ArticleCell communication and signaling : CCS2026
Bone morphogenetic protein receptor 2 signaling mediates mitochondrial Ca
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundBone morphogenetic proteins (BMPs) are highly conserved multifunctional signaling proteins with pleotropic effects throughout embryonic development. BMPs are aberrantly expressed in many diseases including cancer and Alzheimer's disease. Recent studies suggested that BMP signaling negatively regulates mitochondrial bioenergetics. The mechanisms by which BMP signaling regulates bioenergetics and cell survival are not known.
methodsWe utilized BMP type 2 receptor (BMPR2) inhibitor (JL189), BMPR2 kinase domain KO, BMPR2 siRNA, and BMP loss of function mutants in C. elegans to inhibit BMP signaling (BMPR2i). The effects of BMPR2i on mitochondrial bioenergetics were examined by measuring differences in TCA cycle intermediates (mass spectrometer), mitochondrial respiration (Agilent Seahorse), and mitochondrial mass (MitoTracker Green/TFAM). Fluorescent mitochondrial Ca
resultsBMPR2i increased mitochondrial Ca
conclusionThese studies reveal that BMPR2 signaling regulates TAK1-d splice variant to mediate mitochondrial Ca
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