Magic™ Anti-hCG monoclonal antibody, clone N29723ID2

Chlorogenic acids (CGAs) and the biopolymer lignin are both products of the phenylpropanoid pathway. Whereas CGAs have been reported to play a role during stress responses, lignin is a major component of secondary cell walls, providing physical strength and hydrophobicity to supportive and water-conducting tissues. Because the chemical structure of CGAs largely resembles those of some lignin intermediates and because CGAs can be converted back to hydroxycinnamoyl-CoAs in vitro, CGAs have been considered authentic intermediates of the lignin biosynthetic pathway. However, it is still unclear whether and how the CGA pool can be channeled towards the production of lignin monomers in response to developmental or environmental signals. Comprehensive studies on the catalytic activity of recombinant enzymes together with functional characterizations in planta have been very useful in understanding the potential interdependence between these two metabolic routes. Here we present the current understanding on CGA metabolism and discuss the biochemical and molecular evidence of the metabolic re-routing of CGAs towards lignin.

Malnutrition is one of the factors that induces reproductive disorders. However, the underlying biological processes are unclear. AMP-activated protein kinase (AMPK) is an enzyme that plays crucial role as a cellular energy sensor. In the present study, we examined the effects of AMPK activation on the transcription of the murine gonadotropin subunit genes Cga, Lhb, and Fshb, and the gonadotropin-releasing hormone receptor Gnrh-r. Real-time PCR and transcription assay using L beta T2 cells demonstrated that 5-amino-imidazole carboxamide riboside (AICAR), a cell-permeable AMP analog, repressed the expression of Lhb. Next, we examined deletion mutants of the upstream region of Lhb and found that the upstream regulatory region of Lhb (-2527 to -2198 b) was responsible for the repression by AICAR. Furthermore, putative transcription factors (SP1, STAT5a, and TEF) that might mediate transcriptional control of the Lhb repression induced by AICAR were identified. In addition, it was confirmed that both AICAR and a competitive inhibitor of glucose metabolism, 2-deoxy-D-glucose, induced AMPK phosphorylation in L beta T2 cells. Therefore, the upstream region of Lhb is one of the target sites for glucoprivation inducing AMPK activation. In addition, AMPK plays a role in repressing Lhb expression through the distal -2527 to -2198 b region.