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L1cam acts as a modifier gene for members of the endothelin signalling pathway during enteric nervous system development.

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L1cam acts as a modifier gene for members of the endothelin signalling pathway during enteric nervous system development. / Wallace, A S; Tan, M X; Schachner, Melitta; Anderson, R B.

In: NEUROGASTROENT MOTIL, Vol. 23, No. 11, 11, 2011, p. 510-522.

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

Harvard

Wallace, AS, Tan, MX, Schachner, M & Anderson, RB 2011, 'L1cam acts as a modifier gene for members of the endothelin signalling pathway during enteric nervous system development.', NEUROGASTROENT MOTIL, vol. 23, no. 11, 11, pp. 510-522. <http://www.ncbi.nlm.nih.gov/pubmed/21395909?dopt=Citation>

APA

Wallace, A. S., Tan, M. X., Schachner, M., & Anderson, R. B. (2011). L1cam acts as a modifier gene for members of the endothelin signalling pathway during enteric nervous system development. NEUROGASTROENT MOTIL, 23(11), 510-522. [11]. http://www.ncbi.nlm.nih.gov/pubmed/21395909?dopt=Citation

Vancouver

Wallace AS, Tan MX, Schachner M, Anderson RB. L1cam acts as a modifier gene for members of the endothelin signalling pathway during enteric nervous system development. NEUROGASTROENT MOTIL. 2011;23(11):510-522. 11.

Bibtex

@article{65e023587c9e4c24a7f1db8b892c379b,
title = "L1cam acts as a modifier gene for members of the endothelin signalling pathway during enteric nervous system development.",
abstract = "The enteric nervous system originates from neural crest cells that migrate into the embryonic foregut and then sequentially colonize the midgut and hindgut. Defects in neural crest migration result in regions of the gut that lack enteric ganglia, a condition in humans called Hirschsprung's disease. The high degree of phenotypic variability reported in Hirschsprung's disease suggests the involvement of modifier genes.",
keywords = "Animals, Humans, Mice, Mice, Knockout, Cell Proliferation, Apoptosis/physiology, Signal Transduction/*physiology, Cell Movement/physiology, Endothelins/genetics/*metabolism, Enteric Nervous System/abnormalities/*embryology, *Genes, Modifier, *Genes, X-Linked, Genetic Complementation Test, Hirschsprung Disease/embryology/genetics/metabolism, Intestines/embryology/innervation, Neural Cell Adhesion Molecule L1/*genetics/metabolism, Receptors, Endothelin/genetics/*metabolism, Animals, Humans, Mice, Mice, Knockout, Cell Proliferation, Apoptosis/physiology, Signal Transduction/*physiology, Cell Movement/physiology, Endothelins/genetics/*metabolism, Enteric Nervous System/abnormalities/*embryology, *Genes, Modifier, *Genes, X-Linked, Genetic Complementation Test, Hirschsprung Disease/embryology/genetics/metabolism, Intestines/embryology/innervation, Neural Cell Adhesion Molecule L1/*genetics/metabolism, Receptors, Endothelin/genetics/*metabolism",
author = "Wallace, {A S} and Tan, {M X} and Melitta Schachner and Anderson, {R B}",
year = "2011",
language = "English",
volume = "23",
pages = "510--522",
journal = "NEUROGASTROENT MOTIL",
issn = "1350-1925",
publisher = "Wiley-Blackwell",
number = "11",

}

RIS

TY - JOUR

T1 - L1cam acts as a modifier gene for members of the endothelin signalling pathway during enteric nervous system development.

AU - Wallace, A S

AU - Tan, M X

AU - Schachner, Melitta

AU - Anderson, R B

PY - 2011

Y1 - 2011

N2 - The enteric nervous system originates from neural crest cells that migrate into the embryonic foregut and then sequentially colonize the midgut and hindgut. Defects in neural crest migration result in regions of the gut that lack enteric ganglia, a condition in humans called Hirschsprung's disease. The high degree of phenotypic variability reported in Hirschsprung's disease suggests the involvement of modifier genes.

AB - The enteric nervous system originates from neural crest cells that migrate into the embryonic foregut and then sequentially colonize the midgut and hindgut. Defects in neural crest migration result in regions of the gut that lack enteric ganglia, a condition in humans called Hirschsprung's disease. The high degree of phenotypic variability reported in Hirschsprung's disease suggests the involvement of modifier genes.

KW - Animals

KW - Humans

KW - Mice

KW - Mice, Knockout

KW - Cell Proliferation

KW - Apoptosis/physiology

KW - Signal Transduction/physiology

KW - Cell Movement/physiology

KW - Endothelins/genetics/metabolism

KW - Enteric Nervous System/abnormalities/embryology

KW - Genes, Modifier

KW - Genes, X-Linked

KW - Genetic Complementation Test

KW - Hirschsprung Disease/embryology/genetics/metabolism

KW - Intestines/embryology/innervation

KW - Neural Cell Adhesion Molecule L1/genetics/metabolism

KW - Receptors, Endothelin/genetics/metabolism

KW - Animals

KW - Humans

KW - Mice

KW - Mice, Knockout

KW - Cell Proliferation

KW - Apoptosis/physiology

KW - Signal Transduction/physiology

KW - Cell Movement/physiology

KW - Endothelins/genetics/metabolism

KW - Enteric Nervous System/abnormalities/embryology

KW - Genes, Modifier

KW - Genes, X-Linked

KW - Genetic Complementation Test

KW - Hirschsprung Disease/embryology/genetics/metabolism

KW - Intestines/embryology/innervation

KW - Neural Cell Adhesion Molecule L1/genetics/metabolism

KW - Receptors, Endothelin/genetics/metabolism

M3 - SCORING: Journal article

VL - 23

SP - 510

EP - 522

JO - NEUROGASTROENT MOTIL

JF - NEUROGASTROENT MOTIL

SN - 1350-1925

IS - 11

M1 - 11

ER -