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Protein Wnt-9b
Protein-coding gene in the species Homo sapiens From Wikipedia, the free encyclopedia
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Protein Wnt-9b (formerly WNT15[5]) is a protein that in humans is encoded by the WNT9B gene.[6]
The WNT family of genes produce glycolipoproteins that are involved with signaling and developmental processes. Like other Wnt genes, WNT9B codes for the WNT9B protein which participates in the canonical Wnt/β-catenin signaling pathway. WNT9B is a gene found on chromosome 17 in region 17q21. It can be traced to function in the establishment of the kidneys, because WNT9 is critical for morphogenesis of the nephron.[7]
This gene can impact kidney function in more than one way. Improper expression of the gene can cause cyst development on the kidney tubules, and in mice, mutant WNT9 genes that cause lower protein concentrations resulted in failure of the kidneys to thrive shortly after birth.[8]
WNT9B is a gene that often expressed in the epithelial cells of the Wolffian duct in early male and female embryos. In the embryos, Wnt11 is expressed at the branching points of the kidney tubules while WNT9B is expressed in a higher concentration at the stalk of the tubules.[9] WNT9B has also been tied to the involvement of neural differentiation by induction of retinoic acid, according to the NCBI.[10]
WNT9B is expressed in the developing urogenital sinus epithelium (anlage of the prostate) and in the Wollfian duct.[11][12][13] Autosomal dominant WNT9B pathogenic variants cause embryonic developmental sequence defects: Mayer-Rokitansky-Küster-Hauser syndrome in females, and Zinner syndrome in males.[14] Syndrome presentation in males includes prostatic and seminal vesicle cysts, enlarged prostate, kidney agenesis, and ejaculatory duct obstruction. WNT9B mutant mice have absent Wolffian ducts, epididymis and vas deferens, without urogenital sinus-derived mesonephric duct and mesenchymal-derived tubular epithelia.[15] HNF1B transcriptionally regulates WNT9B;[16] HNF1B too has been cited as a cause of Mayer-Rokitansky-Küster-Hauser syndrome.[17] Inheritance of a rare pathogenic mutation of WNT9B has been shown to carry significant risk of the subsequent development of prostate cancer.[18] Estimated risk ranged from 2- to 12-fold across numerous independent study populations. Common genetic variation of HNF1B too has been established to impact prostate cancer risk.[19][20] In mouse models, activation of the WNT pathway causes prostate intraepithelial neoplasia.[21]
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References
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