Now, researchers have found that GUN1 -- a gene that integrates numerous chloroplast-to-nucleus retrograde signaling pathways -- also plays an important role in how proteins are made in damaged chloroplasts, which provides a new insight into how plants respond to stress.
Now, Salk Institute researchers have found that GUN1 -- a gene that integrates numerous chloroplast-to-nucleus retrograde signaling pathways -- also plays an important role in how proteins are made in damaged chloroplasts, which provides a new insight into how plants respond to stress.
The fourth breakthrough, which is functionally most important, is the discovery that endocannabinoids mediate retrograde signaling at synapses.
(45)) Because DSI requires postsynaptic [Ca.sup.2+] elevation and causes suppression of transmitter release from presynaptic terminals, some mechanisms of "retrograde signaling" were thought to exist.
C) FOR CHRONIC CASES-LTP (LONG TERM POTENTIATION) The endocannabinoids anandamide and 2-AG are the primary retrograde messengers in the brain and may also play an important role in
retrograde signaling in long-term-potentiation (LTP), meant for memory and learning (12,13,14,15, 16,17,18,19,20,21,22,23, 24) as is nitric-oxide.
al., "The IRA-induced up regulation of MMP-1 was different from that induced by UV at the mechanistic level, since it involves the formation of mitochondrial reactive oxygen species (RCVS) and the subsequent initiation of a
retrograde signaling response (i.e.
This book highlights recent work on cell adhesion, the binding of one cell to another cell or to a surface or matrix, and looks at the role of cell adhesion in mitochondrial
retrograde signaling, a recently discovered mammalian cellular signaling pathway that might be activated by radiation.
Can a synaptic mark at distal synapses persist long enough to allow
retrograde signaling from the synapse to the soma, followed by anterograde signaling back to the synapse?
Endocannabinoids mediate
retrograde signaling at synapses in the brain by diffusing from postsynaptic sites of synthesis to act on presynaptic [CB.sub.1] receptors, which results in an inhibition of "classical" neurotransmitter release (7, 8, 9, 10, 11, 12).