonism has been primarily reported as a phenomenon of synthetic ligands and the biologic prevalence and importance of such Signaling is unclear. Here, to assess the presence of biased agonism that may underlie Differential Signaling by chemokines targeting the same receptor, we performed a detailed pharmacologic analysis of a set of chemokine receptors with multiple endogenous ligands using assays for G protein Signaling, beta-arrestin (barr) recruitment and receptor internalization. We found that chemokines targeting the same receptor can display marked differences in their efficacies for G protein- or barr-mediated Signaling or receptor internalization. This ligand bias correlates with changes in leukocyte migration, consistent with different mechanisms underlying the Signaling downstream of these receptors induced by their ligands. These findings demonstrate that biased agonism is a common and likely evolutionarily conserved biological mechanism for generating qualitatively distinct patterns of Signaling via the same receptor in response to different endogenous ligands.
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biased agonism as a mechanism for Differential Signaling by chemokine receptors
Journal of Biological Chemistry, 2013Co-Authors: Sudarshan Rajagopal, Daniel Bassoni, Norma P Gerard, Craig Gerard, James Campbell, Tom S WehrmanAbstract:Chemokines display considerable promiscuity with multiple ligands and receptors shared in common, a phenomenon that is thought to underlie their biochemical "redundancy." Their receptors are part of a larger seven-transmembrane receptor superfamily, commonly referred to as G protein-coupled receptors, which have been demonstrated to be able to signal with different efficacies to their multiple downstream Signaling pathways, a phenomenon referred to as biased agonism. Biased agonism has been primarily reported as a phenomenon of synthetic ligands, and the biologic prevalence and importance of such Signaling are unclear. Here, to assess the presence of biased agonism that may underlie Differential Signaling by chemokines targeting the same receptor, we performed a detailed pharmacologic analysis of a set of chemokine receptors with multiple endogenous ligands using assays for G protein Signaling, β-arrestin recruitment, and receptor internalization. We found that chemokines targeting the same receptor can display marked differences in their efficacies for G protein- or β-arrestin-mediated Signaling or receptor internalization. This ligand bias correlates with changes in leukocyte migration, consistent with different mechanisms underlying the Signaling downstream of these receptors induced by their ligands. These findings demonstrate that biased agonism is a common and likely evolutionarily conserved biological mechanism for generating qualitatively distinct patterns of Signaling via the same receptor in response to different endogenous ligands.
Noriyuki Nishioka - One of the best experts on this subject based on the ideXlab platform.
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the hippo Signaling pathway components lats and yap pattern tead4 activity to distinguish mouse trophectoderm from inner cell mass
Developmental Cell, 2009Co-Authors: Noriyuki Nishioka, Kenichi Inoue, Kenjiro Adachi, Hiroshi Kiyonari, Amy Ralston, Norikazu Yabuta, Shino Hirahara, Robert O Stephenson, Narumi Ogonuki, Ryosuke MakitaAbstract:Outside cells of the preimplantation mouse embryo form the trophectoderm (TE), a process requiring the transcription factor Tead4. Here, we show that transcriptionally active Tead4 can induce Cdx2 and other trophoblast genes in parallel in embryonic stem cells. In embryos, the Tead4 coactivator protein Yap localizes to nuclei of outside cells, and modulation of Tead4 or Yap activity leads to changes in Cdx2 expression. In inside cells, Yap is phosphorylated and cytoplasmic, and this involves the Hippo Signaling pathway component Lats. We propose that active Tead4 promotes TE development in outside cells, whereas Tead4 activity is suppressed in inside cells by cell contact- and Lats-mediated inhibition of nuclear Yap localization. Thus, Differential Signaling between inside and outside cell populations leads to changes in cell fate specification during TE formation.
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the hippo Signaling pathway components lats and yap pattern tead4 activity to distinguish mouse trophectoderm from inner cell mass
Developmental Cell, 2009Co-Authors: Noriyuki Nishioka, Kenichi Inoue, Kenjiro Adachi, Hiroshi Kiyonari, Amy Ralston, Norikazu Yabuta, Shino Hirahara, Robert O Stephenson, Mitsunori Ota, Narumi OgonukiAbstract:Outside cells of the preimplantation mouse embryo form the trophectoderm (TE), a process requiring the transcription factor Tead4. Here, we show that transcriptionally active Tead4 can induce Cdx2 and other trophoblast genes in parallel in embryonic stem cells. In embryos, the Tead4 coactivator protein Yap localizes to nuclei of outside cells, and modulation of Tead4 or Yap activity leads to changes in Cdx2 expression. In inside cells, Yap is phosphorylated and cytoplasmic, and this involves the Hippo Signaling pathway component Lats. We propose that active Tead4 promotes TE development in outside cells, whereas Tead4 activity is suppressed in inside cells by cell contact- and Lats-mediated inhibition of nuclear Yap localization. Thus, Differential Signaling between inside and outside cell populations leads to changes in cell fate specification during TE formation.