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1 sitides phosphatidylinositol 4-phosphate and phosphatidylinositol 5-phosphate.
5 n wild-type littermates, female mice lacking phosphatidylinositol 5-phosphate 4-kinase beta have incr
10 hanistically, C24-Ceramide directly bound to phosphatidylinositol 5-phosphate 4-kinase type-2 gamma (
11 pe II phosphatidylinositol-phosphate kinase (phosphatidylinositol 5-phosphate 4-kinase) also inhibite
13 alpha-granule secretion involves the type II phosphatidylinositol 5-phosphate 4-kinase-dependent path
14 r role in many important signaling pathways, phosphatidylinositol 5-phosphate 4-kinases (PI5P4Ks) are
15 e in regulating cell signaling pathways, the phosphatidylinositol 5-phosphate 4-kinases (PI5P4Ks) are
20 w that mice with germline deletion of type 2 phosphatidylinositol-5-phosphate 4-kinase gamma (Pip4k2c
21 2 or decreased cellular PIP2 by knockdown of phosphatidylinositol-5-phosphate 4-kinase impaired apoA1
24 st cancers express high levels of the type 2 phosphatidylinositol-5-phosphate 4-kinases alpha and/or
25 by PIP5K1A, PIP5K1B and PIP5K1C, and type 2 phosphatidylinositol-5-phosphate 4-kinases, encoded by P
26 tide phosphatases, PLIP has a preference for phosphatidylinositol 5-phosphate, a newly discovered pho
27 Apoptotic body-like liposomes loaded with phosphatidylinositol 5-phosphate (ABL/PI5P) were tested
28 ated disruption of the extracellular matrix, phosphatidylinositol 5 phosphate binding, and roundabout
29 The mutant reduces catalytic activity toward phosphatidylinositol 5-phosphate by approximately 50-fol
30 )P(3)) >> phosphatidylinositol 3-phosphate > phosphatidylinositol 5-phosphate >> other phosphoinositi
31 involved in elevating the cellular level of phosphatidylinositol 5-phosphate in response to dehydrat
32 tase (PLIP) exhibits a unique preference for phosphatidylinositol 5-phosphate (PI(5)P) as a substrate
33 4-phosphate (PI(4)P), but much less by d-myo-phosphatidylinositol-5-phosphate (PI(5)P) or d-myo-phosp
36 t al. (2014) identify the signaling molecule phosphatidylinositol 5-phosphate (PI5P) as an allosteric
37 the cellular content of its substrate lipid phosphatidylinositol 5-phosphate (PI5P), suggesting that
38 ipid kinase that catalyzes the conversion of phosphatidylinositol-5-phosphate (PI5P) into phosphatidy
42 scovered phosphatidylinositol monophosphate, phosphatidylinositol 5-phosphate (PtdIns-5-P), plays an
43 nositol-3,5-bisphosphate (PtdIns-3,5-P2) and phosphatidylinositol- 5-phosphate (PtdIns-5-P), have bee
44 on of ING2 with the nuclear phosphoinositide phosphatidylinositol-5-phosphate (PtdIns(5)P) regulates
49 en consumption and promotes the synthesis of phosphatidylinositol-5-phosphate (PtdIns5P), which trigg
51 alpha (PIP4K2A) regulates cellular levels of phosphatidylinositol-5-phosphate (PtsIns5P) and phosphat
52 proteins is not allosterically regulated by phosphatidylinositol 5-phosphate that interacts with a s
53 atidylinositol 5-phosphate 4-kinases convert phosphatidylinositol 5-phosphate to phosphatidylinositol
54 sitol-5-phosphate 4-kinase (PI5P4K) converts phosphatidylinositol-5-phosphate to phosphatidylinositol
55 ain enzyme responsible for the production of phosphatidylinositol 5-phosphate, which in turn fuels PI
56 atase in complex with a surrogate substrate, phosphatidylinositol 5-phosphate, which sheds light on t