Put simply, it claims that signalling factors are exported from the chloroplast, traverse the cytosol, and act in the nucleus. Pertinent signals are thought to derive from various sources, including
the tetrapyrrole pathway, protein synthesis, reactive oxygen species, or the redox state of the organelle. Recent studies have cast doubt on the most popular candidate signalling molecule, the tetrapyrrole pathway intermediate Mg-protoporphyrin IX, indicating that chloroplast activity might control NGE indirectly by affecting cytosolic metabolite levels or redox states (metabolic signalling). Here, we focus on recent developments and confusions in the field of plastid signalling ICG-001 research and highlight alternative scenarios of plastid-nucleus signal transduction.
Future analyses of chloroplast-nucleus communication should focus on providing Belnacasan chemical structure an integrated view of plastid signalling under physiologically relevant conditions.”
“Rationale Tumor necrosis factor-alpha (TNF alpha) acts within the brain to induce sickness behavior, but the molecular mechanisms are still unknown. TNF alpha binding induces receptor trimerization, activation of c-Jun N-terminal kinase (JNK), and induction of downstream transcription factors.
Objectives We hypothesized that TNF alpha-induced sickness behavior can be blocked by a novel JNK inhibitor.
Methods To test this idea, we used a bipartite protein consisting of a ten-amino-acid sequence of the trans-activating domain of the viral TAT protein 17-DMAG (Alvespimycin) HCl (D-TAT) linked to a 19-amino-acid peptide that specifically inhibits JNK activation (D-JNKI-1). C57BL/6J mice were pre-treated intracerebroventricularly (i.c.v.) with D-JNKI-1 or the control peptide containing only the protein transduction domain, D-TAT.
Mice were then injected centrally with an optimal amount of TNF alpha (50 ng/mouse) to induce sickness behavior. Sickness was assessed as a decrease in social exploration of a novel juvenile, an increase in duration of immobility and loss of body weight.
Results Pre-treatment with D-JNKI-1 (10 ng/mouse), but not D-TAT, significantly inhibited all three indices of sickness induced by central TNF alpha.
Conclusions These findings demonstrate that D-JNKI-1 can abrogate TNF alpha-induced sickness behavior and suggest a potential therapeutic target for treating major depressive disorders that develop on a background of cytokine-induced sickness behavior.”
“The maintenance of a stable temperature is of the utmost importance for the proper functioning of the brain. Brain temperature is tightly linked to mitochondrial energetics. Although Parkinson’s disease is characterized by mitochondrial dysfunction, no data are available on brain temperature.