Wnt16
| Wnt16; | ||
|---|---|---|
| Mass / length primary structure | 40.7 kilodaltons / 365 amino acids (isoform 1)
40.4 kilodaltons / 361 amino acids (isoform 2) |
|
| Isoforms | 2 | |
| Identifier | ||
| Gene name (s) | WNT16 | |
| External IDs | ||
| Occurrence | ||
| Parent taxon | Eukaryotes | |
| Orthologue | ||
| homo sapiens | Mus musculus | |
| Entrez | 51384 | 93735 |
| Ensemble | ENSG00000002745 | ENSMUSG00000029671 |
| UniProt | Q9UBV4 | Q9QYS1 |
| Refseq (mRNA) | NM_016087 | NM_053116 |
| Refseq (protein) | NP_057171 | NP_444346 |
| Gene locus | Chr 7: 121.33 - 121.34 Mb | Chr 6: 22.29 - 22.3 Mb |
| PubMed search | 51384 |
93735
|
The Wnt16 protein is a secreted protein from the Wnt signaling pathway which , among other things, serves to control development in multicellular cells . Wnt16 exists in two isoforms , Wnt16A is produced in the pancreas and Wnt16B is produced in cells of the lymphatic system (with the exception of the bone marrow ) and in the kidney .
properties
Wnt16B is a marker for cellular senescence that regulates the activity of p53 and the protein kinase B signaling pathway. Furthermore, Wnt16 regulates the bone density , the cortical bone thickness, the fracture strength of the bones and the risk of fracture in osteoporosis .
Wnt16B is induced in mice during chemotherapy . This protein can growth in mice prostate - cancer cells promote and protect them from further treatment. The damaged cells release the protein into the environment by secretion. The secreted WNT16B interacts with the tumor cells nearby and allows them to grow, which can cause therapy resistance. The result of a mouse model cannot be automatically transferred to humans. It is not yet known whether the observed effect also occurs in human tumor therapy.
Wnt16 is palmitoylated twice , first on S227 and then on C81, whereby it becomes a membrane-bound protein and remains bound to the cell surface after exocytosis . Wnt16 is N-glycosylated at N143, N189 and N311 .
Web links
- Human Wnt16 in the NCBI database. Retrieved August 2, 2013.
Individual evidence
- Jump up ↑ R. Binet, D. Ythier, AI Robles, M. Collado, D. Larrieu, C. Fonti, E. Brambilla, C. Brambilla, M. Serrano, CC Harris, R. Pedeux: WNT16B is a new marker of cellular senescence that regulates p53 activity and the phosphoinositide 3-kinase / AKT pathway. In: Cancer Research (2009), Vol. 69, No. 24, pp. 9183-9191. doi : 10.1158 / 0008-5472.CAN-09-1016 . PMID 19951988 . PDF .
- ↑ Hou-Feng Zheng, Jon H. Tobias, Emma Duncan, David M. Evans, Joel Eriksson, Lavinia Paternoster, Laura M. Yerges-Armstrong, Terho Lehtimäki, Ulrica Bergström, Mika Kähönen, Paul J. Leo, Olli Raitakari, Marika Laaksonen, Geoffrey C. Nicholson, Jorma Viikari, Martin Ladouceur, Leo-Pekka Lyytikäinen, Carolina Medina-Gomez, Fernando Rivadeneira, Richard L. Prince, Harri Sievanen, William D. Leslie, Dan Mellström, John A. Eisman, Sofia Movérare- Skrtic, David Goltzman, David A. Hanley, Graeme Jones, Beate St. Pourcain, Yongjun Xiao, Nicholas J. Timpson, George Davey Smith, Ian R. Reid, Susan M. Ring, Philip N. Sambrook, Magnus Karlsson, Elaine M Dennison, John P. Kemp, Patrick Danoy, Adrian Sayers, Scott G. Wilson, Maria Nethander, Eugene McCloskey, Liesbeth Vandenput, Richard Eastell, Jeff Liu, Tim Spector, Braxton D. Mitchell, Elizabeth A. Streeten, Robert Brommage, Ulrika Pettersson-Kymmer, Matthew A. Brown, Claes Ohlsson, J. Brent Richards, Mattias Lorentzon: WNT16 influences bone mine ral density, cortical bone thickness, bone strength, and osteoporotic fracture risk. In: PLoS Genetics (2012), Volume 8, No. 7, p. E1002745. doi : 10.1371 / journal.pgen.1002745 . PMID 22792071 ; PMC 3390364 (free full text).
- ↑ Yu Sun, Judith Campisi, Celestia Higano, Tomasz M. Beer, Peggy Porter, Ilsa Coleman, Lawrence True, Peter S. Nelson: Treatment-induced damage to the tumor microenvironment promotes prostate cancer therapy resistance through WNT16B In: Nature (2013) , Volume 18, No. 9, pp. 1359-1368. PMID 22863786 ; PMC 3677971 (free full text).
