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Last Updated: 3 years ago

Possible Interaction: Bradykinin and Phosphatidylinositol 4,5-Diphosphate

Research Papers that Mention the Interaction

In conclusion, bradykinin inhibits TREK-2 channels through the activation of B2Rs resulting in PIP2 depletion, much like we have demonstrated for muscarinic agonists.
International journal of molecular sciences  •  2020  |  View Paper
Bradykinin promotes phosphatidylinositol 4,5-bisphosphate ( PIP2 ) hydrolysis by PLC and translocation of various PKC isoforms from the cytosolic fraction to the particulate fraction.
British Journal of Cancer  •  2003  |  View Paper
In ventricular myocytes cultured from neonatal rat hearts, bradykinin (BK), kallidin or BK(1-8) [(Des-Arg9)BK] stimulated PtdinsP2 hydrolysis by 3-4-fold.
Thus, like hypertrophic agents such as endothelin-1 (ET-1) and phenylephrine (PE), BK activates PtdInsP2 hydrolysis, translocates nPKC-delta, and nPKC-epsilon, and activates p42/p44-MAPK.
The Biochemical journal  •  1996  |  View Paper
In neuroblastoma x glioma hybrid cells (NG 108-15) labelled with [32P]-trisodium phosphate, [3H]-inositol and [14C]-arachidonic acid, bradykinin stimulated the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) while it had no effect on the release of [14C]-arachidonic acid (AA).
Cellular signalling  •  1989  |  View Paper
At 37 degrees C, bradykinin induced a rapid rise in lysophosphatidylinositol (lyso-PI) and inositol 1,4,5-trisphosphate (IP3) as well as a decrease in PIP2.
The Journal of biological chemistry  •  1989  |  View Paper
We conclude that bradykinin stimulates PLC hydrolysis of PIP2 with rapid release of IP3 in sufficient amount to account for the increase in cytosolic Ca++.
Biochemical and biophysical research communications  •  1986  |  View Paper
These observations are consistent with the model that bradykinin induces hydrolysis of phosphatidylinositol 4,5-bisphosphate which precedes hydrolysis of phosphatidylinositol in renal papillary collecting tubule cells.
Biochimica et biophysica acta  •  1986  |  View Paper
A mathematical model of phosphoinositide turnover based on this data predicted that PIP2 synthesis is also stimulated by bradykinin , causing an early transient increase in its concentration.
The Journal of cell biology  •  2003  |  View Paper
Treatment of F‐11 cells with bradykinin (BK) stimulated the hydrolysis of a different polyphosphoinositide, PtdIns(4,5)P2 , and enhanced both wortmannin‐induced caspase‐3 (CPP32) activation and subsequent apoptosis.
Journal of neuroscience research  •  2000  |  View Paper
Bradykinin , but not angiotensin, caused a rapid (within 2 s) fall in the levels of PtdIns(4,5)P2 and PtdIns(4)P. Serum pretreatment of the cells caused a 2-3-fold potentiation of both the responses to bradykinin and angiotensin.
The Biochemical journal  •  1990  |  View Paper
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