Difference between revisions of "Phosphatase Subfamily PRL"
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=== Domain === | === Domain === | ||
| − | PRL has a | + | PRL has a [[Phosphatase_Fold_CC1|CC1]] fold phosphatase domain followed by a consensus prenylation motif. |
=== Function === | === Function === | ||
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PRL3 is implicated in cancer. For instance, deletion of PRL3 reduces clonogenicity and tumor-initiation ability of colitis-associated cancer cells in mice <cite>Cramer15</cite>. PRL3 (PTP4A3) independently predicts metastasis and survival in upper tract urothelial carcinoma treated with radical nephroureterectomy <cite>Yeh15</cite>. | PRL3 is implicated in cancer. For instance, deletion of PRL3 reduces clonogenicity and tumor-initiation ability of colitis-associated cancer cells in mice <cite>Cramer15</cite>. PRL3 (PTP4A3) independently predicts metastasis and survival in upper tract urothelial carcinoma treated with radical nephroureterectomy <cite>Yeh15</cite>. | ||
| + | |||
| + | PTP4A3 has a number of protein substrates including ezrin <cite>Forte<cite> and p130cas <cite>Matter</cite>. All three human genes have activity against tyrosine-phosphorylated peptides <cite>Pathak</cite>. | ||
=== References === | === References === | ||
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#Von-Hoff06 pmid=16275986 | #Von-Hoff06 pmid=16275986 | ||
#tremblay14 pmid=24632616 | #tremblay14 pmid=24632616 | ||
| + | #Forte pmid=18078820 | ||
#kohn12 pmid=22413991 | #kohn12 pmid=22413991 | ||
| + | #Matter pmid=11355880 | ||
| + | #Pathak pmid=12516958 | ||
#Yeh15 pmid=26070892 | #Yeh15 pmid=26070892 | ||
</biblio> | </biblio> | ||
Revision as of 00:32, 26 October 2016
Phosphatase Classification: Fold CC1: Superfamily CC1: Family DSP: Subfamily PRL (PTP4A)
Evolution
PRL subfamily is present in animals, amoeba, and many basal eukaryotes, but is absent from fungi and plants (unpublish data from gOrtholog).
Domain
PRL has a CC1 fold phosphatase domain followed by a consensus prenylation motif.
Function
PRL is short for Phosphatases of Regenerating Liver. There are three PRLs in human, PRL1, PRL2, PRL3, all of which have been identified as key contributors to metastasis in several human cancers [1, 2]. The molecular mechanisms of PRL phosphatases is reviewed at here [3] in 2012.
PRL3 is implicated in cancer. For instance, deletion of PRL3 reduces clonogenicity and tumor-initiation ability of colitis-associated cancer cells in mice [4]. PRL3 (PTP4A3) independently predicts metastasis and survival in upper tract urothelial carcinoma treated with radical nephroureterectomy [5].
PTP4A3 has a number of protein substrates including ezrin [6, 7, 7, 8, 9, 10]. All three human genes have activity against tyrosine-phosphorylated peptides [11].
References
Error fetching PMID 16275986:
Error fetching PMID 24632616:
Error fetching PMID 18078820:
Error fetching PMID 22413991:
Error fetching PMID 11355880:
Error fetching PMID 12516958:
Error fetching PMID 26070892:
- Error fetching PMID 24632616:
- Error fetching PMID 16275986:
- Error fetching PMID 22413991:
- Error fetching PMID 24950307:
- Error fetching PMID 26070892:
- Error fetching PMID 18078820:
- Error fetching PMID 11355880:
- Error fetching PMID 12516958:
