The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform

Haruhiko Bito - One of the best experts on this subject based on the ideXlab platform.

  • control of Axon Elongation via an sdf 1α rho mdia pathway in cultured cerebellar granule neurons
    Journal of Cell Biology, 2003
    Co-Authors: Yoshiki Arakawa, Haruhiko Bito, Tomoyuki Furuyashiki, Takahiro Tsuji, Kazuhiro Kimura, Kazuhiko Nozaki, Sayaka Takemotokimura, Nobuo Hashimoto
    Abstract:

    Rho–GTPase has been implicated in Axon outgrowth. However, not all of the critical steps controlled by Rho have been well characterized. Using cultured cerebellar granule neurons, we show here that stromal cell–derived factor (SDF)-1α, a neural chemokine, is a physiological ligand that can turn on two distinct Rho-dependent pathways with opposite consequences. A low concentration of the ligand stimulated a Rho-dependent pathway that mediated facilitation of Axon Elongation. In contrast, Rho/ROCK activation achieved by a higher concentration of SDF-1α caused repression of Axon formation and induced no more increase in Axon length. However, even at this higher concentration a Rho-dependent Axon elongating activity could be recovered upon removal of ROCK activity using Y-27632. SDF-1α–induced Axon elongating activity under ROCK inhibition was replicated by the dominant-active form of the mammalian homologue of the Drosophila gene Diaphanous (mDia)1 and counteracted by its dominant-negative form. Furthermore, RNAi knockdown of mDia1 abolished SDF-1α–induced Axon Elongation. Together, our results support a critical role for an SDF-1α/Rho/mDia1 pathway in mediating Axon Elongation.

  • Control of Axon Elongation via an SDF-1α/Rho/mDia pathway in cultured cerebellar granule neurons
    Journal of Cell Biology, 2003
    Co-Authors: Yoshiki Arakawa, Haruhiko Bito, Tomoyuki Furuyashiki, Takahiro Tsuji, Sayaka Takemoto-kimura, Kazuhiro Kimura, Kazuhiko Nozaki, Nobuo Hashimoto, Shuh Narumiya
    Abstract:

    Rho–GTPase has been implicated in Axon outgrowth. However, not all of the critical steps controlled by Rho have been well characterized. Using cultured cerebellar granule neurons, we show here that stromal cell–derived factor (SDF)-1α, a neural chemokine, is a physiological ligand that can turn on two distinct Rho-dependent pathways with opposite consequences. A low concentration of the ligand stimulated a Rho-dependent pathway that mediated facilitation of Axon Elongation. In contrast, Rho/ROCK activation achieved by a higher concentration of SDF-1α caused repression of Axon formation and induced no more increase in Axon length. However, even at this higher concentration a Rho-dependent Axon elongating activity could be recovered upon removal of ROCK activity using Y-27632. SDF-1α–induced Axon elongating activity under ROCK inhibition was replicated by the dominant-active form of the mammalian homologue of the Drosophila gene Diaphanous (mDia)1 and counteracted by its dominant-negative form. Furthermore, RNAi knockdown of mDia1 abolished SDF-1α–induced Axon Elongation. Together, our results support a critical role for an SDF-1α/Rho/mDia1 pathway in mediating Axon Elongation.

Nobuo Hashimoto - One of the best experts on this subject based on the ideXlab platform.

  • control of Axon Elongation via an sdf 1α rho mdia pathway in cultured cerebellar granule neurons
    Journal of Cell Biology, 2003
    Co-Authors: Yoshiki Arakawa, Haruhiko Bito, Tomoyuki Furuyashiki, Takahiro Tsuji, Kazuhiro Kimura, Kazuhiko Nozaki, Sayaka Takemotokimura, Nobuo Hashimoto
    Abstract:

    Rho–GTPase has been implicated in Axon outgrowth. However, not all of the critical steps controlled by Rho have been well characterized. Using cultured cerebellar granule neurons, we show here that stromal cell–derived factor (SDF)-1α, a neural chemokine, is a physiological ligand that can turn on two distinct Rho-dependent pathways with opposite consequences. A low concentration of the ligand stimulated a Rho-dependent pathway that mediated facilitation of Axon Elongation. In contrast, Rho/ROCK activation achieved by a higher concentration of SDF-1α caused repression of Axon formation and induced no more increase in Axon length. However, even at this higher concentration a Rho-dependent Axon elongating activity could be recovered upon removal of ROCK activity using Y-27632. SDF-1α–induced Axon elongating activity under ROCK inhibition was replicated by the dominant-active form of the mammalian homologue of the Drosophila gene Diaphanous (mDia)1 and counteracted by its dominant-negative form. Furthermore, RNAi knockdown of mDia1 abolished SDF-1α–induced Axon Elongation. Together, our results support a critical role for an SDF-1α/Rho/mDia1 pathway in mediating Axon Elongation.

  • Control of Axon Elongation via an SDF-1α/Rho/mDia pathway in cultured cerebellar granule neurons
    Journal of Cell Biology, 2003
    Co-Authors: Yoshiki Arakawa, Haruhiko Bito, Tomoyuki Furuyashiki, Takahiro Tsuji, Sayaka Takemoto-kimura, Kazuhiro Kimura, Kazuhiko Nozaki, Nobuo Hashimoto, Shuh Narumiya
    Abstract:

    Rho–GTPase has been implicated in Axon outgrowth. However, not all of the critical steps controlled by Rho have been well characterized. Using cultured cerebellar granule neurons, we show here that stromal cell–derived factor (SDF)-1α, a neural chemokine, is a physiological ligand that can turn on two distinct Rho-dependent pathways with opposite consequences. A low concentration of the ligand stimulated a Rho-dependent pathway that mediated facilitation of Axon Elongation. In contrast, Rho/ROCK activation achieved by a higher concentration of SDF-1α caused repression of Axon formation and induced no more increase in Axon length. However, even at this higher concentration a Rho-dependent Axon elongating activity could be recovered upon removal of ROCK activity using Y-27632. SDF-1α–induced Axon elongating activity under ROCK inhibition was replicated by the dominant-active form of the mammalian homologue of the Drosophila gene Diaphanous (mDia)1 and counteracted by its dominant-negative form. Furthermore, RNAi knockdown of mDia1 abolished SDF-1α–induced Axon Elongation. Together, our results support a critical role for an SDF-1α/Rho/mDia1 pathway in mediating Axon Elongation.

Yoshiki Arakawa - One of the best experts on this subject based on the ideXlab platform.

  • control of Axon Elongation via an sdf 1α rho mdia pathway in cultured cerebellar granule neurons
    Journal of Cell Biology, 2003
    Co-Authors: Yoshiki Arakawa, Haruhiko Bito, Tomoyuki Furuyashiki, Takahiro Tsuji, Kazuhiro Kimura, Kazuhiko Nozaki, Sayaka Takemotokimura, Nobuo Hashimoto
    Abstract:

    Rho–GTPase has been implicated in Axon outgrowth. However, not all of the critical steps controlled by Rho have been well characterized. Using cultured cerebellar granule neurons, we show here that stromal cell–derived factor (SDF)-1α, a neural chemokine, is a physiological ligand that can turn on two distinct Rho-dependent pathways with opposite consequences. A low concentration of the ligand stimulated a Rho-dependent pathway that mediated facilitation of Axon Elongation. In contrast, Rho/ROCK activation achieved by a higher concentration of SDF-1α caused repression of Axon formation and induced no more increase in Axon length. However, even at this higher concentration a Rho-dependent Axon elongating activity could be recovered upon removal of ROCK activity using Y-27632. SDF-1α–induced Axon elongating activity under ROCK inhibition was replicated by the dominant-active form of the mammalian homologue of the Drosophila gene Diaphanous (mDia)1 and counteracted by its dominant-negative form. Furthermore, RNAi knockdown of mDia1 abolished SDF-1α–induced Axon Elongation. Together, our results support a critical role for an SDF-1α/Rho/mDia1 pathway in mediating Axon Elongation.

  • Control of Axon Elongation via an SDF-1α/Rho/mDia pathway in cultured cerebellar granule neurons
    Journal of Cell Biology, 2003
    Co-Authors: Yoshiki Arakawa, Haruhiko Bito, Tomoyuki Furuyashiki, Takahiro Tsuji, Sayaka Takemoto-kimura, Kazuhiro Kimura, Kazuhiko Nozaki, Nobuo Hashimoto, Shuh Narumiya
    Abstract:

    Rho–GTPase has been implicated in Axon outgrowth. However, not all of the critical steps controlled by Rho have been well characterized. Using cultured cerebellar granule neurons, we show here that stromal cell–derived factor (SDF)-1α, a neural chemokine, is a physiological ligand that can turn on two distinct Rho-dependent pathways with opposite consequences. A low concentration of the ligand stimulated a Rho-dependent pathway that mediated facilitation of Axon Elongation. In contrast, Rho/ROCK activation achieved by a higher concentration of SDF-1α caused repression of Axon formation and induced no more increase in Axon length. However, even at this higher concentration a Rho-dependent Axon elongating activity could be recovered upon removal of ROCK activity using Y-27632. SDF-1α–induced Axon elongating activity under ROCK inhibition was replicated by the dominant-active form of the mammalian homologue of the Drosophila gene Diaphanous (mDia)1 and counteracted by its dominant-negative form. Furthermore, RNAi knockdown of mDia1 abolished SDF-1α–induced Axon Elongation. Together, our results support a critical role for an SDF-1α/Rho/mDia1 pathway in mediating Axon Elongation.

Shuh Narumiya - One of the best experts on this subject based on the ideXlab platform.

  • Control of Axon Elongation via an SDF-1α/Rho/mDia pathway in cultured cerebellar granule neurons
    Journal of Cell Biology, 2003
    Co-Authors: Yoshiki Arakawa, Haruhiko Bito, Tomoyuki Furuyashiki, Takahiro Tsuji, Sayaka Takemoto-kimura, Kazuhiro Kimura, Kazuhiko Nozaki, Nobuo Hashimoto, Shuh Narumiya
    Abstract:

    Rho–GTPase has been implicated in Axon outgrowth. However, not all of the critical steps controlled by Rho have been well characterized. Using cultured cerebellar granule neurons, we show here that stromal cell–derived factor (SDF)-1α, a neural chemokine, is a physiological ligand that can turn on two distinct Rho-dependent pathways with opposite consequences. A low concentration of the ligand stimulated a Rho-dependent pathway that mediated facilitation of Axon Elongation. In contrast, Rho/ROCK activation achieved by a higher concentration of SDF-1α caused repression of Axon formation and induced no more increase in Axon length. However, even at this higher concentration a Rho-dependent Axon elongating activity could be recovered upon removal of ROCK activity using Y-27632. SDF-1α–induced Axon elongating activity under ROCK inhibition was replicated by the dominant-active form of the mammalian homologue of the Drosophila gene Diaphanous (mDia)1 and counteracted by its dominant-negative form. Furthermore, RNAi knockdown of mDia1 abolished SDF-1α–induced Axon Elongation. Together, our results support a critical role for an SDF-1α/Rho/mDia1 pathway in mediating Axon Elongation.

Carlos A. Saura - One of the best experts on this subject based on the ideXlab platform.

  • Presenilin/γ-secretase-dependent EphA3 processing mediates Axon Elongation through non-muscle myosin IIA.
    eLife, 2019
    Co-Authors: Míriam Javier-torrent, Sergi Marco, Daniel Rocandio, Maria Pons-vizcarra, Peter W. Janes, Martin Lackmann, Joaquim Egea, Carlos A. Saura
    Abstract:

    EphA/ephrin signaling regulates Axon growth and guidance of neurons, but whether this process occurs also independently of ephrins is unclear. We show that presenilin-1 (PS1)/γ-secretase is required for Axon growth in the developing mouse brain. PS1/γ-secretase mediates Axon growth by inhibiting RhoA signaling and cleaving EphA3 independently of ligand to generate an intracellular domain (ICD) fragment that reverses Axon defects in PS1/γ-secretase- and EphA3-deficient hippocampal neurons. Proteomic analysis revealed that EphA3 ICD binds to non-muscle myosin IIA (NMIIA) and increases its phosphorylation (Ser1943), which promotes NMIIA filament disassembly and cytoskeleton rearrangement. PS1/γ-secretase-deficient neurons show decreased phosphorylated NMIIA and NMIIA/actin colocalization. Moreover, pharmacological NMII inhibition reverses Axon retraction in PS-deficient neurons suggesting that NMIIA mediates PS/EphA3-dependent Axon Elongation. In conclusion, PS/γ-secretase-dependent EphA3 cleavage mediates Axon growth by regulating filament assembly through RhoA signaling and NMIIA, suggesting opposite roles of EphA3 on inhibiting (ligand-dependent) and promoting (receptor processing) Axon growth in developing neurons.

  • presenilin γ secretase dependent epha3 processing mediates Axon Elongation through non muscle myosin iia
    eLife, 2019
    Co-Authors: Miriam Javiertorrent, Sergi Marco, Daniel Rocandio, Peter W. Janes, Martin Lackmann, Joaquim Egea, Maria Ponsvizcarra, Carlos A. Saura
    Abstract:

    EphA/ephrin signaling regulates Axon growth and guidance of neurons, but whether this process occurs also independently of ephrins is unclear. We show that presenilin-1 (PS1)/γ-secretase is required for Axon growth in the developing mouse brain. PS1/γ-secretase mediates Axon growth by inhibiting RhoA signaling and cleaving EphA3 independently of ligand to generate an intracellular domain (ICD) fragment that reverses Axon defects in PS1/γ-secretase- and EphA3-deficient hippocampal neurons. Proteomic analysis revealed that EphA3 ICD binds to non-muscle myosin IIA (NMIIA) and increases its phosphorylation (Ser1943), which promotes NMIIA filament disassembly and cytoskeleton rearrangement. PS1/γ-secretase-deficient neurons show decreased phosphorylated NMIIA and NMIIA/actin colocalization. Moreover, pharmacological NMII inhibition reverses Axon retraction in PS-deficient neurons suggesting that NMIIA mediates PS/EphA3-dependent Axon Elongation. In conclusion, PS/γ-secretase-dependent EphA3 cleavage mediates Axon growth by regulating filament assembly through RhoA signaling and NMIIA, suggesting opposite roles of EphA3 on inhibiting (ligand-dependent) and promoting (receptor processing) Axon growth in developing neurons.