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NK-cytolytic T lymphocytes
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[late gestation lung 1; late gestation lung protein 1] The gene encoding this secreted glycoprotein (Oyewumi et al, 2003) has been identified in a search for glucocorticoid inducible genes that regulate lung development in late gestation. LGL1 shows 81 % homology to P25TI, a polypeptide trypsin inhibitor identified in human glioblastoma and neuroblastoma cells but not detected in normal human tissues (Kaplan et al, 1999). The sequence contains an LCCL module of unknown function.
LGL1 is expressed in human, rat, and mouse fetal lungs, induced by glucocorticoid, developmentally regulated in fibroblasts. The protein is not detectable in epithelial cells (Kaplan et al, 1999) but imported by fetal distal lung epithelial cells aqt a late stage of gestation (Oyewumi et al, 2003).
The protein plays a role in fetal lung airway branching morphogenesis, as demonstrated by the inhibition of this process when the expression of this gene is inhibited by suitable antisense oligonucleotides (Oyewumi et al, 2003).
Ruttenstock et al (2011) have reported that prenatal retinoic acid treatment upregulates LGL1 expression in the nitrofen-induced hypoplastic lung in late gestation and thus promotes alveologenesis.
Quinlan et al (2007) have shown that LGL1 is expressed also in mesenchymally derived lineages of fetal kidney and acts as a branching morphogen in the developing kidney.
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ENTRY LAST MODIFIED: September 2012
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