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esults show that Aichi virus 3A protein activates the lipid kinase activity of PI4KIIIb,which activation is sensitized by the protein ACBD3 (显示 Acbd3 ELISA试剂盒). The interfaces between PI4KIIIbeta-ACBD3 (显示 Acbd3 ELISA试剂盒) and ACBD3 (显示 Acbd3 ELISA试剂盒)-3A were mapped with hydrogen-deuterium exchange mass spectrometry.
The results showed that, in contrast to the enteroviruses and the cardioviruses, foot-and-mouth disease virus replication does not require PI4KIII (PI4KIIIalpha and PI4KIIIbeta), and phosphatidylinositol 4-phosphate levels do not increase in foot-and-mouth disease virus-infected cells and phosphatidylinositol 4-phosphate is not seen at replication organelles.
Data show that ACBD3 (显示 Acbd3 ELISA试剂盒) can recruit PI4KB to model membranes as well as redirect PI4KB to cellular membranes where it is not naturally found. Also, results show that ACBD3 (显示 Acbd3 ELISA试剂盒) regulates the enzymatic activity of PI4KB kinase through membrane recruitment rather than allostery.
Analysis reveals novel aspects of the PI4KIIIb-Rab11 complex and determines binding and catalytic sites of the kinase.
PI4KIIIbeta likely plays a role in breast oncogenesis and that cooperation between Rab11a (显示 RAB11A ELISA试剂盒) and PI4KIIIbeta represents a novel Akt (显示 AKT1 ELISA试剂盒) activation pathway.
Although human rhinovirus 3A protein was previously shown to interact with ACBD3 (显示 Acbd3 ELISA试剂盒), these data suggest that PI4KIIIbeta recruitment occurred independently of both GBF1 (显示 GBF1 ELISA试剂盒) and ACBD3 (显示 Acbd3 ELISA试剂盒).
Authors found that NS5A and PI4KB competed for association of acyl-coenzyme A (显示 SOAT2 ELISA试剂盒) binding domain containing protein 3 (显示 HSPB3 ELISA试剂盒) (ACBD3 (显示 Acbd3 ELISA试剂盒)), which inhibited hepatitis C virus replication.
These results suggest that poliovirus proteins modulate PI4KB activity and provide PI4P for recruitment of OSBP (显示 OSBP ELISA试剂盒) to accumulate unesterified cholesterol on virus-induced membrane structure for formation of a virus replication complex.
Host ACBD3 (显示 Acbd3 ELISA试剂盒), PI4KIIIBETA and Aichi virus proteins complexes enhances phosphatidylinositol 4-phosphate synthesis and is critical for viral replication.
these data provide a mechanism for how PI4KIIIbeta coordinates Rab11 (显示 RAB11A ELISA试剂盒) and its effectors on PI4P-enriched membranes and also provide strategies for the design of specific inhibitors that could potentially target plasmodial PI4KIIIbeta to combat malaria.
findings reveal a novel signalling pathway involved in development of the semicircular canal system, and suggest a previously unrecognized role for NCS-1 (显示 NCS1 ELISA试剂盒) in mitochondrial function via its association with several mitochondrial proteins.
Depolarization increases phosphatidylinositol (PI) 4,5-bisphosphate level and KCNQ currents through PI 4-kinase mechanisms
Phosphorylates phosphatidylinositol (PI) in the first committed step in the production of the second messenger inositol- 1,4,5,-trisphosphate (PIP) (By similarity).
phosphatidylinositol 4-kinase, catalytic, beta polypeptide
, phosphatidylinositol 4-kinase, catalytic, beta
, phosphatidylinositol 4-kinase beta
, PtdIns 4-kinase beta
, phosphatidylinositol 4-kinase beta-like
, phosphatidylinositol 4-kinase, wortmannin-sensitive
, type III phosphatidylinositol 4-kinase beta
, catalytic phosphatidylinositol 4-kinase beta
, ptdIns 4-kinase beta
, phosphatidylinositol 4-kinase III beta