phosphatidylinositol-4-phosphate has been researched along with Schizophrenia* in 2 studies
1 review(s) available for phosphatidylinositol-4-phosphate and Schizophrenia
| Article | Year |
|---|---|
The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection.
The discovery that apolipoprotein L1 (APOL1) is the trypanolytic factor of human serum raised interest about the function of APOLs, especially following the unexpected finding that in addition to their protective action against sleeping sickness, APOL1 C-terminal variants also cause kidney disease. Based on the analysis of the structure and trypanolytic activity of APOL1, it was proposed that APOLs could function as ion channels of intracellular membranes and be involved in mechanisms triggering programmed cell death. In this review, the recent finding that APOL1 and APOL3 inversely control the synthesis of phosphatidylinositol-4-phosphate (PI(4)P) by the Golgi PI(4)-kinase IIIB (PI4KB) is commented. APOL3 promotes Ca Topics: Actomyosin; Animals; Apolipoprotein L1; Apolipoproteins L; Autistic Disorder; Autophagosomes; Calcium; Gene Expression Regulation; Golgi Apparatus; Humans; Neoplasms; Phosphatidylinositol Phosphates; Phosphotransferases (Alcohol Group Acceptor); Renal Insufficiency; Schizophrenia; Trypanosomiasis, African; Virus Diseases | 2021 |
1 trial(s) available for phosphatidylinositol-4-phosphate and Schizophrenia
| Article | Year |
|---|---|
Phosphoinositide signalling system in platelets of schizophrenic patients and the effect of neuroleptic therapy.
Alterations in the phosphoinositide signalling system have been proposed as a possible biological marker of schizophrenia. We studied the levels of inositol 1,4,5-trisphosphate (IP3), cytosolic Ca2+ concentrations ([Ca2+]i), and the incorporation of [32P]-orthophosphate into inositol phospholipids and phosphatidic acid (PA) in blood platelets of neuroleptic-treated schizophrenics in comparison with controls. The [Ca2+]i was significantly higher in platelets of one month neuroleptic-treated patients (155+/-5.8 nM) in comparison with controls (95+/-5.4 nM). Neuroleptic therapy decreased the [Ca2+]i, but even after long-term therapy it remained significantly higher (114+/-5.7 nM) than in controls. Differences were also found in the level of IP3 between controls (30+/-4.0 pmol/10(9) platelets), drug-free schizophrenics (52+/-9.0 pmol/10(9) platelets) and treated patients (50+/-6.0 pmol/10(9) platelets). The increased turnover of PA was observed in platelets of neuroleptic-treated schizophrenic patients. The study suggests that the regulation of calcium homeostasis and pathways involved in the phosphoinositide signalling system are altered in the platelets of schizophrenics. Neuroleptic therapy did not remove the observed changes in [Ca2+]i and IP3 levels. Topics: Adolescent; Adult; Antipsychotic Agents; Blood Platelets; Calcium; Female; Humans; Inositol 1,4,5-Trisphosphate; Male; Middle Aged; Phosphatidic Acids; Phosphatidylinositol 4,5-Diphosphate; Phosphatidylinositol Phosphates; Phosphatidylinositols; Phosphorus Radioisotopes; Schizophrenia; Signal Transduction; Time Factors | 1999 |