Molekulargenetisches Labor
Zentrum für Nephrologie und Stoffwechsel
Moldiag Erkrankungen Gene Support Kontakt

Gliazellen neurotrophischer Faktor

Das GDNF-Gen kodiert einen von Glia-Zellen gebildeten neutrotrophischen Faktor der zusammen mit dem Produkt des RET-Gens die Bildung und Apoptose von Nervenzellen steuert. Mutationen führen zu verschiedenen autosomal dominanten Erkrankungen, dem zentralen Hypoventilationssyndrom, der Hirschsprung-Erkrankung und dem Phäochromozytom.

Gentests:

Klinisch Untersuchungsmethoden Familienuntersuchung
Bearbeitungszeit 5 Tage
Probentyp genomische DNS
Klinisch Untersuchungsmethoden Hochdurchsatz-Sequenzierung
Bearbeitungszeit 25 Tage
Probentyp genomische DNS
Klinisch Untersuchungsmethoden Direkte Sequenzierung der proteinkodierenden Bereiche eines Gens
Bearbeitungszeit 25 Tage
Probentyp genomische DNS
Klinisch Untersuchungsmethoden Multiplex ligationsabhängige Amplifikation
Bearbeitungszeit 25 Tage
Probentyp genomische DNS

Verknüpfte Erkrankungen:

Phäochromozytom
GDNF
KIF1B
MAX
OCLN
RET
SDHB
SDHD
TMEM127
VHL

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139.

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140.

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146.

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147.

Ramer MS et al. (2000) Functional regeneration of sensory axons into the adult spinal cord.

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148.

Meng X et al. (2000) Regulation of cell fate decision of undifferentiated spermatogonia by GDNF.

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149.

Messer CJ et al. (2000) Role for GDNF in biochemical and behavioral adaptations to drugs of abuse.

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150.

Martucciello G et al. (2000) Pathogenesis of Hirschsprung's disease.

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151.

Boucher TJ et al. (2000) Potent analgesic effects of GDNF in neuropathic pain states.

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152.

Kordower JH et al. (2000) Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson's disease.

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153.

Bahuau M et al. (2001) GDNF as a candidate modifier in a type 1 neurofibromatosis (NF1) enteric phenotype.

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154.

Wang CY et al. (2001) Ca(2+) binding protein frequenin mediates GDNF-induced potentiation of Ca(2+) channels and transmitter release.

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155.

Shen L et al. (2002) Gdnf haploinsufficiency causes Hirschsprung-like intestinal obstruction and early-onset lethality in mice.

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156.

Eketjäll S et al. (2002) Functional characterization of mutations in the GDNF gene of patients with Hirschsprung disease.

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157.

Japón MA et al. (2002) Glial-derived neurotropic factor and RET gene expression in normal human anterior pituitary cell types and in pituitary tumors.

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158.

Borghini S et al. (2002) Hirschsprung associated GDNF mutations do not prevent RET activation.

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159.

Nair SK et al. (2003) X-ray structures of Myc-Max and Mad-Max recognizing DNA. Molecular bases of regulation by proto-oncogenic transcription factors.

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160.

Amiel J et al. (2003) Polyalanine expansion and frameshift mutations of the paired-like homeobox gene PHOX2B in congenital central hypoventilation syndrome.

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161.

Gill SS et al. (2003) Direct brain infusion of glial cell line-derived neurotrophic factor in Parkinson disease.

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162.

Iwashita T et al. (2003) Hirschsprung disease is linked to defects in neural crest stem cell function.

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163.

Lawrence JM et al. (2004) Transplantation of Schwann cell line clones secreting GDNF or BDNF into the retinas of dystrophic Royal College of Surgeons rats.

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164.

Dahia PL et al. (2005) Novel pheochromocytoma susceptibility loci identified by integrative genomics.

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165.

Anitha M et al. (2006) GDNF rescues hyperglycemia-induced diabetic enteric neuropathy through activation of the PI3K/Akt pathway.

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166.

Carnicella S et al. (2008) GDNF is a fast-acting potent inhibitor of alcohol consumption and relapse.

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167.

Qin Y et al. (2010) Germline mutations in TMEM127 confer susceptibility to pheochromocytoma.

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168.

Comino-Méndez I et al. (2011) Exome sequencing identifies MAX mutations as a cause of hereditary pheochromocytoma.

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169.

NCBI article

NCBI 2668 external link
170.

OMIM.ORG article

Omim 600837 external link
171.

Orphanet article

Orphanet ID 122076 external link
Update: 14. August 2020
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