214383_Ch21
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Fig. 21.1 (a) The proposed model for the role of DAG-activated Ca 2+ influx mediated by TRPC3 in BCR signaling. (b) DAG-activated TRPC3 is essential for Ang II-induced NFAT activation and cardiac hypertrophy. Activation of TRPC3 causes cation influx responsible for depolarization of membrane potentials to a positive direction (Δψ) and concomitantly increases the frequency of spontaneous firing due to activation of voltage-dependent Ca 2+ channel (VDCC) Transient Receptor Potential Channels, Md. Shahidul Islam (Ed.) ISBN: 978-94-007-0264-6, Springer
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Fig. 21.1 (a) The proposed model for the role of DAG-activated Ca2+ influx mediated by TRPC3 in BCR signaling. (b) DAG-activated TRPC3 is essential for Ang II-induced NFAT activation and cardiac hypertrophy. Activation of TRPC3 causes cation influx responsible for depolarization of membrane potentials to a positive direction (Δψ) and concomitantly increases the frequency of spontaneous firing due to activation of voltage-dependent Ca2+ channel (VDCC)
Transient Receptor Potential Channels, Md. Shahidul Islam (Ed.)ISBN: 978-94-007-0264-6, Springer
Fig. 21.2 Proposed model for TRPC5-mediated feedback cycle of receptor-activated Ca2+ and NO signaling in caveolae of endothelial cells
Transient Receptor Potential Channels, Md. Shahidul Islam (Ed.)ISBN: 978-94-007-0264-6, Springer
Fig. 21.3 A key role of the TRPM2 on H2O2-induced chemokine production in monocytes and macrophages
Transient Receptor Potential Channels, Md. Shahidul Islam (Ed.)ISBN: 978-94-007-0264-6, Springer
