2.7.1.150: 1-phosphatidylinositol-3-phosphate 5-kinase
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For detailed information about 1-phosphatidylinositol-3-phosphate 5-kinase, go to the full flat file.
Word Map on EC 2.7.1.150
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2.7.1.150
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mating
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pheromone
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vacuole
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endosomal
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ptdins3,5p2
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haploid
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3,5-bisphosphate
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ptdins5p
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endolysosomal
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apilimod
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pheromone-induced
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pseudohyphal
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phosphatidylinositol-3,5-bisphosphate
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pheromone-responsive
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charcot-marie-tooth
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mating-type
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mating-specific
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fleck
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alpha-specific
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matalpha
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a-specific
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trpml1
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a-factor
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insulin-regulated
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drug development
- 2.7.1.150
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mating
- pheromone
- vacuole
- endosomal
-
ptdins3,5p2
-
haploid
- 3,5-bisphosphate
-
ptdins5p
-
endolysosomal
- apilimod
-
pheromone-induced
-
pseudohyphal
- phosphatidylinositol-3,5-bisphosphate
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pheromone-responsive
-
charcot-marie-tooth
-
mating-type
-
mating-specific
-
fleck
-
alpha-specific
-
matalpha
-
a-specific
-
trpml1
- a-factor
-
insulin-regulated
- drug development
Reaction
Synonyms
CgFab1, class III lipid kinase, Fab1, Fab1 phosphatidylinositol 3-phosphate 5-kinase, FAB1/FYVE finger-containing phosphoinositide kinase, Fab1/PIKfyve, Fab1p, formation of aploid and binucleate cells1/FYVE finger-containing phosphoinositide kinase, FYVE domain-containing phosphatidylinositol 3-phosphate 5-kinase, kinase (phosphorylating), phosphatidylinositol 3-phosphate 5-, More, phosphatidylinositol 3-phosphate 5-kinase, phosphatidylinositol 5-OH kinase, phosphatidylinositol phosphate kinase 3, Phosphatidylinositol-3-phosphate 5-kinase, phosphatidylinositol-3-phosphate-5-kinase PIKfyve, phosphatidylinositol-3-phosphate/phosphatidylinositol 5-kinase, PI(3)P-5-kinase, PI-3P-5-kinase, PI3P 5-kinase, PI3P-5 kinase, PIKfyve, PIKfyve/Fab1p, PIP5K3, PPK-3, PtdIns 3-phosphate 5-kinase, PtdIns(3) 5-kinase, PtdIns(3)P 5-kinase, PtdIns3P 5-kinase, PtdIns3P 5-OH kinase, Ste12, type III PIP kinase
ECTree
2.7.1.150 1-phosphatidylinositol-3-phosphate 5-kinaseAdvanced search results
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results (Engineering
Engineering on EC 2.7.1.150 - 1-phosphatidylinositol-3-phosphate 5-kinase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
S1448L
naturally occuring mutation yq24, yq24 mutants exhibit embryonic vacuoles similar to slc-36.1 mutants. Double mutants of yq24 with ced-4(n1162) show neither button-like apoptotic cell corpses nor vacuolar structures. The yq24 embryonic vacuoles are enriched for both LAAT-1::GFP and HIS-24::mCh. Mutant yq24 embryonic vacuoles are phagolysosomes arising from apoptosis
S318A
in Xenopus oocytes expressing mammalian excitatory amino acid transporter EAAT4, glutamate induces a current which is significantly enhanced by coexpression of isoform PIKfyve and glucocorticoid inducible kinase SGK1. The stimulating effect of PIKfyve is abrogated by mutation S318A in the SGK consensus sequence of PIKfyve. Coexpression of PIKfyve S318A mutant significantly blunts the stimulating effect of SGK1 on EAAT4 activity
D2134R
site-directed mutagenesis, in vivo abrogation of lipid kinase activity of the enzyme
K2059M
site-directed mutagenesis, in vitro abrogation of lipid kinase activity of the enzyme
W1037stop
G1867/1870V
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site-directed mutagenesis, the Cgfab1DELTA mutant carrying CgFab1G1867/1870V is sensitive to both azole and metal ion stress
additional information
W1037stop
gene ste12 next generation sequencing reveals a truncating, premature stop codon at position W1037 of the Ste12PIKFYVE-phosphatidylinositol-3-phosphate 5-kinase. The advancement of cell division is markedly compromised in ste12PIKFYVE. Mutant W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE.W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. No significant changes in TORC1 and TORC2 activities are observed in ste12PIKFYVE-W1037STOP mutants. Phenotype, overview
W1037stop
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gene ste12 next generation sequencing reveals a truncating, premature stop codon at position W1037 of the Ste12PIKFYVE-phosphatidylinositol-3-phosphate 5-kinase. The advancement of cell division is markedly compromised in ste12PIKFYVE. Mutant W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE.W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. No significant changes in TORC1 and TORC2 activities are observed in ste12PIKFYVE-W1037STOP mutants. Phenotype, overview
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W1037stop
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gene ste12 next generation sequencing reveals a truncating, premature stop codon at position W1037 of the Ste12PIKFYVE-phosphatidylinositol-3-phosphate 5-kinase. The advancement of cell division is markedly compromised in ste12PIKFYVE. Mutant W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE.W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. No significant changes in TORC1 and TORC2 activities are observed in ste12PIKFYVE-W1037STOP mutants. Phenotype, overview
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additional information
ppk-3(n2668) strong loss-of-function mutants embryos contain many vacuolar structures of different sizes, a subset of which are positive for both LAAT-1::GFP and HIS-24::mCh, indicating that they are phagolysosomes. The double mutant of slc-36.1(yq110) with ppk-3(n2668) contains enlarged autolysosomes similar to ppk-3(n2668) single mutants
additional information
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ppk-3(n2668) strong loss-of-function mutants embryos contain many vacuolar structures of different sizes, a subset of which are positive for both LAAT-1::GFP and HIS-24::mCh, indicating that they are phagolysosomes. The double mutant of slc-36.1(yq110) with ppk-3(n2668) contains enlarged autolysosomes similar to ppk-3(n2668) single mutants
additional information
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enzyme defect leads to enlarged vacuoles that do not acidify correctly, the defect can be complemented by enzyme overexpression, mutants grow poorly at elevated temperature
additional information
FAB1 null mutants possess no phosphatidylinositol 3,5-bisphosphate and shows vacuolar defects, expression of murine enzyme PIKfyve, but of the enzyme from Schizosaccharomyces pombe, can revert the vacuolar defects in vivo, while the enzyme from Schizosaccharomyces pombe can restore catalytic activity in response to hyperosmotic stress
additional information
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enzyme defect leads to enlarged vacuoles that do not acidify correctly, the defect can be complemented by enzyme overexpression, mutants grow poorly at elevated temperature
additional information
identification of a non-functional ste12PIKFYVE mutant that is unable to invoke the normal advancement of mitotic onset and adjust cell size at division in response to nitrogen stress
additional information
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identification of a non-functional ste12PIKFYVE mutant that is unable to invoke the normal advancement of mitotic onset and adjust cell size at division in response to nitrogen stress
additional information
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identification of a non-functional ste12PIKFYVE mutant that is unable to invoke the normal advancement of mitotic onset and adjust cell size at division in response to nitrogen stress
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additional information
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identification of a non-functional ste12PIKFYVE mutant that is unable to invoke the normal advancement of mitotic onset and adjust cell size at division in response to nitrogen stress
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additional information
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generation of a deletion strain for the CgFAB1 gene, using the homologous recombination-based strategy. The mutant is sensitive to azoles (fluconazole, clotrimazole and ketoconazole), and cell membrane (SDS) and cell wall (caffeine) stressors. The growth of the Cgfab1DELTA mutant is also slightly impaired in the presence of the oxidative stressor, hydrogen peroxide, and at high temperature. MDR genes are activated in the Cgfab1DELTA mutant upon fluconazole exposure
