Difference between revisions of "Phosphatase Subfamily DSP6"
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__NOTOC__ | __NOTOC__ | ||
[[Phosphatase classification|Phosphatase Classification]]: [[Phosphatase_Fold_CC1|Fold CC1]]: [[Phosphatase_Superfamily_CC1|Superfamily CC1]]: [[Phosphatase_Family_DSP|Family DSP]]: [[Phosphatase_Subfamily_DSP6|Subfamily DSP6]] | [[Phosphatase classification|Phosphatase Classification]]: [[Phosphatase_Fold_CC1|Fold CC1]]: [[Phosphatase_Superfamily_CC1|Superfamily CC1]]: [[Phosphatase_Family_DSP|Family DSP]]: [[Phosphatase_Subfamily_DSP6|Subfamily DSP6]] | ||
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=== Evolution === | === Evolution === | ||
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=== Function === | === Function === | ||
| + | ====== DUSP6 (MKP3/PYST1) ====== | ||
| + | |||
| + | |||
| + | ====== DUSP7 (MKPX/PYST2) ====== | ||
| + | DUSP7 is constitutively expressed in a wide variety of human cell lines. DUSP7 is predominantly cytosolic when expressed in COS-1 cells. In common with other members of DSP6 subfamily, DUSP7 shows substrate selectivity ERK > p38 = JNK. DUSP7 binds ERK in vivo. Both ERK and JNK activate DUSP7 phosphatase activity in vitro <cite>Dowd98</cite>. | ||
| + | |||
| + | DUSP7 has at least two isoforms. The longer isoform is constitutively highly expressed in myeloid leukemia and other malignant cells <cite>Levy-Nissenbaum03a, Levy-Nissenbaum03b, Levy-Nissenbaum04</cite>. | ||
| + | |||
| + | ====== DUSP9 (MKP4) ====== | ||
| + | DUSP6 blocks activation of MAP kinases with the selectivity ERK > p38 = JNK. Same as other members in the subfamily, it locates in cytosol <cite>Muda97, Liu07</cite>. DUSP9 is unique among these cytoplasmic MKPs in containing a conserved PKA consensus phosphorylation site (55)RRXSer-58 immediately adjacent to the kinase interaction motif. DUSP9 is phosphorylated on Ser-58 by PKA in vitro, and phosphorylation abrogates the binding of DUSP9 to both ERK2 and p38alpha MAP kinases <cite>Dickinson11</cite>. | ||
| + | |||
| + | Decreased expression of DUSP-9 is associated with poor prognosis in clear cell renal cell carcinomas <cite>Wu11</cite>. | ||
=== References === | === References === | ||
<biblio> | <biblio> | ||
| − | + | #Dickinson11 pmid=21908610 | |
| + | #Levy-Nissenbaum03a pmid=14576828 | ||
| + | #Levy-Nissenbaum03b pmid=14674243 | ||
| + | #Levy-Nissenbaum04 pmid=14603440 | ||
| + | #Liu07 pmid=18006813 | ||
| + | #Muda96 pmid=8626780 | ||
| + | #Muda97 pmid=9030581 | ||
| + | #Wu11 pmid=21943117 | ||
</biblio> | </biblio> | ||
Revision as of 19:45, 6 March 2015
Phosphatase Classification: Fold CC1: Superfamily CC1: Family DSP: Subfamily DSP6
Evolution
Domain
Function
DUSP6 (MKP3/PYST1)
DUSP7 (MKPX/PYST2)
DUSP7 is constitutively expressed in a wide variety of human cell lines. DUSP7 is predominantly cytosolic when expressed in COS-1 cells. In common with other members of DSP6 subfamily, DUSP7 shows substrate selectivity ERK > p38 = JNK. DUSP7 binds ERK in vivo. Both ERK and JNK activate DUSP7 phosphatase activity in vitro [1].
DUSP7 has at least two isoforms. The longer isoform is constitutively highly expressed in myeloid leukemia and other malignant cells [2, 3, 4].
DUSP9 (MKP4)
DUSP6 blocks activation of MAP kinases with the selectivity ERK > p38 = JNK. Same as other members in the subfamily, it locates in cytosol [5, 6]. DUSP9 is unique among these cytoplasmic MKPs in containing a conserved PKA consensus phosphorylation site (55)RRXSer-58 immediately adjacent to the kinase interaction motif. DUSP9 is phosphorylated on Ser-58 by PKA in vitro, and phosphorylation abrogates the binding of DUSP9 to both ERK2 and p38alpha MAP kinases [7].
Decreased expression of DUSP-9 is associated with poor prognosis in clear cell renal cell carcinomas [8].
References
Error fetching PMID 14576828:
Error fetching PMID 14674243:
Error fetching PMID 14603440:
Error fetching PMID 18006813:
Error fetching PMID 8626780:
Error fetching PMID 9030581:
Error fetching PMID 21943117:
- Error fetching PMID 14576828:
- Error fetching PMID 14674243:
- Error fetching PMID 14603440:
- Error fetching PMID 9030581:
- Error fetching PMID 18006813:
- Error fetching PMID 21908610:
- Error fetching PMID 21943117:
- Error fetching PMID 8626780: