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A TAG1-APP signalling pathway through Fe65 negatively modulates neurogenesis.

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A TAG1-APP signalling pathway through Fe65 negatively modulates neurogenesis. / Ma, Quanhong; Futagawa, Toshitaka; Yang, Wu-Lin; Jiang, Xiao-Dan; Zeng, Li; Takeda, Yasuo; Xu, Ru-Xiang; Bagnard, Dominique; Schachner, Melitta; Furley, Andrew J; Karagogeos, Domna; Watanabe, Kazutada; Dawe, Gavin S; Xiao, Zhi-Cheng.

In: NAT CELL BIOL, Vol. 10, No. 3, 3, 2008, p. 283-294.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ma, Q, Futagawa, T, Yang, W-L, Jiang, X-D, Zeng, L, Takeda, Y, Xu, R-X, Bagnard, D, Schachner, M, Furley, AJ, Karagogeos, D, Watanabe, K, Dawe, GS & Xiao, Z-C 2008, 'A TAG1-APP signalling pathway through Fe65 negatively modulates neurogenesis.', NAT CELL BIOL, vol. 10, no. 3, 3, pp. 283-294. <http://www.ncbi.nlm.nih.gov/pubmed/18278038?dopt=Citation>

APA

Ma, Q., Futagawa, T., Yang, W-L., Jiang, X-D., Zeng, L., Takeda, Y., Xu, R-X., Bagnard, D., Schachner, M., Furley, A. J., Karagogeos, D., Watanabe, K., Dawe, G. S., & Xiao, Z-C. (2008). A TAG1-APP signalling pathway through Fe65 negatively modulates neurogenesis. NAT CELL BIOL, 10(3), 283-294. [3]. http://www.ncbi.nlm.nih.gov/pubmed/18278038?dopt=Citation

Vancouver

Ma Q, Futagawa T, Yang W-L, Jiang X-D, Zeng L, Takeda Y et al. A TAG1-APP signalling pathway through Fe65 negatively modulates neurogenesis. NAT CELL BIOL. 2008;10(3):283-294. 3.

Bibtex

@article{0aea34e39370419ba877c4e54d5e7ddc,
title = "A TAG1-APP signalling pathway through Fe65 negatively modulates neurogenesis.",
abstract = "The release of amyloid precursor protein (APP) intracellular domain (AICD) may be triggered by extracellular cues through gamma-secretase-dependent cleavage. AICD binds to Fe65, which may have a role in AICD-dependent signalling; however, the functional ligand has not been characterized. In this study, we have identified TAG1 as a functional ligand of APP. We found that, through an extracellular interaction with APP, TAG1 increased AICD release and triggered Fe65-dependent activity in a gamma-secretase-dependent manner. TAG1, APP and Fe65 colocalized in the neural stem cell niche of the fetal ventricular zone. Neural precursor cells from TAG1-/-, APP-/- and TAG1-/-;APP-/- mice had aberrantly enhanced neurogenesis, which was significantly reversed in TAG1-/- mice by TAG1 or AICD but not by AICD mutated at the Fe65 binding site. Notably, TAG1 reduced normal neurogenesis in Fe65+/+ mice. Abnormally enhanced neurogenesis also occurred in Fe65-/- mice but could not be reversed by TAG1. These results describe a TAG1-APP signalling pathway that negatively modulates neurogenesis through Fe65.",
author = "Quanhong Ma and Toshitaka Futagawa and Wu-Lin Yang and Xiao-Dan Jiang and Li Zeng and Yasuo Takeda and Ru-Xiang Xu and Dominique Bagnard and Melitta Schachner and Furley, {Andrew J} and Domna Karagogeos and Kazutada Watanabe and Dawe, {Gavin S} and Zhi-Cheng Xiao",
year = "2008",
language = "Deutsch",
volume = "10",
pages = "283--294",
journal = "NAT CELL BIOL",
issn = "1465-7392",
publisher = "NATURE PUBLISHING GROUP",
number = "3",

}

RIS

TY - JOUR

T1 - A TAG1-APP signalling pathway through Fe65 negatively modulates neurogenesis.

AU - Ma, Quanhong

AU - Futagawa, Toshitaka

AU - Yang, Wu-Lin

AU - Jiang, Xiao-Dan

AU - Zeng, Li

AU - Takeda, Yasuo

AU - Xu, Ru-Xiang

AU - Bagnard, Dominique

AU - Schachner, Melitta

AU - Furley, Andrew J

AU - Karagogeos, Domna

AU - Watanabe, Kazutada

AU - Dawe, Gavin S

AU - Xiao, Zhi-Cheng

PY - 2008

Y1 - 2008

N2 - The release of amyloid precursor protein (APP) intracellular domain (AICD) may be triggered by extracellular cues through gamma-secretase-dependent cleavage. AICD binds to Fe65, which may have a role in AICD-dependent signalling; however, the functional ligand has not been characterized. In this study, we have identified TAG1 as a functional ligand of APP. We found that, through an extracellular interaction with APP, TAG1 increased AICD release and triggered Fe65-dependent activity in a gamma-secretase-dependent manner. TAG1, APP and Fe65 colocalized in the neural stem cell niche of the fetal ventricular zone. Neural precursor cells from TAG1-/-, APP-/- and TAG1-/-;APP-/- mice had aberrantly enhanced neurogenesis, which was significantly reversed in TAG1-/- mice by TAG1 or AICD but not by AICD mutated at the Fe65 binding site. Notably, TAG1 reduced normal neurogenesis in Fe65+/+ mice. Abnormally enhanced neurogenesis also occurred in Fe65-/- mice but could not be reversed by TAG1. These results describe a TAG1-APP signalling pathway that negatively modulates neurogenesis through Fe65.

AB - The release of amyloid precursor protein (APP) intracellular domain (AICD) may be triggered by extracellular cues through gamma-secretase-dependent cleavage. AICD binds to Fe65, which may have a role in AICD-dependent signalling; however, the functional ligand has not been characterized. In this study, we have identified TAG1 as a functional ligand of APP. We found that, through an extracellular interaction with APP, TAG1 increased AICD release and triggered Fe65-dependent activity in a gamma-secretase-dependent manner. TAG1, APP and Fe65 colocalized in the neural stem cell niche of the fetal ventricular zone. Neural precursor cells from TAG1-/-, APP-/- and TAG1-/-;APP-/- mice had aberrantly enhanced neurogenesis, which was significantly reversed in TAG1-/- mice by TAG1 or AICD but not by AICD mutated at the Fe65 binding site. Notably, TAG1 reduced normal neurogenesis in Fe65+/+ mice. Abnormally enhanced neurogenesis also occurred in Fe65-/- mice but could not be reversed by TAG1. These results describe a TAG1-APP signalling pathway that negatively modulates neurogenesis through Fe65.

M3 - SCORING: Zeitschriftenaufsatz

VL - 10

SP - 283

EP - 294

JO - NAT CELL BIOL

JF - NAT CELL BIOL

SN - 1465-7392

IS - 3

M1 - 3

ER -